Reproductive biology最新文献

Impact of vitrification conditions on genetic and functional competence of prepubertal mouse oocytes

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-24 DOI: 10.1016/j.repbio.2025.101022

Akshatha Daddangadi , Siyona Saruparia , Dhakshanya Predheepan , Shubhashree Uppangala , Shama Prasada Kabekkodu , G. Nadeem Khan , Guruprasad Kalthur , Riccardo Talevi , Satish Kumar Adiga

Oocyte in vitro maturation (IVM) and vitrification are being considered as fertility preservation strategies for prepubertal cancer patients. Since prepubertal oocytes have differential sensitivity and response to vitrification compared to adult oocytes, there is a need to optimize the technique to improve the outcome. This study specifically looked into the effect of varying equilibration time and temperatures on the survival and functional competence of prepubertal mouse oocytes. Germinal vesicle (GV) stage and in vitro matured, metaphase II stage sibling oocytes retrieved from 2-week-old Swiss albino mice were equilibrated at 24 °C and 37 °C for 10 and 15 min during vitrification. GV vitrified-IVM (GVV) and GV IVM-vitrified (MIIV) oocytes that survived post-warming were assessed for mitochondrial potential, spindle integrity, spindle checkpoint transcripts, and DNA integrity. The GVV oocytes equilibrated at 37 °C for 15 min had a significantly lower maturation rate (P < 0.01). Survival was reduced when MIIV oocytes were equilibrated at 37 °C, regardless of equilibration duration (P < 0.05). The meiotic spindle and DNA integrity were affected at 37 °C/15 min equilibration (P < 0.01). IVM prepubertal mouse oocytes are at higher risk of experiencing cryo-damage with 37 °C equilibration. Hence, fertility preservation protocols must be refined and individualized for prepubertal age to safeguard the genetic and functional integrity of such oocytes.

{"title":"Impact of vitrification conditions on genetic and functional competence of prepubertal mouse oocytes","authors":"Akshatha Daddangadi , Siyona Saruparia , Dhakshanya Predheepan , Shubhashree Uppangala , Shama Prasada Kabekkodu , G. Nadeem Khan , Guruprasad Kalthur , Riccardo Talevi , Satish Kumar Adiga","doi":"10.1016/j.repbio.2025.101022","DOIUrl":"10.1016/j.repbio.2025.101022","url":null,"abstract":"<div><div>Oocyte <em>in vitro</em> maturation (IVM) and vitrification are being considered as fertility preservation strategies for prepubertal cancer patients. Since prepubertal oocytes have differential sensitivity and response to vitrification compared to adult oocytes, there is a need to optimize the technique to improve the outcome. This study specifically looked into the effect of varying equilibration time and temperatures on the survival and functional competence of prepubertal mouse oocytes. Germinal vesicle (GV) stage and in vitro matured, metaphase II stage sibling oocytes retrieved from 2-week-old <em>Swiss albino</em> mice were equilibrated at 24 °C and 37 °C for 10 and 15 min during vitrification. GV vitrified-IVM (GVV) and GV IVM-vitrified (MIIV) oocytes that survived post-warming were assessed for mitochondrial potential, spindle integrity, spindle checkpoint transcripts, and DNA integrity. The GVV oocytes equilibrated at 37 °C for 15 min had a significantly lower maturation rate (P < 0.01). Survival was reduced when MIIV oocytes were equilibrated at 37 °C, regardless of equilibration duration (P < 0.05). The meiotic spindle and DNA integrity were affected at 37 °C/15 min equilibration (P < 0.01). IVM prepubertal mouse oocytes are at higher risk of experiencing cryo-damage with 37 °C equilibration. Hence, fertility preservation protocols must be refined and individualized for prepubertal age to safeguard the genetic and functional integrity of such oocytes.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101022"},"PeriodicalIF":2.5,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868902","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}

引用次数: 0

Anti-mullerian hormone in felids: A systematic review

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-19 DOI: 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}

引用次数: 0

Tributyltin affects the growth of ovarian granulosa cells in polycystic ovary syndrome by upregulating YY1-mediated CDKN1C via the PI3K/AKT pathway

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-19 DOI: 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.

{"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}

引用次数: 0

The effect of amphiregulin on equine endometrial fibroblasts: in vitro responses of fibroblast derived from non-fibrotic and fibrotic endometrium 安非他酮对马子宫内膜成纤维细胞的影响：非纤维化和纤维化子宫内膜成纤维细胞的体外反应

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-14 DOI: 10.1016/j.repbio.2025.101018

Anna Wójtowicz, Agnieszka Sadowska, Katarzyna Piotrowska-Tomala, Anna Szóstek-Mioduchowska

The role of AREG in the development of fibrosis in the progression of endometrosis in mare remains unknown. We aimed to determine the effects of AREG on fibroblast functional characteristics as well as the expression of extracellular matrix (ECM)-associated genes in fibroblast derived from non-fibrotic and fibrotic equine endometria. Our findings suggest that the mechanisms associated with ECM remodeling regulated by AREG in non-fibrotic fibroblasts may be dysregulated in the progression of fibrosis in endometrosis.

引用次数: 0

Increased circulating T helper 17 (TH17) cells and endometrial tissue IL-17-producing cells in patients with endometriosis compared with non-endometriotic subjects 与非子宫内膜异位症患者相比，子宫内膜异位症患者体内循环 T 辅助细胞 17 (TH17) 和子宫内膜组织 IL-17 生成细胞增多

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-12 DOI: 10.1016/j.repbio.2025.101019

Ali-Akbar Delbandi , Mahmoud Mahmoudi , Adel Shervin , Pooya Farhangnia , Tahereh Mohammadi , Amir-Hassan Zarnani

Endometriosis, an inflammatory disease, is characterized by the aberrant presence of endometrial tissues at ectopic locations. Accumulating evidence suggests that inflammatory cells, such as interleukin-17 (IL-17)-producing cells, may be involved in the pathogenesis of endometriosis. This investigation assessed the frequency of IL-17A (commonly known as IL-17)-producing cells in peripheral blood mononuclear cells (PBMCs), ectopic, and eutopic endometrial tissues in patients with endometriosis compared to non-endometriotic subjects. PBMCs, ectopic, and eutopic endometrial tissues were collected from 23 patients with endometriosis. PBMCs and endometrial tissues from 20 non-endometriotic women were used as the control group. The frequency of T helper 17 (T_H17) lymphocytes in PBMCs was assessed using flow cytometry, and the expression level of IL-17 in eutopic and ectopic endometrial tissues was evaluated through immunohistochemistry. The percentage of T_H17 and IL-17-producing lymphocytes was significantly higher in the PBMCs of patients with endometriosis compared to non-endometriotic subjects (P < 0.01 and P < 0.001, respectively). The expression of IL-17 protein in ectopic (P < 0.001) and eutopic (P < 0.05) endometrial tissues of patients with endometriosis increased compared to controls' endometrial tissue. Furthermore, the eutopic endometrium of patients with endometriosis showed a higher expression of IL-17 protein than the eutopic endometrial tissue of control subjects (P < 0.05). The findings suggest that the higher frequency of IL-17-producing cells in the PBMCs and endometrial tissues of patients with endometriosis contributes to the pathogenesis of endometriosis.

{"title":"Increased circulating T helper 17 (TH17) cells and endometrial tissue IL-17-producing cells in patients with endometriosis compared with non-endometriotic subjects","authors":"Ali-Akbar Delbandi , Mahmoud Mahmoudi , Adel Shervin , Pooya Farhangnia , Tahereh Mohammadi , Amir-Hassan Zarnani","doi":"10.1016/j.repbio.2025.101019","DOIUrl":"10.1016/j.repbio.2025.101019","url":null,"abstract":"<div><div>Endometriosis, an inflammatory disease, is characterized by the aberrant presence of endometrial tissues at ectopic locations. Accumulating evidence suggests that inflammatory cells, such as interleukin-17 (IL-17)-producing cells, may be involved in the pathogenesis of endometriosis. This investigation assessed the frequency of IL-17A (commonly known as IL-17)-producing cells in peripheral blood mononuclear cells (PBMCs), ectopic, and eutopic endometrial tissues in patients with endometriosis compared to non-endometriotic subjects. PBMCs, ectopic, and eutopic endometrial tissues were collected from 23 patients with endometriosis. PBMCs and endometrial tissues from 20 non-endometriotic women were used as the control group. The frequency of T helper 17 (T<sub>H</sub>17) lymphocytes in PBMCs was assessed using flow cytometry, and the expression level of IL-17 in eutopic and ectopic endometrial tissues was evaluated through immunohistochemistry. The percentage of T<sub>H</sub>17 and IL-17-producing lymphocytes was significantly higher in the PBMCs of patients with endometriosis compared to non-endometriotic subjects (<em>P</em> < 0.01 and <em>P</em> < 0.001, respectively). The expression of IL-17 protein in ectopic (<em>P</em> < 0.001) and eutopic (<em>P</em> < 0.05) endometrial tissues of patients with endometriosis increased compared to controls' endometrial tissue. Furthermore, the eutopic endometrium of patients with endometriosis showed a higher expression of IL-17 protein than the eutopic endometrial tissue of control subjects (<em>P</em> < 0.05). The findings suggest that the higher frequency of IL-17-producing cells in the PBMCs and endometrial tissues of patients with endometriosis contributes to the pathogenesis of endometriosis.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101019"},"PeriodicalIF":2.5,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143820837","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}

引用次数: 0

PCOS and genetics: Exploring the heterogeneous role of potential genes in ovarian dysfunction, a hallmark of PCOS – A review

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-12 DOI: 10.1016/j.repbio.2025.101017

V. Dharani , S. Nishu , L. Hariprasath

PCOS is an endocrine disorder that affects women of reproductive age. The root of PCOS is ovarian dysfunction, which presents as hormonal disturbances affecting normal ovarian function to cause the symptoms and complications of the disease. This dysfunction causes symptoms like impaired maturation of follicles and disorders of various origins with multiple treatment regimens that are not always clear. Therefore, the present review mainly concentrates on the genetic level of ovarian dysfunction of PCOS. The articles were identified through a vigorous literature search where search engines such as PubMed, Google Scholar, databases, and Science Direct were used, and the articles published from 2015 to 2025 were referred. We identified that the key genes involved in the ovarian dysfunctions in PCOS include CYP11A1, CYP17A1, CYP19A1, AR, FSHR, LHCGR, AMH, INSR, SHBG, IRS1, GATA4, ADIPOQ, YAP1, TCF7L2, and DENND1A, which play a role in gonadotropin action, steroidogenesis, and folliculogenesis. Furthermore, epigenetic factors and miRNAs miR-93, 222, 155, 146a, 132, 320, 27a, 483, 21, 378, 17–92 Cluster, and 375, 221 are also involved in it. Abnormal expression of these genes is known to play a critical role in the etiology and pathogenesis of PCOS. Present treatment includes the use of oral contraceptives, anti-androgen agents, insulin-sensitizing agents, and ovulation-inducing agents, and future treatment may consist of miRNA therapy, drug repositioning, and genetic markers that might be used for early identification and better management of ovarian dysfunction. Thus, the current review discusses ovarian dysfunction in PCOS, the involvement of potential genes and epigenetic factors, and miRNAs concerning ovulation and its therapeutic implications.

{"title":"PCOS and genetics: Exploring the heterogeneous role of potential genes in ovarian dysfunction, a hallmark of PCOS – A review","authors":"V. Dharani , S. Nishu , L. Hariprasath","doi":"10.1016/j.repbio.2025.101017","DOIUrl":"10.1016/j.repbio.2025.101017","url":null,"abstract":"<div><div>PCOS is an endocrine disorder that affects women of reproductive age. The root of PCOS is ovarian dysfunction, which presents as hormonal disturbances affecting normal ovarian function to cause the symptoms and complications of the disease. This dysfunction causes symptoms like impaired maturation of follicles and disorders of various origins with multiple treatment regimens that are not always clear. Therefore, the present review mainly concentrates on the genetic level of ovarian dysfunction of PCOS. The articles were identified through a vigorous literature search where search engines such as PubMed, Google Scholar, databases, and Science Direct were used, and the articles published from 2015 to 2025 were referred. We identified that the key genes involved in the ovarian dysfunctions in PCOS include CYP11A1, CYP17A1, CYP19A1, AR, FSHR, LHCGR, AMH, INSR, SHBG, IRS1, GATA4, ADIPOQ, YAP1, TCF7L2, and DENND1A, which play a role in gonadotropin action, steroidogenesis, and folliculogenesis. Furthermore, epigenetic factors and miRNAs miR-93, 222, 155, 146a, 132, 320, 27a, 483, 21, 378, 17–92 Cluster, and 375, 221 are also involved in it. Abnormal expression of these genes is known to play a critical role in the etiology and pathogenesis of PCOS. Present treatment includes the use of oral contraceptives, anti-androgen agents, insulin-sensitizing agents, and ovulation-inducing agents, and future treatment may consist of miRNA therapy, drug repositioning, and genetic markers that might be used for early identification and better management of ovarian dysfunction. Thus, the current review discusses ovarian dysfunction in PCOS, the involvement of potential genes and epigenetic factors, and miRNAs concerning ovulation and its therapeutic implications.</div></div>","PeriodicalId":21018,"journal":{"name":"Reproductive biology","volume":"25 2","pages":"Article 101017"},"PeriodicalIF":2.5,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823591","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}

引用次数: 0

Investigating the clinical significance of immune and thyroid biomarkers in women with breast cancer and Hashimoto's thyroiditis

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-12 DOI: 10.1016/j.repbio.2025.101011

Israa Khalaf Aneed , Noori Mohammed Luaibi , Sajid Nader Abdulqader

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":"2025-04-12","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}

引用次数: 0

Evaluation of mitochondrial copy number and gene expression changes in the spermatozoa of buffalo bulls under heat stress

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-04-02 DOI: 10.1016/j.repbio.2025.101014

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

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}

引用次数: 0

The impact of extracellular glucose concentrations on antioxidant capacity, viability, and microRNA expression in TM4 Sertoli cells

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-03-30 DOI: 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}

引用次数: 0

The special phenotypic characteristics of Dummerstorf superfertile mouse lines could depend on the expression levels of IGF-axis genes

IF 2.5 3区生物学 Q3 REPRODUCTIVE BIOLOGY

Reproductive biology

Pub Date : 2025-03-29 DOI: 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}

引用次数: 0