Breast cancer with Hashimoto’s thyroiditis (BC-HT) presents a unique immuno-thyroid interplay that remains poorly understood. This study investigates the relationships between thyroid function markers (TSH, T3, T4), immune markers (CD33, CD44), and thyroid autoantibodies (Anti-TPO, Anti-Tg) in BC-HT patients and healthy controls. Normality testing confirmed non-parametric data distribution, necessitating Mann-Whitney U tests for group comparisons. BC-HT patients exhibited significantly elevated TSH, CD33, Anti-TPO, and Anti-Tg levels, alongside reduced T3 and T4, compared to controls, indicating thyroid dysfunction. Spearman’s correlation analysis revealed strong negative correlations between TSH and T3/T4 in controls, which were lost in BC-HT, suggesting disruption of normal thyroid feedback mechanisms. Additionally, CD33 and CD44 correlations with thyroid hormones were evident in controls but absent in BC-HT, highlighting altered immune-thyroid interactions. ROC analysis demonstrated high diagnostic performance for TSH, Anti-Tg, and Anti-TPO, with sensitivities exceeding 0.75, whereas CD33 and CD44 showed limited diagnostic utility. These findings suggest a distinct immuno-thyroid dysregulation in BC-HT patients and highlight the potential of thyroid-specific markers for disease stratification. Future research should focus on longitudinal studies and mechanistic investigations to further delineate the role of immune markers in breast cancer pathophysiology within the context of thyroid autoimmunity.
{"title":"Investigating the clinical significance of immune and thyroid biomarkers in women with breast cancer and Hashimoto's thyroiditis","authors":"Israa Khalaf Aneed , Noori Mohammed Luaibi , Sajid Nader Abdulqader","doi":"10.1016/j.repbio.2025.101011","DOIUrl":"10.1016/j.repbio.2025.101011","url":null,"abstract":"<div><div>Breast cancer with Hashimoto’s thyroiditis (BC-HT) presents a unique immuno-thyroid interplay that remains poorly understood. This study investigates the relationships between thyroid function markers (TSH, T3, T4), immune markers (CD33, CD44), and thyroid autoantibodies (Anti-TPO, Anti-Tg) in BC-HT patients and healthy controls. Normality testing confirmed non-parametric data distribution, necessitating Mann-Whitney <em>U</em> tests for group comparisons. BC-HT patients exhibited significantly elevated TSH, CD33, Anti-TPO, and Anti-Tg levels, alongside reduced T3 and T4, compared to controls, indicating thyroid dysfunction. Spearman’s correlation analysis revealed strong negative correlations between TSH and T3/T4 in controls, which were lost in BC-HT, suggesting disruption of normal thyroid feedback mechanisms. Additionally, CD33 and CD44 correlations with thyroid hormones were evident in controls but absent in BC-HT, highlighting altered immune-thyroid interactions. ROC analysis demonstrated high diagnostic performance for TSH, Anti-Tg, and Anti-TPO, with sensitivities exceeding 0.75, whereas CD33 and CD44 showed limited diagnostic utility. These findings suggest a distinct immuno-thyroid dysregulation in BC-HT patients and highlight the potential of thyroid-specific markers for disease stratification. Future research should focus on longitudinal studies and mechanistic investigations to further delineate the role of immune markers in breast cancer pathophysiology within the context of thyroid autoimmunity.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101011"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143820838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-03-27DOI: 10.1016/j.repbio.2025.101013
Anna Monallysa Silva de Oliveira , Nívia Maria Rocha Brandão , Anailson De Oliveira Maciel , Nágylla Santos De Almeida , Nayonara Santos De Almeida , Thiago Santos Santos , Izakiel Reis Marinho , Francisco Cardoso Figueiredo , Yndyra Nayan Teixeira Carvalho Castelo Branco , José Adalmir Torres de Souza
The objective was to evaluate the effects of different concentrations of hydroxypropylmethylcellulose (HPMC) on the cryopreservation of bovine semen. Semen was collected from seven bulls by electroejaculation and diluted in Tris-egg yolk medium with and without glycerol (G) in the following treatments: C: Tris-Egg Yolk + 6 %G; T1: Tris-Egg Yolk + 3 % G; T2: Tris-Egg Yolk + 0 % G; T3: Tris-Egg Yolk + 0.5 % HPMC; T4: Tris-Egg Yolk + 1.0 % HPMC; T5: Tris-Egg Yolk + 1.5 % HPMC; T6: Tris-Egg Yolk + 5.5 % G + 0.5 % HPMC. Samples were frozen and stored at −196°C. After thawing, sperm quality was assessed using the rapid thermoresistance test (RTRT), sperm morphology, hypoosmotic swelling test, plasma membrane integrity, mitochondrial activity, and in vitro fertilization (IVF) test. RTRT results showed that the control group had better motility and vigor at 0’, 15’, and 30’ compared to the T6 group. The T6 group had better results than other groups supplemented with 0.5 %, 1.0 %, and 1.5 % HPMC. No significant differences were observed at 45’ for RTRT, hypoosmotic swelling, morphology, membrane integrity, mitochondrial activity, or IVF rates. In conclusion, the addition of HPMC reduced sperm motility and vigor but did not negatively affect other cryopreservation parameters.
目的是评价不同浓度羟丙基甲基纤维素(HPMC)对牛精液冷冻保存的影响。采用电射精法采集7头公牛的精液,在添加和不添加甘油(G)的tris -卵黄培养基中稀释,处理如下:C: tris -卵黄+ 6 %G;T1: Tris-Egg yellow + 3 % G;T2: Tris-Egg yellow + 0 % G;T3: tris -蛋黄+ 0.5 % HPMC;T4: tris -蛋黄+ 1.0 % HPMC;T5: tris -蛋黄+ 1.5 % HPMC;T6: tris -蛋黄+ 5.5 % G + 0.5 % HPMC。样品冷冻保存于- 196°C。解冻后,通过快速耐热性试验(RTRT)、精子形态、低渗肿胀试验、质膜完整性、线粒体活性和体外受精(IVF)试验评估精子质量。RTRT结果显示,与T6组相比,对照组在0 ‘,15 ’和30 '时具有更好的运动性和活力。T6组效果优于添加0.5 %、1.0 %、1.5 % HPMC组。在45 '时,RTRT、低渗肿胀、形态学、膜完整性、线粒体活性或体外受精率均无显著差异。总之,HPMC的加入降低了精子活力和活力,但对其他低温保存参数没有负面影响。
{"title":"Evaluation of the quality of bovine semen subjected to cryopreservation with hydroxypropylmethylcellulose","authors":"Anna Monallysa Silva de Oliveira , Nívia Maria Rocha Brandão , Anailson De Oliveira Maciel , Nágylla Santos De Almeida , Nayonara Santos De Almeida , Thiago Santos Santos , Izakiel Reis Marinho , Francisco Cardoso Figueiredo , Yndyra Nayan Teixeira Carvalho Castelo Branco , José Adalmir Torres de Souza","doi":"10.1016/j.repbio.2025.101013","DOIUrl":"10.1016/j.repbio.2025.101013","url":null,"abstract":"<div><div>The objective was to evaluate the effects of different concentrations of hydroxypropylmethylcellulose (HPMC) on the cryopreservation of bovine semen. Semen was collected from seven bulls by electroejaculation and diluted in Tris-egg yolk medium with and without glycerol (G) in the following treatments: C: Tris-Egg Yolk + 6 %G; T1: Tris-Egg Yolk + 3 % G; T2: Tris-Egg Yolk + 0 % G; T3: Tris-Egg Yolk + 0.5 % HPMC; T4: Tris-Egg Yolk + 1.0 % HPMC; T5: Tris-Egg Yolk + 1.5 % HPMC; T6: Tris-Egg Yolk + 5.5 % G + 0.5 % HPMC. Samples were frozen and stored at −196°C. After thawing, sperm quality was assessed using the rapid thermoresistance test (RTRT), sperm morphology, hypoosmotic swelling test, plasma membrane integrity, mitochondrial activity, and in vitro fertilization (IVF) test. RTRT results showed that the control group had better motility and vigor at 0’, 15’, and 30’ compared to the T6 group. The T6 group had better results than other groups supplemented with 0.5 %, 1.0 %, and 1.5 % HPMC. No significant differences were observed at 45’ for RTRT, hypoosmotic swelling, morphology, membrane integrity, mitochondrial activity, or IVF rates. In conclusion, the addition of HPMC reduced sperm motility and vigor but did not negatively affect other cryopreservation parameters.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101013"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-03-24DOI: 10.1016/j.repbio.2025.101010
Qin Yao, Yuejuan Zhang, Qizhi Yan, Junhui Qian
Endometritis is an infectious disease of the female reproductive system and commonly treated with antibiotics. However, the high resistance rates to antibiotics necessitate the urgent research for new and effective therapeutic strategies. The aim of this research is to explore the effect of fucoxanthin (FX) on endometritis through in vitro and in vivo assays. The effect of FX on inflammation was first explored in vitro using LPS-induced bovine endometrial epithelial (BEND) cell injury model. After the anti-inflammation effect of FX was confirmed in vitro, the effect of FX on endometritis was investigated in vivo using LPS-induced mice model. The female mice were randomly assigned into control, control + FX, LPS, and LPS + FX (100, 200 mg/kg) groups. The histological features of the uterus and expression levels of NF-κBp65 and inflammatory mediators (COX-2, iNOS, IL-1β, IL-6, and TNF-α) in the uterine tissue were compared among the animal groups. Our in vitro results showed that LPS induced BEND cell damage while significantly enhancing the expression of NF-κBp65 and inflammatory mediators (COX-2, iNOS, IL-1β, IL-6, and TNF-α). Nevertheless, pretreatment with FX reversed the abnormal phenomena caused by LPS. In vivo, LPS treatment resulted in obvious histopathological uterus damages, which were alleviated by FX treatment. Consistent with the in vitro assay, FX treatment also inhibited the expression of NF-κBp65 and inflammatory mediators in the animal experiments. Our study implies that FX is a potential therapeutic agent for endometritis. The beneficial function of FX on endometritis was achieved by inhibiting the inflammatory factors through the NF-κB pathway.
{"title":"Fucoxanthin attenuates LPS-induced endometritis via inhibiting inflammatory factors through the NF-κB pathway","authors":"Qin Yao, Yuejuan Zhang, Qizhi Yan, Junhui Qian","doi":"10.1016/j.repbio.2025.101010","DOIUrl":"10.1016/j.repbio.2025.101010","url":null,"abstract":"<div><div>Endometritis is an infectious disease of the female reproductive system and commonly treated with antibiotics. However, the high resistance rates to antibiotics necessitate the urgent research for new and effective therapeutic strategies. The aim of this research is to explore the effect of fucoxanthin (FX) on endometritis through in vitro and in vivo assays. The effect of FX on inflammation was first explored in vitro using LPS-induced bovine endometrial epithelial (BEND) cell injury model. After the anti-inflammation effect of FX was confirmed in vitro, the effect of FX on endometritis was investigated in vivo using LPS-induced mice model. The female mice were randomly assigned into control, control + FX, LPS, and LPS + FX (100, 200 mg/kg) groups. The histological features of the uterus and expression levels of NF-κBp65 and inflammatory mediators (COX-2, iNOS, IL-1β, IL-6, and TNF-α) in the uterine tissue were compared among the animal groups. Our in vitro results showed that LPS induced BEND cell damage while significantly enhancing the expression of NF-κBp65 and inflammatory mediators (COX-2, iNOS, IL-1β, IL-6, and TNF-α). Nevertheless, pretreatment with FX reversed the abnormal phenomena caused by LPS. In vivo, LPS treatment resulted in obvious histopathological uterus damages, which were alleviated by FX treatment. Consistent with the in vitro assay, FX treatment also inhibited the expression of NF-κBp65 and inflammatory mediators in the animal experiments. Our study implies that FX is a potential therapeutic agent for endometritis. The beneficial function of FX on endometritis was achieved by inhibiting the inflammatory factors through the NF-κB pathway.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101010"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-24DOI: 10.1016/j.repbio.2025.101027
Habit Medina , Alejandra Flores , Lizbeth Juárez-Rojas , Fahiel Casillas , Mohammad Mehdi Ommati , Reza Heidari , Sara Vázquez , Denise Clavijo-Cornejo , Sheila Peña-Corona , Socorro Retana-Márquez
Currently, stress is considered one of the risk factors for infertility in male humans, altering sperm function. Sperm production and maturation depends on the hypothalamic-pituitary-testis axis control. Therefore, the objective of the current study was to evaluate the effects of chronic stress on the neuroendocrine control of male reproduction, the oxidative status in the epididymis, and male fertility. Adult male rats were assigned to control or chronic stress groups. Chronically stressed males were exposed to cold-water immersion (CWI) for 50 consecutive days. After euthanasia, the hypothalamus was dissected for Kisspeptin (Kiss1) and Gonadotropin releasing hormone (GnRH) evaluation; serum luteinizing hormone (LH), testosterone (T), and corticosterone concentrations were determined. In the epididymis, reactive oxygen species (ROS), lipid peroxides, and content of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx4) were assessed. Sperm motility, viability, concentration, morphology and acrosomal reaction were assessed. Epididymal sperm were used for in-vitro fertilization with oocytes from intact female rats. Stressed males showed lower hypothalamic Kiss1 and GnRH content, lower LH and T concentration, together with higher serum corticosterone concentration. ROS production, and lipid peroxides increased in all epididymal regions, while SOD, CAT, and GPx4 content decreased after chronic stress; sperm quality was also lower. The percentage of fertilized oocytes decreased, and embryonic development was low, compared to controls. Together, these results show that chronic stress disrupts neuroendocrine control of male reproduction and generates oxidative stress in the epididymis. These effects disturb sperm quality, leading to low fertilizing potential and poor embryonic development.
{"title":"Chronic stress disturbs neuroendocrine control of reproduction and fertility in male rats","authors":"Habit Medina , Alejandra Flores , Lizbeth Juárez-Rojas , Fahiel Casillas , Mohammad Mehdi Ommati , Reza Heidari , Sara Vázquez , Denise Clavijo-Cornejo , Sheila Peña-Corona , Socorro Retana-Márquez","doi":"10.1016/j.repbio.2025.101027","DOIUrl":"10.1016/j.repbio.2025.101027","url":null,"abstract":"<div><div>Currently, stress is considered one of the risk factors for infertility in male humans, altering sperm function. Sperm production and maturation depends on the hypothalamic-pituitary-testis axis control. Therefore, the objective of the current study was to evaluate the effects of chronic stress on the neuroendocrine control of male reproduction, the oxidative status in the epididymis, and male fertility. Adult male rats were assigned to control or chronic stress groups. Chronically stressed males were exposed to cold-water immersion (CWI) for 50 consecutive days. After euthanasia, the hypothalamus was dissected for Kisspeptin (Kiss1) and Gonadotropin releasing hormone (GnRH) evaluation; serum luteinizing hormone (LH), testosterone (T), and corticosterone concentrations were determined. In the epididymis, reactive oxygen species (ROS), lipid peroxides, and content of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx4) were assessed. Sperm motility, viability, concentration, morphology and acrosomal reaction were assessed. Epididymal sperm were used for in-vitro fertilization with oocytes from intact female rats. Stressed males showed lower hypothalamic Kiss1 and GnRH content, lower LH and T concentration, together with higher serum corticosterone concentration. ROS production, and lipid peroxides increased in all epididymal regions, while SOD, CAT, and GPx4 content decreased after chronic stress; sperm quality was also lower. The percentage of fertilized oocytes decreased, and embryonic development was low, compared to controls. Together, these results show that chronic stress disrupts neuroendocrine control of male reproduction and generates oxidative stress in the epididymis. These effects disturb sperm quality, leading to low fertilizing potential and poor embryonic development.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 3","pages":"Article 101027"},"PeriodicalIF":2.5,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-28DOI: 10.1016/j.repbio.2025.101023
Haoyu Yang , Cancan Wang , Wenxuan Li , Xin Su , Mengyuan Li , Qian Li , Xiang-Hong Xu , Liping Jin
Decidualization is a multistep and complex physiological process used to aid the development of an implanting embryo. To date, the potential genes regulating decidualization have not been elucidated. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) is widely used in gene expression studies, with relative quantification being the predominant method due to its simplicity, cost-effectiveness, and lower sample requirements. This method determines gene expression levels by normalizing to reference genes. However, the selection of stable reference genes for studies on decidualization remains a challenge. Based on the RNA-seq dataset from human endometrial stromal cells (ESCs) and differentiated ESCs (DESCs), ten new candidate reference genes were identified. The expression of these ten candidates, along with the commonly used reference gene β-actin, was measured in ESCs, DESCs, and decidual stromal cells (DSCs) through RTqPCR. Five algorithms were used to systematically identify suitable reference genes. The results indicated that Staufen double-stranded RNA binding protein 1 (STAU1) was most stable for induced decidualization in vitro, showing consistent expression in ESCs and DSCs. Using STAU1 as the reference gene, the expression levels of insulin like growth factor binding protein 1 and prolactin in DESCs were significantly higher than those in ESCs. Stau1 was further validated with both natural pregnancy and artificially induced decidualization mouse models. Based on our bioinformatics analysis, we also propose that kelch like family member 9 and TSC complex subunit 1 may serve as additional reference genes. Our findings offer valuable insights for gene expression studies of endometrial decidualization.
{"title":"Selection and validation of reference genes for gene expression studies of decidualization based on RNA sequencing","authors":"Haoyu Yang , Cancan Wang , Wenxuan Li , Xin Su , Mengyuan Li , Qian Li , Xiang-Hong Xu , Liping Jin","doi":"10.1016/j.repbio.2025.101023","DOIUrl":"10.1016/j.repbio.2025.101023","url":null,"abstract":"<div><div>Decidualization is a multistep and complex physiological process used to aid the development of an implanting embryo. To date, the potential genes regulating decidualization have not been elucidated. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) is widely used in gene expression studies, with relative quantification being the predominant method due to its simplicity, cost-effectiveness, and lower sample requirements. This method determines gene expression levels by normalizing to reference genes. However, the selection of stable reference genes for studies on decidualization remains a challenge. Based on the RNA-seq dataset from human endometrial stromal cells (ESCs) and differentiated ESCs (DESCs), ten new candidate reference genes were identified. The expression of these ten candidates, along with the commonly used reference gene β-actin, was measured in ESCs, DESCs, and decidual stromal cells (DSCs) through RT<img>qPCR. Five algorithms were used to systematically identify suitable reference genes. The results indicated that <em>Staufen double-stranded RNA binding protein 1 (STAU1)</em> was most stable for induced decidualization in vitro, showing consistent expression in ESCs and DSCs. Using <em>STAU1</em> as the reference gene, the expression levels of <em>insulin like growth factor binding protein 1</em> and <em>prolactin</em> in DESCs were significantly higher than those in ESCs. <em>Stau1</em> was further validated with both natural pregnancy and artificially induced decidualization mouse models. Based on our bioinformatics analysis, we also propose that <em>kelch like family member 9</em> and <em>TSC complex subunit 1</em> may serve as additional reference genes. Our findings offer valuable insights for gene expression studies of endometrial decidualization.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101023"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143883125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-19DOI: 10.1016/j.repbio.2025.101016
Camila Lapuente , Augusto Lantermino , Sol Arioni , Paula G. Blanco , Cristina Gobello
Anti-Müllerian hormone (AMH) is a dimeric glycoprotein that belongs to the transforming growth factor-β (TGF-β) superfamily. This hormone that is produced by gonadal Sertoli cells in males and granulosa cells in females has been extensively studied in humans, rodents, and livestock species. Research on AMH in felids began in 2011 and given the increasing number of studies over recent years, an updated literature review is necessary to clarify and organize future research directions. The objective of this article was to conduct a systematic review of AMH in domestic and wild felids. From a literature search of international publications, 23 were selected for inclusion. AMH determinations were performed using commercial enzyme-linked immunosorbent assays (ELISA) and electrochemiluminescence immunoassays (EQLIA). In female felids, AMH concentrations decrease with age, along with follicular reserve diminution. AMH can also be used to diagnose granulosa cell ovarian tumors and cryptorchidism in females and males, respectively. This hormone serves as a marker for reproductive status and can reflect gonadal function in both genders. Furthermore, AMH may prove to be a valuable predictive tool for reproductive biotechnologies in both domestic and wild felids. Several aspects of this hormone still remain to be elucidated, including its variations throughout the estrous cycle and the effect of photoperiod. Finally, standardization of assays and the establishment of reference ranges for both domestic and wild animals are necessary for widespread clinical application and future research development.
{"title":"Anti-mullerian hormone in felids: A systematic review","authors":"Camila Lapuente , Augusto Lantermino , Sol Arioni , Paula G. Blanco , Cristina Gobello","doi":"10.1016/j.repbio.2025.101016","DOIUrl":"10.1016/j.repbio.2025.101016","url":null,"abstract":"<div><div>Anti-Müllerian hormone (AMH) is a dimeric glycoprotein that belongs to the transforming growth factor-β (TGF-β) superfamily. This hormone that is produced by gonadal Sertoli cells in males and granulosa cells in females has been extensively studied in humans, rodents, and livestock species. Research on AMH in felids began in 2011 and given the increasing number of studies over recent years, an updated literature review is necessary to clarify and organize future research directions. The objective of this article was to conduct a systematic review of AMH in domestic and wild felids. From a literature search of international publications, 23 were selected for inclusion. AMH determinations were performed using commercial enzyme-linked immunosorbent assays (ELISA) and electrochemiluminescence immunoassays (EQLIA). In female felids, AMH concentrations decrease with age, along with follicular reserve diminution. AMH can also be used to diagnose granulosa cell ovarian tumors and cryptorchidism in females and males, respectively. This hormone serves as a marker for reproductive status and can reflect gonadal function in both genders. Furthermore, AMH may prove to be a valuable predictive tool for reproductive biotechnologies in both domestic and wild felids. Several aspects of this hormone still remain to be elucidated, including its variations throughout the estrous cycle and the effect of photoperiod. Finally, standardization of assays and the establishment of reference ranges for both domestic and wild animals are necessary for widespread clinical application and future research development.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101016"},"PeriodicalIF":2.5,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-19DOI: 10.1016/j.repbio.2025.101020
Shitao Dong, Youbin Liu, Zhimin Yang
Polycystic ovary syndrome (PCOS) poses a significant threat to women's fertility and quality of life. Studies have found a close association between the environmental contaminant tributyltin (TBT) and the occurrence of PCOS. The main objective of this study was to investigate the specific mechanisms by which TBT adversely affects the growth of ovarian granulosa cells. Cell viability, cycle, proliferation, and apoptosis were measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2’-deoxyuridine (EdU), and flow cytometry. Simultaneously, lactate dehydrogenase (LDH) leakage and Caspase-3 activity were measured by the corresponding kits. Besides, western blot was used to analyze the protein levels of cyclin-dependent kinase inhibitor 1 C (CDKN1C) and the transcription factor Yin Yang 1 (YY1). TBT severely impaired the viability, cell cycle, and proliferation capacity of granulosa cells, and induced their apoptosis. Silencing CDKN1C and YY1 alleviated the damage caused by TBT to the cells, but these repair effects were weakened by CDKN1C overexpressed. By inhibiting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, TBT upregulated the YY1-mediated CDNK1C, and further exacerbated the damage to granulosa cells. This study revealed the mechanism that TBT induced the loss of ovarian granulosa cells in PCOS patients by upregulating YY1-mediated CDKN1C expression, which provided new ideas and targets for the pathogenesis and treatment of PCOS.
多囊卵巢综合征(PCOS)严重威胁妇女的生育能力和生活质量。研究发现环境污染物三丁基锡(TBT)与多囊卵巢综合征的发生密切相关。本研究的主要目的是探讨TBT对卵巢颗粒细胞生长不利的具体机制。采用3-(4,5 -二甲基-2-噻唑基)- 2,5 -二苯基-2- h -溴化四唑(MTT)、5-乙基-2 ' -脱氧尿苷(EdU)和流式细胞术检测细胞活力、周期、增殖和凋亡。同时用相应的试剂盒检测乳酸脱氢酶(LDH)渗漏量和Caspase-3活性。western blot检测细胞周期蛋白依赖性激酶抑制剂1 C (CDKN1C)和转录因子阴阳1 (YY1)蛋白水平。TBT严重损害颗粒细胞的活力、细胞周期和增殖能力,诱导颗粒细胞凋亡。沉默CDKN1C和YY1可减轻TBT对细胞的损伤,但这些修复作用因CDKN1C过表达而减弱。TBT通过抑制磷脂酰肌醇3-激酶/蛋白激酶B (PI3K/AKT)信号通路,上调yy1介导的CDNK1C,进一步加重对颗粒细胞的损伤。本研究揭示了TBT通过上调yy1介导的CDKN1C表达诱导PCOS患者卵巢颗粒细胞丢失的机制,为PCOS的发病机制和治疗提供了新的思路和靶点。
{"title":"Tributyltin affects the growth of ovarian granulosa cells in polycystic ovary syndrome by upregulating YY1-mediated CDKN1C via the PI3K/AKT pathway","authors":"Shitao Dong, Youbin Liu, Zhimin Yang","doi":"10.1016/j.repbio.2025.101020","DOIUrl":"10.1016/j.repbio.2025.101020","url":null,"abstract":"<div><div>Polycystic ovary syndrome (PCOS) poses a significant threat to women's fertility and quality of life. Studies have found a close association between the environmental contaminant tributyltin (TBT) and the occurrence of PCOS. The main objective of this study was to investigate the specific mechanisms by which TBT adversely affects the growth of ovarian granulosa cells. Cell viability, cycle, proliferation, and apoptosis were measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2’-deoxyuridine (EdU), and flow cytometry. Simultaneously, lactate dehydrogenase (LDH) leakage and Caspase-3 activity were measured by the corresponding kits. Besides, western blot was used to analyze the protein levels of cyclin-dependent kinase inhibitor 1 C (CDKN1C) and the transcription factor Yin Yang 1 (YY1). TBT severely impaired the viability, cell cycle, and proliferation capacity of granulosa cells, and induced their apoptosis. Silencing CDKN1C and YY1 alleviated the damage caused by TBT to the cells, but these repair effects were weakened by CDKN1C overexpressed. By inhibiting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, TBT upregulated the YY1-mediated CDNK1C, and further exacerbated the damage to granulosa cells. This study revealed the mechanism that TBT induced the loss of ovarian granulosa cells in PCOS patients by upregulating YY1-mediated CDKN1C expression, which provided new ideas and targets for the pathogenesis and treatment of PCOS.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101020"},"PeriodicalIF":2.5,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Relative copy number of mitochondria was estimated for the potential association with the expression of mitochondrial coded stress related genes in bubaline spermatozoa. Semen samples were collected from buffalo bulls under two extreme temperature-humidity index conditions: hot summer and winter. Based on the semen quality, the bulls were categorized: exhibiting poor semen quality during hot summer as "seasonally affected," while those maintaining good semen quality throughout the year, as "seasonally not affected". The average mitochondrial copy numbers were lower during hot summer (15.42 ± 1.2368) compared to winter (17.29 ± 0.72) in both the groups. Furthermore, within the hot summer period, bulls classified as seasonally affected exhibited significantly lower mitochondrial copy numbers (12.86 ± 1.343) than their seasonally unaffected counterpart (17.97 ± 1.34). These results suggest a potential role of mitochondria in influencing semen quality, particularly in response to impaired scrotal thermoregulation during the summer season. Although the fold change in apoptotic genes (BCL2, MCL1, CASP3, and BAK) and oxidative panel genes (CAT, SOD, GPx, ATF4, and FOXO-3), did not differ significantly across the groups, differences were observed between the seasons. Further, to understand the role of copy number in apoptosis and ROS scavenging across the seasons and the groups, the generalized mixed model was employed. The results conveyed a significant negative interaction of copy number with the expression of CAT gene and significant positive interaction of copy number with the apoptotic gene panel. Our findings underscore the significant role of mitochondrial copy numbers in domestic buffalo spermatozoa in managing the challenges of thermoregulation posed by harsh tropical conditions.
{"title":"Evaluation of mitochondrial copy number and gene expression changes in the spermatozoa of buffalo bulls under heat stress","authors":"Meenakshi Chitkara , Harsimran Kaur , Rashi Vasisth , Karpenahalli Ranganatha Sriranga , Ankita Gurao , Karan Mahar , Mahesh Shivanand Dige , R.A.K. Aggarwal , Manishi Mukesh , Pradeep Kumar , Pawan Singh , Ranjit Singh Kataria","doi":"10.1016/j.repbio.2025.101014","DOIUrl":"10.1016/j.repbio.2025.101014","url":null,"abstract":"<div><div>Relative copy number of mitochondria was estimated for the potential association with the expression of mitochondrial coded stress related genes in bubaline spermatozoa. Semen samples were collected from buffalo bulls under two extreme temperature-humidity index conditions: hot summer and winter. Based on the semen quality, the bulls were categorized: exhibiting poor semen quality during hot summer as \"seasonally affected,\" while those maintaining good semen quality throughout the year, as \"seasonally not affected\". The average mitochondrial copy numbers were lower during hot summer (15.42 ± 1.2368) compared to winter (17.29 ± 0.72) in both the groups. Furthermore, within the hot summer period, bulls classified as seasonally affected exhibited significantly lower mitochondrial copy numbers (12.86 ± 1.343) than their seasonally unaffected counterpart (17.97 ± 1.34). These results suggest a potential role of mitochondria in influencing semen quality, particularly in response to impaired scrotal thermoregulation during the summer season. Although the fold change in apoptotic genes (<em>BCL2</em>, <em>MCL1</em>, <em>CASP3</em>, and <em>BAK</em>) and oxidative panel genes (<em>CAT</em>, <em>SOD</em>, <em>GPx</em>, <em>ATF4</em>, and <em>FOXO-3</em>), did not differ significantly across the groups, differences were observed between the seasons. Further, to understand the role of copy number in apoptosis and ROS scavenging across the seasons and the groups, the generalized mixed model was employed. The results conveyed a significant negative interaction of copy number with the expression of <em>CAT</em> gene and significant positive interaction of copy number with the apoptotic gene panel. Our findings underscore the significant role of mitochondrial copy numbers in domestic buffalo spermatozoa in managing the challenges of thermoregulation posed by harsh tropical conditions.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101014"},"PeriodicalIF":2.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143747099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-30DOI: 10.1016/j.repbio.2025.101015
Farha A. Ali Shafi , Ali Thoulfikar A. Imeer , Hassan Ali Abood Nassrullah , Ali Mutashar Naeemah
This study investigates the impact of extracellular glucose concentrations on antioxidant capacity, viability, and microRNA (miR) expression in TM4 Sertoli cell lines. TM4 cells were cultured in high-glucose (115 µm) and low-glucose (<505 µm) conditions to simulate hyperglycemia and glucose starvation, respectively. The study measured total antioxidant capacity (TAC), malondialdehyde (MDA), total oxidant status (TOS), glutathione (GSH), glutathione disulfide (GSSG), NADP/NADPH, glutathione peroxidase (GPX), and glutathione reductase (GR) levels. MiR-17, miR-34, miR-106a, and miR-200a expression levels were assessed. Cell viability and apoptosis were evaluated using MTT assay and acridine-orange staining. Results indicated that high glucose reduced miR-17 expression while low glucose increased it. Both glucose conditions elevated miR-34, miR-106a, and miR-200a expressions. TAC levels decreased, while TOS and MDA levels increased significantly under both conditions. High glucose had no significant effect on GPX and GR levels, whereas low glucose decreased them. Both conditions led to reduced GSH levels, increased GSSG levels, and altered NADP/NADPH ratio. Increased apoptosis and decreased cell viability were observed under both glucose conditions. These findings suggest that extracellular glucose levels significantly dysregulate miRNA expression, antioxidant capacities, and redox buffer systems in TM4 cells. High glucose conditions suppress miR-17 expression, increase miR-34 and miR-106a levels, and induce reductive buffer imbalance. Conversely, low glucose conditions trigger compensatory mechanisms via increased miR-17 expression to enhance antioxidant status while reducing GPX and GR levels. These results provide insights into the molecular responses of Sertoli cells under varying glucose environments, highlighting potential therapeutic pathways for conditions like diabetes and metabolic dysfunctions.
{"title":"The impact of extracellular glucose concentrations on antioxidant capacity, viability, and microRNA expression in TM4 Sertoli cells","authors":"Farha A. Ali Shafi , Ali Thoulfikar A. Imeer , Hassan Ali Abood Nassrullah , Ali Mutashar Naeemah","doi":"10.1016/j.repbio.2025.101015","DOIUrl":"10.1016/j.repbio.2025.101015","url":null,"abstract":"<div><div>This study investigates the impact of extracellular glucose concentrations on antioxidant capacity, viability, and microRNA (miR) expression in TM4 Sertoli cell lines. TM4 cells were cultured in high-glucose (115 µm) and low-glucose (<505 µm) conditions to simulate hyperglycemia and glucose starvation, respectively. The study measured total antioxidant capacity (TAC), malondialdehyde (MDA), total oxidant status (TOS), glutathione (GSH), glutathione disulfide (GSSG), NADP/NADPH, glutathione peroxidase (GPX), and glutathione reductase (GR) levels. MiR-17, miR-34, miR-106a, and miR-200a expression levels were assessed. Cell viability and apoptosis were evaluated using MTT assay and acridine-orange staining. Results indicated that high glucose reduced miR-17 expression while low glucose increased it. Both glucose conditions elevated miR-34, miR-106a, and miR-200a expressions. TAC levels decreased, while TOS and MDA levels increased significantly under both conditions. High glucose had no significant effect on GPX and GR levels, whereas low glucose decreased them. Both conditions led to reduced GSH levels, increased GSSG levels, and altered NADP/NADPH ratio. Increased apoptosis and decreased cell viability were observed under both glucose conditions. These findings suggest that extracellular glucose levels significantly dysregulate miRNA expression, antioxidant capacities, and redox buffer systems in TM4 cells. High glucose conditions suppress miR-17 expression, increase miR-34 and miR-106a levels, and induce reductive buffer imbalance. Conversely, low glucose conditions trigger compensatory mechanisms via increased miR-17 expression to enhance antioxidant status while reducing GPX and GR levels. These results provide insights into the molecular responses of Sertoli cells under varying glucose environments, highlighting potential therapeutic pathways for conditions like diabetes and metabolic dysfunctions.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101015"},"PeriodicalIF":2.5,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143734743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-29DOI: 10.1016/j.repbio.2025.101012
Michela Calanni-Pileri , Joachim M. Weitzel , Andreas Hoeflich , Martina Langhammer , Marten Michaelis
To date, animal models with reproductive phenotypes are knockout or transgenic and typically exhibit reduced fertility or infertility. This limits research to studying single-gene effects or loss of fertility. By contrast, Dummerstorf high-fertility mouse lines 1 and 2 (FL1 and FL2) are two unique outbred selection models that demonstrate exceptional reproductive performance. After approximately 50 years of selection, both lines have doubled the number of ovulated oocytes per cycle and consequently their litter size (>20 vs ∼11) compared to the unselected mice of the same founder population (Dummerstorf FZTDU, ctrl line). FL1 and FL2 exhibit atypical estrous cycle length and altered levels of hormones, such as insulin and leptin, which are associated with GnRH release and/or increased body fat content. Unlike typical cases where these factors impair fertility, they instead contribute to the FLs’ high reproductive capacity: the increased ovulation rate results from an upgrade in the quality of their oocytes, influenced by different ovarian lipid profile. In the present study, we analyzed the expression of IGF-axis marker genes linked to reproductive performance and FL-specific traits in three tissues. We found that lepr, which plays a critical role in implantation, was upregulated in the FL1 uterus (1.5-fold vs. ctrl, p < 0.05). In FL1 follicles, igf1, IGF-biding proteins (IGFBP2, IGFBP4) and hsf1—which is involved in gametogenesis—were significantly upregulated (1–4-fold vs. ctrl, p < 0.05 for igf1, hsf1 and IGFBP4; p < 0.01 for igfbp2). In FL2, uterine size was reduced relatively to the body weight (∼0.2 % FL2 vs. 0.25 % in ctrl and 0.28 % in FL1, p < 0.001), indicating that uterus dimensions do not drive their increased litter size. These findings provide new insights into the molecular basis of high fertility and could serve as a foundation for further studies on genotype-phenotype relationships in reproductive biology.
{"title":"The special phenotypic characteristics of Dummerstorf superfertile mouse lines could depend on the expression levels of IGF-axis genes","authors":"Michela Calanni-Pileri , Joachim M. Weitzel , Andreas Hoeflich , Martina Langhammer , Marten Michaelis","doi":"10.1016/j.repbio.2025.101012","DOIUrl":"10.1016/j.repbio.2025.101012","url":null,"abstract":"<div><div>To date, animal models with reproductive phenotypes are knockout or transgenic and typically exhibit reduced fertility or infertility. This limits research to studying single-gene effects or loss of fertility. By contrast, Dummerstorf high-fertility mouse lines 1 and 2 (FL1 and FL2) are two unique outbred selection models that demonstrate exceptional reproductive performance. After approximately 50 years of selection, both lines have doubled the number of ovulated oocytes per cycle and consequently their litter size (>20 vs ∼11) compared to the unselected mice of the same founder population (Dummerstorf FZTDU, ctrl line). FL1 and FL2 exhibit atypical estrous cycle length and altered levels of hormones, such as insulin and leptin, which are associated with GnRH release and/or increased body fat content. Unlike typical cases where these factors impair fertility, they instead contribute to the FLs’ high reproductive capacity: the increased ovulation rate results from an upgrade in the quality of their oocytes, influenced by different ovarian lipid profile. In the present study, we analyzed the expression of IGF-axis marker genes linked to reproductive performance and FL-specific traits in three tissues. We found that lepr, which plays a critical role in implantation, was upregulated in the FL1 uterus (1.5-fold vs. ctrl, p < 0.05). In FL1 follicles, igf1, IGF-biding proteins (IGFBP2, IGFBP4) and hsf1—which is involved in gametogenesis—were significantly upregulated (1–4-fold vs. ctrl, p < 0.05 for igf1, hsf1 and IGFBP4; p < 0.01 for igfbp2). In FL2, uterine size was reduced relatively to the body weight (∼0.2 % FL2 vs. 0.25 % in ctrl and 0.28 % in FL1, p < 0.001), indicating that uterus dimensions do not drive their increased litter size. These findings provide new insights into the molecular basis of high fertility and could serve as a foundation for further studies on genotype-phenotype relationships in reproductive biology.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101012"},"PeriodicalIF":2.5,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}