Premature ovarian failure (POF) is a refractory disease for clinical treatment with the goal of restoring fertility. In this study, umbilical cord mesenchymal stem cells on a collagen scaffold (collagen/UC-MSCs) can activate primordial follicles in vitro via phosphorylation of FOXO3a and FOXO1. Transplantation of collagen/UC-MSCs to the ovaries of POF patients rescued overall ovarian function, evidenced by elevated estradiol concentrations, improved follicular development, and increased number of antral follicles. Successful clinical pregnancy was achieved in women with POF after transplantation of collagen/UC-MSCs or UC-MSCs. In summary, collagen/UC-MSC transplantation may provide an effective treatment for POF.
Polycystic ovary syndrome (PCOS) is a common endocrine, metabolic and heterogeneous disorder in women of reproductive age, the exact etiology of which remains unknown. To unravel the molecular mechanisms underlying the hyperandrogenic phenotype of PCOS, prenatally androgenized (PNA) mice were used to mimic this phenotype in women with PCOS. Using microarray analysis, 1188 differentially expressed genes, including 671 upregulated and 517 downregulated genes, were identified in ovaries from PNA mice. Five differentially expressed genes (Aldh1a7, Bhmt, Mtr, Nrcam, Ptprg) were validated, and decreased MTR expression was shown in ovaries of PNA mice. In addition, results from qRT-PCR showed decreased MTR expression in granulosa cells (GCs) from women with the hyperandrogenic phenotype of PCOS. Serum levels of S-adenosyl methionine (SAM), the downstream product of MTR, were also decreased in PNA mice and women with the hyperandrogenic phenotype of PCOS. Our study provides evidence that the hyperandrogenic phenotype of PCOS is linked to abnormal folate one-carbon metabolism.
Preeclampsia remains a high cause of incidence and death for mothers and fetuses in developing nations. Preeclampsia has numerous clinical and biochemical markers that have been tested, but they have failed to provide a conclusive diagnosis in the different phases of the disease’s progression. Herein, our team intended to determine potential diagnostic biomarkers for preeclampsia and analyzed associations with immune cells. Two microarray data from mankind’s preeclampsia and control specimens were acquired from GSE75010 and GSE44711 datasets. Differentially expressed genes (DEGs) were identified between77 normal samples and 80 preeclampsia samples. Candidate biomarkers were discovered using the least absolute shrinkage and selection operator (LASSO) and the support vector machine recursive feature elimination (SVM-RFE) analysis. The expressions and diagnostic values of genes in preeclampsia were further demonstrated in the GSE44711 dataset (8 control samples and 8 preeclampsia samples). The correlation of critical genes with the proportion of immune cells was analyzed. We identified 20 DEGs in preeclampsia. Diseases enriched by DEGs were mainly related to preeclampsia, gestational diabetes, ovarian disease, female reproductive system disease, and endocrine system disease. COL17A1, FLT1, FSTL3, and SERPINA3 were identified as diagnostic genes of preeclampsia and validated in the GSE44711 datasets. Immune cell infiltration assays suggested that COL17A1, FLT1, FSTL3, and SERPINA3 were related to several immune cells. Overall, we identified four critical diagnostic genes in preeclampsia. Furthermore, more well-designed research studies with larger cohorts were warranted to confirm the value of the four genes for the diagnosis and outcome of preeclampsia patients.
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