Reproductive biology and endocrinology : RB&E最新文献

{"title":"Diverse actions of sirtuin-1 on ovulatory genes and cell death pathways in human granulosa cells.","authors":"Jackson Sapuleni,&nbsp;Magdalena Szymanska,&nbsp;Rina Meidan","doi":"10.1186/s12958-022-00970-x","DOIUrl":"https://doi.org/10.1186/s12958-022-00970-x","url":null,"abstract":"<p><strong>Background: </strong>Human granulosa-lutein cells (hGLCs) amply express sirtuin-1 (SIRT1), a NAD + -dependent deacetylase that is associated with various cellular functions. SIRT1 was shown to elevate cAMP on its own and additively with human chorionic gonadotropin (hCG), it is therefore interesting to examine if SIRT1 affects other essential hGLC functions.</p><p><strong>Methods: </strong>Primary hGLCs, obtained from the follicular aspirates of women undergoing IVF and SV40-transfected, immortalized hGLCs (SVOG cells), were used. Primary cells were treated with SIRT1 specific activator SRT2104, as well as hCG or their combination. Additionally, siRNA-targeting SIRT1 construct was used to silence endogenous SIRT1 in SVOG cells. PTGS2, EREG, VEGFA and FGF2 expression was determined using quantitative polymerase chain reaction (qPCR). Apoptotic and necroptotic proteins were determined by specific antibodies in western blotting. Cell viability/apoptosis was determined by the XTT and flow cytometry analyses. Data were analyzed using student t-test or Mann-Whitney U test or one-way ANOVA followed by Tukey HSD post hoc test.</p><p><strong>Results: </strong>In primary and immortalized hGLCs, SRT2104 significantly upregulated key ovulatory and angiogenic genes: PTGS2, EREG, FGF2 and VEGFA, these effects tended to be further augmented in the presence of hCG. Additionally, SRT2104 dose and time-dependently decreased viable cell numbers. Flow cytometry of Annexin V stained cells confirmed that SIRT1 reduced live cell numbers and increased late apoptotic and necrotic cells. Moreover, we found that SIRT1 markedly reduced anti-apoptotic BCL-XL and MCL1 protein levels and increased cleaved forms of pro-apoptotic proteins caspase-3 and PARP. SIRT1 also significantly induced necroptotic proteins RIPK1 and MLKL. RIPK1 inhibitor, necrostatin-1 mitigated SIRT1 actions on RIPK1 and MLKL but also on cleaved caspase-3 and PARP and in accordance on live and apoptotic cells, implying a role for RIPK1 in SIRT1-induced cell death. SIRT1 silencing produced inverse effects on sorted cell populations, anti-apoptotic, pro-apoptotic and necroptotic proteins, corroborating SIRT1 activation.</p><p><strong>Conclusions: </strong>These findings reveal that in hGLCs, SIRT1 enhances the expression of ovulatory and angiogenic genes while eventually advancing cell death pathways. Interestingly, these seemingly contradictory events may have occurred in a cAMP-dependent manner.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"104"},"PeriodicalIF":4.4,"publicationDate":"2022-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9284863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40527225","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}

{"title":"A loss-of-function variant in SSFA2 causes male infertility with globozoospermia and failed oocyte activation.","authors":"Gelin Huang,&nbsp;Xueguang Zhang,&nbsp;Guanping Yao,&nbsp;Lin Huang,&nbsp;Sixian Wu,&nbsp;Xiaoliang Li,&nbsp;Juncen Guo,&nbsp;Yuting Wen,&nbsp;Yan Wang,&nbsp;Lijun Shang,&nbsp;Na Li,&nbsp;Wenming Xu","doi":"10.1186/s12958-022-00976-5","DOIUrl":"https://doi.org/10.1186/s12958-022-00976-5","url":null,"abstract":"<p><p>Globozoospermia (OMIM: 102530) is a rare type of teratozoospermia (< 0.1%). The etiology of globozoospermia is complicated and has not been fully revealed. Here, we report an infertile patient with globozoospermia. Variational analysis revealed a homozygous missense variant in the SSFA2 gene (NM_001130445.3: c.3671G > A; p.R1224Q) in the patient. This variant significantly reduced the protein expression of SSFA2. Immunofluorescence staining showed positive SSFA2 expression in the acrosome of human sperm. Liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) and Coimmunoprecipitation (Co-IP) analyses identified that GSTM3 and Actin interact with SSFA2. Further investigation revealed that for the patient, regular intracytoplasmic sperm injection (ICSI) treatment had a poor prognosis. However, Artificial oocyte activation (AOA) by a calcium ionophore (A23187) after ICSI successfully rescued the oocyte activation failure for the patient with the SSFA2 variant, and the couple achieved a live birth. This study revealed that SSFA2 plays an important role in acrosome formation, and the homozygous c.3671G > A loss-of-function variant in SSFA2 caused globozoospermia. SSFA2 may represent a new gene in the genetic diagnosis of globozoospermia, especially the successful outcome of AOA-ICSI treatment for couples, which has potential value for clinicians in their treatment regimen selections.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"103"},"PeriodicalIF":4.4,"publicationDate":"2022-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9281110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40604451","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}

{"title":"IGF2 reduces meiotic defects in oocytes from obese mice and improves embryonic developmental competency.","authors":"Yanling Wan,&nbsp;Tahir Muhammad,&nbsp;Tao Huang,&nbsp;Yue Lv,&nbsp;Qianqian Sha,&nbsp;Shuang Yang,&nbsp;Gang Lu,&nbsp;Wai-Yee Chan,&nbsp;Jinlong Ma,&nbsp;Hongbin Liu","doi":"10.1186/s12958-022-00972-9","DOIUrl":"https://doi.org/10.1186/s12958-022-00972-9","url":null,"abstract":"<p><strong>Background: </strong>Maternal obesity is a global issue that has devastating effects across the reproductive spectrum such as meiotic defects in oocytes, consequently worsening pregnancy outcomes. Different studies have shown that such types of meiotic defects originated from the oocytes of obese mothers. Thus, there is an urgent need to develop strategies to reduce the incidence of obesity-related oocyte defects that adversely affect pregnancy outcomes. Multiple growth factors have been identified as directly associated with female reproduction; however, the impact of various growth factors on female fertility in response to obesity remains poorly understood.</p><p><strong>Methods: </strong>The immature GV-stage oocytes from HFD female mice were collected and cultured in vitro in two different groups (HFD oocytes with and without 50 nM IGF2), however; the oocytes from ND mice were used as a positive control. HFD oocytes treated with or without IGF2 were further used to observe the meiotic structure using different analysis including, the spindle and chromosomal analysis, reactive oxygen species levels, mitochondrial functional activities, and early apoptotic index using immunofluorescence. Additionally, the embryonic developmental competency and embryos quality of IGF2-treated zygotes were also determined.</p><p><strong>Results: </strong>In our findings, we observed significantly reduced contents of insulin-like growth factor 2 (IGF2) in the serum and oocytes of obese mice. Our data indicated supplementation of IGF2 in a culture medium improves the blastocyst formation: from 46% in the HFD group to 61% in the HFD + IGF2-treatment group (50 nM IGF2). Moreover, adding IGF2 to the culture medium reduces the reactive oxygen species index and alleviates the frequency of spindle/chromosome defects. We found increased mitochondrial functional activity in oocytes from obese mice after treating the oocytes with IGF2: observed elevated level of adenosine triphosphate, increased mitochondrial distribution, higher mitochondrial membrane potentials, and reduced mitochondrial ultrastructure defects. Furthermore, IGF2 administration also increases the overall protein synthesis and decreases the apoptotic index in oocytes from obese mice.</p><p><strong>Conclusions: </strong>Collectively, our findings are strongly in favor of adding IGF2 in culture medium to overcome obesity-related meiotic structural-developmental defects by helping ameliorate the known sub-optimal culturing conditions that are currently standard with assisted reproduction technologies.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"101"},"PeriodicalIF":4.4,"publicationDate":"2022-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9281013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40506126","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}

{"title":"The expression of IGFBP-5 in the reproductive axis and effect on the onset of puberty in female rats.","authors":"Zhiqiu Yao,&nbsp;Maosen Lin,&nbsp;Tao Lin,&nbsp;Xinbao Gong,&nbsp;Pin Qin,&nbsp;Hailing Li,&nbsp;Tiezhu Kang,&nbsp;Jing Ye,&nbsp;Yanyun Zhu,&nbsp;Qiwen Hong,&nbsp;Ya Liu,&nbsp;Yunsheng Li,&nbsp;Juhua Wang,&nbsp;Fugui Fang","doi":"10.1186/s12958-022-00966-7","DOIUrl":"https://doi.org/10.1186/s12958-022-00966-7","url":null,"abstract":"<p><p>Insulin-like growth factor-binding protein-5 (IGFBP-5) has recently been shown to alter the reproductive capacity by regulating insulin-like growth factor (IGF) bioavailability or IGF-independent effects. The present study aimed to investigate the effect and mechanism of IGFBP-5 on the onset of puberty in female rats. Immunofluorescence and real-time quantitative PCR were used to determine the expression and location of IGFBP-5 mRNA and protein distribution in the infant's hypothalamus-pituitary-ovary (HPO) axis prepuberty, peripuberty, puberty and adult female rats. Prepubertal rats with IGFBP-5 intracerebroventricular (ICV) were injected to determine the puberty-related genes expression and the concentrations of reproductive hormones. Primary hypothalamic cells were treated with IGFBP-5 to determine the expression of puberty-related genes and the Akt and mTOR proteins. Results showed that Igfbp-5 mRNA and protein were present on the HPO axis. The addition of IGFBP-5 to primary hypothalamic cells inhibited the expression of Gnrh and Igf-1 mRNAs (P < 0.05) and increased the expression of AKT and mTOR protein (P < 0.01). IGFBP-5 ICV-injection delayed the onset of puberty, reduced Gnrh, Igf-1, and Fshβ mRNAs, and decreased the concentrations of E2, P4, FSH,serum LH levels and the ovaries weight (P < 0.05). More corpus luteum and fewer primary follicles were found after IGFBP-5 injection (P < 0.05).</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"100"},"PeriodicalIF":4.4,"publicationDate":"2022-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9277959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40515819","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}

{"title":"Regulatory roles of alternative splicing at Ezh2 gene in mouse oocytes.","authors":"Shi-Meng Guo,&nbsp;Xing-Ping Liu,&nbsp;Qing Tian,&nbsp;Cai-Feng Fei,&nbsp;Yi-Ran Zhang,&nbsp;Zhi-Ming Li,&nbsp;Ying Yin,&nbsp;Ximiao He,&nbsp;Li-Quan Zhou","doi":"10.1186/s12958-022-00962-x","DOIUrl":"https://doi.org/10.1186/s12958-022-00962-x","url":null,"abstract":"<p><strong>Background: </strong>Enhancer of zeste homologue 2 (EZH2), the core member of polycomb repressive complex 2 (PRC2), has multiple splicing modes and performs various physiological functions. However, function and mechanism of alternative splicing at Ezh2 exon 3 in reproduction are unknown.</p><p><strong>Methods: </strong>We generated Ezh2^Long and Ezh2^Short mouse models with different point mutations at the Ezh2 exon 3 alternative splicing site, and each mutant mouse model expressed either the long or the short isoform of Ezh2. We examined mutant mouse fertility and oocyte development to assess the function of Ezh2 alternative splicing at exon 3 in the reproductive system.</p><p><strong>Results: </strong>We found that Ezh2^Long female mice had normal fertility. However, Ezh2^Short female mice had significantly decreased fertility and obstructed oogenesis, with compromised mitochondrial function in Ezh2^Short oocytes. Interestingly, increased EZH2 protein abundance and accumulated H3K27me3 were observed in Ezh2^Short oocytes.</p><p><strong>Conclusions: </strong>Our results demonstrate that correct Ezh2 alternative splicing at exon 3 is important for mouse oogenesis.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"99"},"PeriodicalIF":4.4,"publicationDate":"2022-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9254527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40472902","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}

{"title":"Basal and dynamic relationships between serum anti-Müllerian hormone and gonadotropins in patients with functional hypothalamic amenorrhea, with or without polycystic ovarian morphology.","authors":"Marlene Hager,&nbsp;Johannes Ott,&nbsp;Julian Marschalek,&nbsp;Marie-Louise Marschalek,&nbsp;Clemens Kinsky,&nbsp;Rodrig Marculescu,&nbsp;Didier Dewailly","doi":"10.1186/s12958-022-00961-y","DOIUrl":"https://doi.org/10.1186/s12958-022-00961-y","url":null,"abstract":"<p><strong>Background: </strong>To evaluate in women with functional hypothalamic amenorrhea (FHA), whether there is a difference between patients with and without polycystic ovarian morphology (PCOM) concerning the response to a gonadotropin releasing hormone (GnRH) stimulation test and to pulsatile GnRH treatment.</p><p><strong>Methods: </strong>In a retrospective observational study, 64 women with FHA who underwent a GnRH stimulation test and 32 age-matched controls without PCOM were included. Pulsatile GnRH treatment was provided to 31 FHA patients and three-month follow-up data were available for 19 of these.</p><p><strong>Results: </strong>Serum levels of gonadotropins and estradiol were lower in FHA women than in controls (p < 0.05). FHA patients revealed PCOM in 27/64 cases (42.2%). FHA patients without PCOM revealed lower anti-Müllerian hormone (AMH) levels than controls (median 2.03 ng/mL, IQR 1.40-2.50, versus 3.08 ng/mL, IQR 2.24-4.10, respectively, p < 0.001). Comparing FHA patients with and without PCOM, the latter revealed lower AMH levels, a lower median LH increase after the GnRH stimulation test (240.0%, IQR 186.4-370.0, versus 604.9%, IQR 360.0-1122.0; p < 0.001) as well as, contrary to patients with PCOM, a significant increase in AMH after three months of successful pulsatile GnRH treatment (median 1.69 ng/mL at baseline versus 2.02 ng/mL after three months of treatment; p = 0.002).</p><p><strong>Conclusions: </strong>In women with FHA without PCOM, the phenomenon of low AMH levels seems to be based on relative gonadotropin deficiency rather than diminished ovarian reserve. AMH tended to rise after three months of pulsatile GnRH treatment. The differences found between patients with and without PCOM suggest the former the existence of some PCOS-specific systemic and/or intra-ovarian abnormalities.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"98"},"PeriodicalIF":4.4,"publicationDate":"2022-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9251918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40583753","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}

{"title":"Myostatin: a multifunctional role in human female reproduction and fertility - a short review.","authors":"Sijia Wang,&nbsp;Lanlan Fang,&nbsp;Luping Cong,&nbsp;Jacqueline Pui Wah Chung,&nbsp;Tin Chiu Li,&nbsp;David Yiu Leung Chan","doi":"10.1186/s12958-022-00969-4","DOIUrl":"https://doi.org/10.1186/s12958-022-00969-4","url":null,"abstract":"<p><p>Myostatin (MSTN) is member of the transforming growth factor β (TGF-β) superfamily and was originally identified in the musculoskeletal system as a negative regulator of skeletal muscle growth. The functional roles of MSTN outside of the musculoskeletal system have aroused researchers' interest in recent years, with an increasing number of studies being conducted in this area. Notably, the expression of MSTN and its potential activities in various reproductive organs, including the ovary, placenta, and uterus, have recently been examined. Numerous studies published in the last few years demonstrate that MSTN plays a critical role in human reproduction and fertility, including the regulation of follicular development, ovarian steroidogenesis, granule-cell proliferation, and oocyte maturation regulation. Furthermore, findings from clinical samples suggest that MSTN may play a key role in the pathogenesis of several reproductive disorders such as uterine myoma, preeclampsia (PE), ovary hyperstimulation syndrome (OHSS), and polycystic ovarian syndrome (PCOS). There is no comprehensive review regarding to MSTN related to the female reproductive system in the literature. This review serves as a summary of the genes in reproductive medicine and their potential influence. We summarized MSTN expression in different compartments of the female reproductive system. Subsequently, we discuss the role of MSTN in both physiological and several pathological conditions related to the female fertility and reproduction-related diseases.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"96"},"PeriodicalIF":4.4,"publicationDate":"2022-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9250276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40465853","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}

{"title":"Follicle-stimulating hormone signaling in Sertoli cells: a licence to the early stages of spermatogenesis.","authors":"Jia-Ming Wang,&nbsp;Zhen-Fang Li,&nbsp;Wan-Xi Yang,&nbsp;Fu-Qing Tan","doi":"10.1186/s12958-022-00971-w","DOIUrl":"https://doi.org/10.1186/s12958-022-00971-w","url":null,"abstract":"<p><p>Follicle-stimulating hormone signaling is essential for the initiation and early stages of spermatogenesis. Follicle-stimulating hormone receptor is exclusively expressed in Sertoli cells. As the only type of somatic cell in the seminiferous tubule, Sertoli cells regulate spermatogenesis not only by controlling their own number and function but also through paracrine actions to nourish germ cells surrounded by Sertoli cells. After follicle-stimulating hormone binds to its receptor and activates the follicle-stimulating hormone signaling pathway, follicle-stimulating hormone signaling will establish a normal Sertoli cell number and promote their differentiation. Spermatogonia pool maintenance, spermatogonia differentiation and their entry into meiosis are also positively regulated by follicle-stimulating hormone signaling. In addition, follicle-stimulating hormone signaling regulates germ cell survival and limits their apoptosis. Our review summarizes the aforementioned functions of follicle-stimulating hormone signaling in Sertoli cells. We also describe the clinical potential of follicle-stimulating hormone treatment in male patients with infertility. Furthermore, our review may be helpful for developing better therapies for treating patients with dysfunctional follicle-stimulating hormone signaling in Sertoli cells.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"97"},"PeriodicalIF":4.4,"publicationDate":"2022-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9250200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40565698","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}

{"title":"The role of ERK-1 and ERK-2 gene polymorphisms in PCOS pathogenesis.","authors":"Gurhan Guney,&nbsp;Mine Islimye Taşkın,&nbsp;Nazli Sener,&nbsp;Ezgi Tolu,&nbsp;Yavuz Dodurga,&nbsp;Levent Elmas,&nbsp;Orkun Cetin,&nbsp;Cengiz Sarigul","doi":"10.1186/s12958-022-00967-6","DOIUrl":"https://doi.org/10.1186/s12958-022-00967-6","url":null,"abstract":"<p><strong>Background: </strong>Ovulation is regulated by extracellular signal-regulated kinase-1 (ERK-1) and ERK-2 signaling mechanisms, and ERK-1/2 kinases modulates the function of most of the LH-regulated genes. Defective ERK kinase signaling that is secondary to a genetic problem contributes to both ovulatory dysfunction and metabolic problems in polycystic ovary syndrome (PCOS). We planned to investigate ERK-1 and ERK-2 gene polymorphisms in PCOS for the first time in the Turkish population.</p><p><strong>Methods: </strong>One hundred two PCOS patients and 102 healthy controls were recruited for this patient control study. HOMA-IR, Ferriman-Gallwey score (FGS), waist-to-hip ratio (WHR), and body mass index (BMI) were assessed. Lipid profile levels, CRP, and total testosterone were determined. ERK-2 rs2276008 (G > C) and ERK-1 rs11865228 (G > A) SNPs were analyzed with a real-time PCR system.</p><p><strong>Results: </strong>ERK-1 and ERK-2 genotypes were found to differ between the PCOS and control groups. In patients with PCOS, ERK-1 GA and ERK-2 GC genotypes were different in terms of BMI, FGS, HOMA-IR, CRP, total testosterone, and total cholesterol levels.</p><p><strong>Conclusions: </strong>ERK-1 and ERK-2 genes are involved in PCOS pathogenesis. BMI, FGS, HOMA-IR, and CRP levels are related to the heterozygote polymorphic types of ERK-1 and ERK-2 genes.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"95"},"PeriodicalIF":4.4,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9241270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40409342","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}

{"title":"Endometrial thickness is an independent risk factor of hypertensive disorders of pregnancy: a retrospective study of 13,458 patients in frozen-thawed embryo transfers.","authors":"Meng Zhang,&nbsp;Jing Li,&nbsp;Xiao Fu,&nbsp;Yiting Zhang,&nbsp;Tao Zhang,&nbsp;Bingjie Wu,&nbsp;Xinyue Han,&nbsp;Shanshan Gao","doi":"10.1186/s12958-022-00965-8","DOIUrl":"https://doi.org/10.1186/s12958-022-00965-8","url":null,"abstract":"<p><strong>Background: </strong>Hypertensive disorders of pregnancy (HDP) are an important cause of maternal and fetal mortality, and its potential risk factors are still being explored. Endometrial thickness (EMT), as one of the important monitoring indicators of endometrial receptivity, has been confirmed to be related to the incidence of HDP in fresh embryo transfer. Our study was designed to investigate whether endometrial thickness is associated with the risk of hypertensive disorders of pregnancy in frozen-thawed embryo transfer (FET).</p><p><strong>Methods: </strong>This respective cohort study enrolled 13,458 women who received vitrified embryo transfer and had a singleton delivery in the Reproductive Hospital affiliated to Shandong University from January 2015 to December 2019. We set strict screening criteria and obtained the information from the hospital electronic medical system. Statistical methods including logistic regression analysis, receiver operating characteristic curve and restricted cubic spline were used to evaluate the relationship between endometrial thickness and the incidence of pregnancy-induced hypertension.</p><p><strong>Results: </strong>The incidences of HDP in a thin endometrial thickness group (< 0.8 cm) and a thick endometrial thickness group (> 1.2 cm) were significantly greater than in a reference group (0.8 cm-1.2 cm) (7.98 and 5.24% vs 4.59%, P <  0.001). A nonlinear relationship between endometrial thickness and risk of hypertensive disorders of pregnancy was examined by restricted cubic spline (P <  0.001). The thin endometrial thickness and thick endometrial thickness groups were significantly associated with the risk of HDP after adjusting for confounding variables by stepwise logistic regression analysis. Subsequently, subgroup logistic regression analysis based on endometrial preparation regimens showed that thin endometria were still significantly associated with a higher morbidity rate in the artificial cycle group, while in the natural cycle group, thick endometria were closely associated with increased morbidity.</p><p><strong>Conclusion: </strong>Our study manifested that both the thin and thick endometria were associated with an increased risk of hypertensive disorders of pregnancy in frozen embryo transfer cycles. Reproductive clinicians should focus on adjusting endometrial thickness in different preparation regimens; and obstetricians should be mindful of the risk of hypertension during pregnancy, when women with thin (< 0.8 cm) or excessively thicker (> 1.2 cm) endometrial thickness achieve pregnancy through frozen-thawed embryo transfer.</p>","PeriodicalId":520764,"journal":{"name":"Reproductive biology and endocrinology : RB&E","volume":" ","pages":"93"},"PeriodicalIF":4.4,"publicationDate":"2022-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9238038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40407774","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}