Pub Date : 2024-11-01DOI: 10.1016/j.xfss.2024.09.001
{"title":"Corrigendum for Bhatt S, Butola A, Acuña S, Hansen DH, Tinguely JC, Nystad M, et al. Characterizing the consistency of motion of spermatozoa through nanoscale motion tracing. F S Sci 2024;5:215–24.","authors":"","doi":"10.1016/j.xfss.2024.09.001","DOIUrl":"10.1016/j.xfss.2024.09.001","url":null,"abstract":"","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Page 404"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142482285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.xfss.2024.07.006
Emmanuel N. Paul Ph.D., Tyler J. Carpenter B.S., Laura A. Pavliscak B.S., Abigail Z. Bennett B.S., Maria Ariadna Ochoa-Bernal Ph.D., Asgerally T. Fazleabas Ph.D., Jose M. Teixeira Ph.D.
Objective
To study the possible role for HMGA2 overexpression in differentiated myometrial cells and its potential to induce a stem cell-like or dedifferentiating phenotype and drive fibroid development.
Design
Myometrial cells were immortalized and transduced with an HMGA2 lentivirus to produce HMGA2hi cells. In vitro stem cell assays were conducted, and ribonucleic acid from HMGA2hi and control cells as well as fibroid-free myometrial and HMGA2 fibroid (HMGA2F) tissues were submitted for ribonucleic acid sequencing.
Setting
University research laboratory.
Patient(s)
Women who underwent hysterectomy for symptomatic uterine fibroids or other gynecological conditions.
Intervention(s)
Not applicable.
Main Outcome Measure(s)
In vitro stem cell-like properties from myometrial cell lines. Ribonucleic acid sequencing and collagen production of HMGA2-overexpressing primary leiomyoma tissue and cell lines.
Result(s)
HMGA2hi cells had enhanced self-renewal capacity, decreased proliferation, and a greater ability to differentiate into other mesenchymal cell types. HMGA2hi cells exhibited a stem cell-like signature and shared transcriptomic similarities with HMGA2F. Moreover, dysregulated extracellular matrix pathways were observed in both HMGA2hi cells and HMGA2F.
Conclusion(s)
Our findings show that HMGA2 overexpression may drive myometrial cells to dedifferentiate into a more plastic phenotype and provide evidence for an alternative mechanism for fibroid etiology, suggesting that fibroids arise not only from a mutated stem cell but also from a mutated differentiated myometrial cell.
{"title":"HMGA2 overexpression induces plasticity in myometrial cells and a transcriptomic profile more similar to that of uterine fibroids","authors":"Emmanuel N. Paul Ph.D., Tyler J. Carpenter B.S., Laura A. Pavliscak B.S., Abigail Z. Bennett B.S., Maria Ariadna Ochoa-Bernal Ph.D., Asgerally T. Fazleabas Ph.D., Jose M. Teixeira Ph.D.","doi":"10.1016/j.xfss.2024.07.006","DOIUrl":"10.1016/j.xfss.2024.07.006","url":null,"abstract":"<div><h3>Objective</h3><div>To study the possible role for <em>HMGA2</em> overexpression in differentiated myometrial cells and its potential to induce a stem cell-like or dedifferentiating phenotype and drive fibroid development.</div></div><div><h3>Design</h3><div>Myometrial cells were immortalized and transduced with an <em>HMGA2</em> lentivirus to produce HMGA2hi cells. In vitro stem cell assays were conducted, and ribonucleic acid from HMGA2hi and control cells as well as fibroid-free myometrial and <em>HMGA2</em> fibroid (HMGA2F) tissues were submitted for ribonucleic acid sequencing.</div></div><div><h3>Setting</h3><div>University research laboratory.</div></div><div><h3>Patient(s)</h3><div>Women who underwent hysterectomy for symptomatic uterine fibroids or other gynecological conditions.</div></div><div><h3>Intervention(s)</h3><div>Not applicable.</div></div><div><h3>Main Outcome Measure(s)</h3><div>In vitro stem cell-like properties from myometrial cell lines. Ribonucleic acid sequencing and collagen production of <em>HMGA2</em>-overexpressing primary leiomyoma tissue and cell lines.</div></div><div><h3>Result(s)</h3><div>HMGA2hi cells had enhanced self-renewal capacity, decreased proliferation, and a greater ability to differentiate into other mesenchymal cell types. HMGA2hi cells exhibited a stem cell-like signature and shared transcriptomic similarities with HMGA2F. Moreover, dysregulated extracellular matrix pathways were observed in both HMGA2hi cells and HMGA2F.</div></div><div><h3>Conclusion(s)</h3><div>Our findings show that <em>HMGA2</em> overexpression may drive myometrial cells to dedifferentiate into a more plastic phenotype and provide evidence for an alternative mechanism for fibroid etiology, suggesting that fibroids arise not only from a mutated stem cell but also from a mutated differentiated myometrial cell.</div></div>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Pages 369-378"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141705225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.xfss.2024.07.004
Charlene Echague D.O. , Minnie Malik Ph.D. , Paul Driggers Ph.D. , William H. Catherino M.D., Ph.D.
Objective
To evaluate the impact of coenzyme Q-10 (CoQ-10) on the dysregulated synthesis of extracellular matrix proteins mediated by transforming growth factor beta 3 (TGF-β3) in uterine leiomyomas.
Design
Laboratory study.
Setting
University.
Patients
None.
Interventions
Treatment of immortalized uterine myometrial and leiomyoma cells to TGF-β3 and CoQ-10.
Main Outcome Measures
The protein concentrations of collagen 1A1 (COL1A1), collagen 3A1 (COL3A1), collagen 11A1 (COL11A1), and fibronectin (FN1) were assessed through western blot analysis after treatment of immortalized uterine myometrial and leiomyoma cells with both transforming growth factor beta (TGF-β) 3 and concentrations of CoQ-10 at 10, 50, and 100 μM concurrently for 24 hours.
Results
Immortalized uterine leiomyoma and myometrial cells exposed to TGF-β3 for 24 hours demonstrated a significant up-regulation of COL1A1, COL3A1, COL11A1, and FN1 compared with untreated cells. In leiomyoma cells, concurrent treatment with CoQ-10 over the same timeframe revealed a dose-dependent decrease in these protein concentrations compared with those in cells treated with TGF-β3 alone. At the highest concentration of 100 μM of CoQ-10, significant decreases in the amounts of COL1A1 (0.59 ± 0.10-fold), COL3A1 (0.46 ± 0.09-fold), COL11A1 (0.53 ± 0.09-fold), and FN1 (0.56 ± 0.09-fold) were observed. Similarly, myometrial cells exposed to both TGF-β3 and CoQ-10 demonstrated a dose-responsive decline in the amount of extracellular matrix protein compared with cells exposed to TGF-β3 alone. Significant reductions in the amounts of COL1A1 (0.75 ± 0.03-fold), COL3A1 (0.48 ± 0.06-fold), COL11A1 (0.38 ± 0.06), and FN1 (0.69 ± 0.04-fold) were appreciated at 100-μM CoQ-10.
Conclusion
Coenzyme Q-10 mitigated the aberrant production of key biomarkers of the extracellular matrix mediated by TGF-β3 in uterine leiomyomas. Our findings highlight a promising nonhormonal compound that can counteract the fibroproliferative process inherent to leiomyomas.
{"title":"Coenzyme Q-10 reduced the aberrant production of extracellular matrix proteins in uterine leiomyomas through transforming growth factor beta 3","authors":"Charlene Echague D.O. , Minnie Malik Ph.D. , Paul Driggers Ph.D. , William H. Catherino M.D., Ph.D.","doi":"10.1016/j.xfss.2024.07.004","DOIUrl":"10.1016/j.xfss.2024.07.004","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate the impact of coenzyme Q-10 (CoQ-10) on the dysregulated synthesis of extracellular matrix proteins mediated by transforming growth factor beta 3 (TGF-β3) in uterine leiomyomas.</div></div><div><h3>Design</h3><div>Laboratory study.</div></div><div><h3>Setting</h3><div>University.</div></div><div><h3>Patients</h3><div>None.</div></div><div><h3>Interventions</h3><div>Treatment of immortalized uterine myometrial and leiomyoma cells to TGF-β3 and CoQ-10.</div></div><div><h3>Main Outcome Measures</h3><div>The protein concentrations of collagen 1A1 (COL1A1), collagen 3A1 (COL3A1), collagen 11A1 (COL11A1), and fibronectin (FN1) were assessed through western blot analysis after treatment of immortalized uterine myometrial and leiomyoma cells with both transforming growth factor beta (TGF-β) 3 and concentrations of CoQ-10 at 10, 50, and 100 μM concurrently for 24 hours.</div></div><div><h3>Results</h3><div>Immortalized uterine leiomyoma and myometrial cells exposed to TGF-β3 for 24 hours demonstrated a significant up-regulation of COL1A1, COL3A1, COL11A1, and FN1 compared with untreated cells. In leiomyoma cells, concurrent treatment with CoQ-10 over the same timeframe revealed a dose-dependent decrease in these protein concentrations compared with those in cells treated with TGF-β3 alone. At the highest concentration of 100 μM of CoQ-10, significant decreases in the amounts of COL1A1 (0.59 ± 0.10-fold), COL3A1 (0.46 ± 0.09-fold), COL11A1 (0.53 ± 0.09-fold), and FN1 (0.56 ± 0.09-fold) were observed. Similarly, myometrial cells exposed to both TGF-β3 and CoQ-10 demonstrated a dose-responsive decline in the amount of extracellular matrix protein compared with cells exposed to TGF-β3 alone. Significant reductions in the amounts of COL1A1 (0.75 ± 0.03-fold), COL3A1 (0.48 ± 0.06-fold), COL11A1 (0.38 ± 0.06), and FN1 (0.69 ± 0.04-fold) were appreciated at 100-μM CoQ-10.</div></div><div><h3>Conclusion</h3><div>Coenzyme Q-10 mitigated the aberrant production of key biomarkers of the extracellular matrix mediated by TGF-β3 in uterine leiomyomas. Our findings highlight a promising nonhormonal compound that can counteract the fibroproliferative process inherent to leiomyomas.</div></div>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Pages 342-351"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141617715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To examine the effect of skoochies, an illicit cocktail drink, on testicular and sperm function in male rats.
Design
Twenty-five adult male Wistar rats were assigned randomly into five groups (n = 5) as follows: normal saline; skoochies; Cannabis sativa; codeine; and tramadol. The cocktail (skoochies) used in this study was formulated with the following composition: codeine (5 mg/kg); tramadol (20 mg/kg); and cannabis extract (2 mg/kg). These doses are as previously reported. Administration was performed once daily for 28 days.
Setting
University.
Animal(s)
Twenty-five (25) male Wistar rats.
Intervention(s)
Skoochies, tramadol, Codeiene, Cannabis.
Main Outcome Measure(s)
Skoochies and its components induced testicular and sperm damage via increased generation of reactive oxygen species and impairment of glutathione system in rats.
Result(s)
Skoochies increased reactive oxygen species generation and impaired the antioxidant system resulting in inflammation that eventually damaged the testicular tissue. Skoochies caused oxidoinflammatory injury to this tissue, leading to impaired testicular function. This was evident by the distorted cytoarchitecture, reduced sperm count and motility, and impaired testicular deoxyribonucleic acid integrity.
Conclusion(s)
Thus, our results infer that skoochies impaired the testicular and sperm function through the increased generation of reactive oxygen species and impairment of the glutathione system.
{"title":"Skoochies and its component substances induced testicular damage and impaired sperm function via increased generation of reactive oxygen species and impairment of the glutathione system in rats","authors":"Ayodeji Folorunsho Ajayi Ph.D. , Olufemi Ogundeji Ogundipe M.Tech. , Moses Agbomhere Hamed B.M.L.S. , David Tolulope Oluwole M.Phil.","doi":"10.1016/j.xfss.2024.07.005","DOIUrl":"10.1016/j.xfss.2024.07.005","url":null,"abstract":"<div><h3>Objective</h3><div>To examine the effect of skoochies, an illicit cocktail drink, on testicular and sperm function in male rats.</div></div><div><h3>Design</h3><div>Twenty-five adult male Wistar rats were assigned randomly into five groups (n = 5) as follows: normal saline; skoochies; <em>Cannabis sativa</em>; codeine; and tramadol. The cocktail (skoochies) used in this study was formulated with the following composition: codeine (5 mg/kg); tramadol (20 mg/kg); and cannabis extract (2 mg/kg). These doses are as previously reported. Administration was performed once daily for 28 days.</div></div><div><h3>Setting</h3><div>University.</div></div><div><h3>Animal(s)</h3><div>Twenty-five (25) male Wistar rats.</div></div><div><h3>Intervention(s)</h3><div>Skoochies, tramadol, Codeiene, Cannabis.</div></div><div><h3>Main Outcome Measure(s)</h3><div>Skoochies and its components induced testicular and sperm damage via increased generation of reactive oxygen species and impairment of glutathione system in rats.</div></div><div><h3>Result(s)</h3><div>Skoochies increased reactive oxygen species generation and impaired the antioxidant system resulting in inflammation that eventually damaged the testicular tissue. Skoochies caused oxidoinflammatory injury to this tissue, leading to impaired testicular function. This was evident by the distorted cytoarchitecture, reduced sperm count and motility, and impaired testicular deoxyribonucleic acid integrity.</div></div><div><h3>Conclusion(s)</h3><div>Thus, our results infer that skoochies impaired the testicular and sperm function through the increased generation of reactive oxygen species and impairment of the glutathione system.</div></div>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Pages 318-330"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141617716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.xfss.2024.07.007
Seifeldin Sadek M.D. , Terry A. Jacot Ph.D. , Diane M. Duffy Ph.D. , David F. Archer M.D.
Objective
To study the role of PGE2 in regulating plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) in human primary endometrial endothelial cells (HEECs) from women with normal menstrual bleeding (NMB) and heavy menstrual bleeding (HMB).
Design
In vitro study using endometrial endothelial cells.
Setting
Research laboratory setting.
Patients
Women with NMB and HMB provided endometrial biopsy samples.
Interventions
Prostaglandin E2 and PGE2 receptor-selective agonists were administered to cultured HEECs.
Main Outcome Measures
Levels of PAI-1 and tPA in NMB-HEECs and HMB-HEECs after treatment with PGE2 and receptor-selective agonists.
Results
Prostaglandin E2 increased total PAI-1 levels in NMB-HEECs, but not in HMB-HEECs, which had higher baseline PAI-1 levels. PGE2 receptors (PTGER)1 and PTGER2 agonists increased PAI-1 in NMB-HEECs, whereas PTGER3 and PTGER4 did not. Prostaglandin E2 had no effect on tPA levels in either NMB-HEECs or HMB-HEECs.
Conclusions
Prostaglandin E2, through PTGER1 and PTGER2, regulates the plasminogen activator system in NMB-HEECs, suggesting a role in reducing fibrinolytic activity during normal menstrual cycles. The lack of PGE2 effect and elevated baseline PAI-1 in HMB-HEECs support using this in vitro model to further understand prostaglandin pathways in NMB and HMB.
{"title":"Prostaglandin E2 regulates the plasminogen activator pathway in human endometrial endothelial cells: a new in vitro model to investigate heavy menstrual bleeding","authors":"Seifeldin Sadek M.D. , Terry A. Jacot Ph.D. , Diane M. Duffy Ph.D. , David F. Archer M.D.","doi":"10.1016/j.xfss.2024.07.007","DOIUrl":"10.1016/j.xfss.2024.07.007","url":null,"abstract":"<div><h3>Objective</h3><div>To study the role of PGE<sub>2</sub> in regulating plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) in human primary endometrial endothelial cells (HEECs) from women with normal menstrual bleeding (NMB) and heavy menstrual bleeding (HMB).</div></div><div><h3>Design</h3><div>In vitro study using endometrial endothelial cells.</div></div><div><h3>Setting</h3><div>Research laboratory setting.</div></div><div><h3>Patients</h3><div>Women with NMB and HMB provided endometrial biopsy samples.</div></div><div><h3>Interventions</h3><div>Prostaglandin E<sub>2</sub> and PGE<sub>2</sub> receptor-selective agonists were administered to cultured HEECs.</div></div><div><h3>Main Outcome Measures</h3><div>Levels of PAI-1 and tPA in NMB-HEECs and HMB-HEECs after treatment with PGE<sub>2</sub> and receptor-selective agonists.</div></div><div><h3>Results</h3><div>Prostaglandin E<sub>2</sub> increased total PAI-1 levels in NMB-HEECs, but not in HMB-HEECs, which had higher baseline PAI-1 levels. PGE<sub>2</sub> receptors (PTGER)1 and PTGER2 agonists increased PAI-1 in NMB-HEECs, whereas PTGER3 and PTGER4 did not. Prostaglandin E<sub>2</sub> had no effect on tPA levels in either NMB-HEECs or HMB-HEECs.</div></div><div><h3>Conclusions</h3><div>Prostaglandin E<sub>2</sub>, through PTGER1 and PTGER2, regulates the plasminogen activator system in NMB-HEECs, suggesting a role in reducing fibrinolytic activity during normal menstrual cycles. The lack of PGE<sub>2</sub> effect and elevated baseline PAI-1 in HMB-HEECs support using this in vitro model to further understand prostaglandin pathways in NMB and HMB.</div></div>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Pages 379-385"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141749911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.xfss.2024.08.003
Ling Guo M.D. , Anliang Guo Ph.D. , Xiangxin Lan M.D. , Siqi Tian M.S. , Fengxuan Sun M.D. , Yaxin Su M.S. , Zi-Jiang Chen M.D., Ph.D. , Yongzhi Cao Ph.D. , Yan Li M.D., Ph.D.
Objective
To evaluate whether intergroup differences in the risk of maternal pregnancy complications after in vitro fertilization (IVF) vary with male factor.
Design
A post hoc exploratory secondary analysis of data from a multicenter, randomized, controlled noninferiority trial (NCT03118141).
Setting
Academic fertility centers.
Patient(s)
A total of 1,131 subfertile women with complete recording of their male partner’s semen parameters during the trial were enrolled. All participants underwent intracytoplasmic sperm injection followed by frozen embryo transfer (ET) as part of their assisted reproductive technology treatment protocol.
Intervention(s)
Women were divided into the oligoasthenospermia (n = 405) and normospermia (n = 726) groups according to the quality of male sperm.
Main Outcome Measure(s)
Pregnancy complications, principally including the incidence of preeclampsia.
Result(s)
Notably, we found that the risk of maternal preeclampsia was significantly higher in the oligoasthenospermia group than in the normospermia group. After adjustments for confounding factors by multivariate logistic regression analysis, the incidence of preeclampsia in the oligoasthenospermia group was still significantly higher than that in the normospermia group (6.55% vs. 3.60%; odds ratio, 0.529; 95% confidence interval, 0.282–0.992). However, there were no significant differences in terms of embryo quality, cumulative live birth rate, other pregnancy complications, or neonatal outcomes between the 2 groups.
Conclusion(s)
Oligoasthenospermia was associated with a higher risk of maternal preeclampsia in subfertile couples undergoing IVF-ET treatment. In clinical practice, it is essential to thoroughly evaluate the sperm quality and quantity of male partners before IVF-ET. Further research is needed to establish the causal relationships between semen quality and adverse pregnancy complications, particularly preeclampsia, and explore potential interventions.
目的评估体外受精(IVF)后母体妊娠并发症风险的组间差异是否因男性因素而异:对一项多中心、随机对照、非劣效试验(NCT03118141)的数据进行事后探索性二次分析:受试者共招募了 1131 名在试验期间完整记录了其男性伴侣精液参数的亚不育女性。作为辅助生殖技术(ART)治疗方案的一部分,所有参与者都接受了卵胞浆内单精子注射(ICSI)和冷冻胚胎移植(FET):干预措施:根据男性精子的质量将女性分为少弱精子症组(405人)和正常精子症组(726人):妊娠并发症,主要包括子痫前期的发生率:值得注意的是,我们发现少精症组产妇子痫前期的风险明显高于正常精子症组(P=0.035)。通过多变量逻辑回归分析调整混杂因素后,少精症组的子痫前期发生率仍明显高于正常精子症组(6.55% vs. 3.60%;OR=0.529;95% CI=0.282-0.992;P-adj=0.047)。然而,两组在胚胎质量、累积活产率、其他妊娠并发症或新生儿结局方面没有明显差异(P>0.05):结论:在接受IVF-ET治疗的亚育夫妇中,低精子症与较高的产妇子痫前期风险有关。在临床实践中,体外受精-胚胎移植前彻底评估男性伴侣的精子质量和数量至关重要。要确定精液质量与不良妊娠并发症(尤其是子痫前期)之间的因果关系,并探索潜在的干预措施,还需要进一步的研究。
{"title":"Oligoasthenospermia is correlated with increased preeclampsia incidence in subfertile couples undergoing in vitro fertilization and embryo transfer: a secondary analysis of a randomized clinical trial","authors":"Ling Guo M.D. , Anliang Guo Ph.D. , Xiangxin Lan M.D. , Siqi Tian M.S. , Fengxuan Sun M.D. , Yaxin Su M.S. , Zi-Jiang Chen M.D., Ph.D. , Yongzhi Cao Ph.D. , Yan Li M.D., Ph.D.","doi":"10.1016/j.xfss.2024.08.003","DOIUrl":"10.1016/j.xfss.2024.08.003","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate whether intergroup differences in the risk of maternal pregnancy complications after in vitro fertilization (IVF) vary with male factor.</div></div><div><h3>Design</h3><div>A post hoc exploratory secondary analysis of data from a multicenter, randomized, controlled noninferiority trial (NCT03118141).</div></div><div><h3>Setting</h3><div>Academic fertility centers.</div></div><div><h3>Patient(s)</h3><div>A total of 1,131 subfertile women with complete recording of their male partner’s semen parameters during the trial were enrolled. All participants underwent intracytoplasmic sperm injection followed by frozen embryo transfer (ET) as part of their assisted reproductive technology treatment protocol.</div></div><div><h3>Intervention(s)</h3><div>Women were divided into the oligoasthenospermia (n = 405) and normospermia (n = 726) groups according to the quality of male sperm.</div></div><div><h3>Main Outcome Measure(s)</h3><div>Pregnancy complications, principally including the incidence of preeclampsia.</div></div><div><h3>Result(s)</h3><div>Notably, we found that the risk of maternal preeclampsia was significantly higher in the oligoasthenospermia group than in the normospermia group. After adjustments for confounding factors by multivariate logistic regression analysis, the incidence of preeclampsia in the oligoasthenospermia group was still significantly higher than that in the normospermia group (6.55% vs. 3.60%; odds ratio, 0.529; 95% confidence interval, 0.282–0.992). However, there were no significant differences in terms of embryo quality, cumulative live birth rate, other pregnancy complications, or neonatal outcomes between the 2 groups.</div></div><div><h3>Conclusion(s)</h3><div>Oligoasthenospermia was associated with a higher risk of maternal preeclampsia in subfertile couples undergoing IVF-ET treatment. In clinical practice, it is essential to thoroughly evaluate the sperm quality and quantity of male partners before IVF-ET. Further research is needed to establish the causal relationships between semen quality and adverse pregnancy complications, particularly preeclampsia, and explore potential interventions.</div></div>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Pages 386-394"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141997010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.xfss.2024.08.001
Virginia-Arlene Go M.D. , Jeffery Chavez , Randal D. Robinson M.D. , Bruce J. Nicholson Ph.D.
Objective
To study the role of the mesothelial cells in early endometriosis lesion formation by assessing in vitro cell-to-cell communication and invasion of endometrial cells across a mesothelial cell monolayer, with both cell types derived from both patients with endometriosis and control patients.
Design
Laboratory-based experimental study.
Setting
University hospital and laboratory.
Patient(s)
Consenting reproductive-age women who underwent laparoscopy for gynecologic reasons and were confirmed to have either endometriosis with pathology tissue diagnosis (n = 8) or no endometriosis n = 8) at the time of surgery.
Intervention(s)
Primary stromal cells cultured from endometrial pipelle biopsies and primary mesothelial cells cultured from peritoneal explants were used in transmesothelial invasion assays and gap junction coupling assays.
Main Outcome Measure(s)
Comparison of potential for lesion formation, using in vitro models, of both primary endometrial and mesothelial cells from patients with endometriosis and control patients, establishing the former as the primary disease driver.
Result(s)
When comparing mesothelial cells from control patients with those from patients with endometriosis, there was no significant difference in the amount of stromal cell invasion across either barrier. In contrast, when comparing stromal cell origin, the amount of invasion by endometriosis stromal cells was greater than control stromal cells regardless of whether the mesothelial cell monolayer was derived from patients with the disease or control patients. Additionally, primary mesothelial cells induced more gap junction coupling, a requirement for invasion, in stromal cells from patients with endometriosis than control patients, again independent of mesothelial origin. The notable exception was mesothelial cells derived from endometriotic lesion-affected areas that showed depressed ability to support invasion.
Conclusion(s)
Although both endometrial and mesothelial cells need to function for establishment of endometriosis lesions, the endometrium seems to be the key player, serving as an ideal target for diagnostic strategies and therapeutic intervention. While this notion is consistent with previous studies, to our knowledge, we are the first to directly test both primary mesothelial and endometrial cells from patients with endometriosis and control patients to compare propensities for mesothelial invasion.
{"title":"A seed or soil problem in early endometriosis: stromal cell origin drives cellular invasion and coupling over mesothelial cell origin","authors":"Virginia-Arlene Go M.D. , Jeffery Chavez , Randal D. Robinson M.D. , Bruce J. Nicholson Ph.D.","doi":"10.1016/j.xfss.2024.08.001","DOIUrl":"10.1016/j.xfss.2024.08.001","url":null,"abstract":"<div><h3>Objective</h3><div>To study the role of the mesothelial cells in early endometriosis lesion formation by assessing in vitro cell-to-cell communication and invasion of endometrial cells across a mesothelial cell monolayer, with both cell types derived from both patients with endometriosis and control patients.</div></div><div><h3>Design</h3><div>Laboratory-based experimental study.</div></div><div><h3>Setting</h3><div>University hospital and laboratory.</div></div><div><h3>Patient(s)</h3><div>Consenting reproductive-age women who underwent laparoscopy for gynecologic reasons and were confirmed to have either endometriosis with pathology tissue diagnosis (n = 8) or no endometriosis n = 8) at the time of surgery.</div></div><div><h3>Intervention(s)</h3><div>Primary stromal cells cultured from endometrial pipelle biopsies and primary mesothelial cells cultured from peritoneal explants were used in transmesothelial invasion assays and gap junction coupling assays.</div></div><div><h3>Main Outcome Measure(s)</h3><div>Comparison of potential for lesion formation, using in vitro models, of both primary endometrial and mesothelial cells from patients with endometriosis and control patients, establishing the former as the primary disease driver.</div></div><div><h3>Result(s)</h3><div>When comparing mesothelial cells from control patients with those from patients with endometriosis, there was no significant difference in the amount of stromal cell invasion across either barrier. In contrast, when comparing stromal cell origin, the amount of invasion by endometriosis stromal cells was greater than control stromal cells regardless of whether the mesothelial cell monolayer was derived from patients with the disease or control patients. Additionally, primary mesothelial cells induced more gap junction coupling, a requirement for invasion, in stromal cells from patients with endometriosis than control patients, again independent of mesothelial origin. The notable exception was mesothelial cells derived from endometriotic lesion-affected areas that showed depressed ability to support invasion.</div></div><div><h3>Conclusion(s)</h3><div>Although both endometrial and mesothelial cells need to function for establishment of endometriosis lesions, the endometrium seems to be the key player, serving as an ideal target for diagnostic strategies and therapeutic intervention. While this notion is consistent with previous studies, to our knowledge, we are the first to directly test both primary mesothelial and endometrial cells from patients with endometriosis and control patients to compare propensities for mesothelial invasion.</div></div>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":"5 4","pages":"Pages 395-403"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141914743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To evaluate the effects of a P2X4 receptor (P2X4R)-specific antagonist on murine endometriotic-like lesions and human endometriotic stromal cells.
Design: Experimental study using an in vivo mouse endometriosis model and in vitro primary culture of human endometriotic stromal cells. NC-2600, an antagonist of the P2X4 ionotropic ATP receptor (P2X4R), was orally administered to the mice and cells. Gene expression analyses for cytokines were conducted in the endometriotic-like cysts and vaginal portion of mice, and immunohistochemistry was performed to evaluate the proliferative activity and localization of macrophages in addition to cytokine expression. The sensation of murine vaginal pain was evaluated using visceromotor responses.
Setting: The study was performed in academic and hospital research laboratories.
Results: NC-2600 reduced the proliferation of the cyst epithelium and vaginal pain sensation. In both cysts and vaginas, P2X4R is mainly expressed in macrophages, and NC-2600 reduces the number of tissue macrophages and reverses the elevated expression of InterleukinL-33 and cyclooxygenase-2 in animals with endometriosis.
Conclusion: These results indicate unknown pathophysiological roles of P2X4R expressed in local macrophages at the injury site of endometriosis and in the vagina, suggesting the potential therapeutic effects of orally administered P2X4R inhibitors for alleviating the symptoms of endometriosis.
{"title":"P2X4 receptor mediates macrophage infiltration leading to endometriotic cyst epithelium proliferation and hyperalgesia in mouse model.","authors":"Hiroki Nagata, Takeshi Y Hiyama, Misaki Inoue, Shanshan Xu, Ikumi Wada, Yuki Yoshimura, Kazuomi Nakamura, Yukihiro Azuma, Tasuku Harada, Fuminori Taniguchi","doi":"10.1016/j.xfss.2024.10.007","DOIUrl":"10.1016/j.xfss.2024.10.007","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the effects of a P2X4 receptor (P2X4R)-specific antagonist on murine endometriotic-like lesions and human endometriotic stromal cells.</p><p><strong>Design: </strong>Experimental study using an in vivo mouse endometriosis model and in vitro primary culture of human endometriotic stromal cells. NC-2600, an antagonist of the P2X4 ionotropic ATP receptor (P2X4R), was orally administered to the mice and cells. Gene expression analyses for cytokines were conducted in the endometriotic-like cysts and vaginal portion of mice, and immunohistochemistry was performed to evaluate the proliferative activity and localization of macrophages in addition to cytokine expression. The sensation of murine vaginal pain was evaluated using visceromotor responses.</p><p><strong>Setting: </strong>The study was performed in academic and hospital research laboratories.</p><p><strong>Results: </strong>NC-2600 reduced the proliferation of the cyst epithelium and vaginal pain sensation. In both cysts and vaginas, P2X4R is mainly expressed in macrophages, and NC-2600 reduces the number of tissue macrophages and reverses the elevated expression of InterleukinL-33 and cyclooxygenase-2 in animals with endometriosis.</p><p><strong>Conclusion: </strong>These results indicate unknown pathophysiological roles of P2X4R expressed in local macrophages at the injury site of endometriosis and in the vagina, suggesting the potential therapeutic effects of orally administered P2X4R inhibitors for alleviating the symptoms of endometriosis.</p>","PeriodicalId":73012,"journal":{"name":"F&S science","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142514111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}