Decidualization of endometrial stromal cells is the pre-requisite for the embryo implantation and establishment of pregnancy. Although known to be regulated by several factors, the process of regulation of decidualization by miRNAs is largely unknown. Previous reports suggest that the upregulated expression of miR-145 is associated with repeated implantation failure. The current study was aimed to identify and validate the role of miR-145 in regulating stromal cell decidualization and the mechanism involved therein. Expression of miR-145 was found to be downregulated during the decidualization period of early pregnancy and also in artificially induced decidualization in rat uterus. During in vitro decidualization in rat endometrial stromal cells (ESCs), the overexpression of mimic miR-145 attenuated the progression of decidualization. Biochemical marker alkaline phosphatase and protein markers (insulin-like growth factor binding protein, cyclin D3) were also suppressed in miR-145 mimic-transfected cells as compared to normal decidualized cells. Bioinformatic analysis and luciferase reporter assay confirmed that Smad1 is the direct target of miR-145. Differentiation of ESCs was inhibited in miR-145 mimic-transfected cells which occurred via downregulating the target Smad1 along with its downstream p-Smad1/5/8 and Wnt-4. Pre-treatment of ESCs with Smad1 siRNA resulted in downregulated expression of p-Smad1/5/8, Wnt-4, Cox-2, and VEGF. In addition, miR-145 overexpression resulted in the loss of angiogenic factors Cox-2, MMP-9, and VEGF, indicating suppression of the process of angiogenesis. Migration of human umbilical vein endothelial cells was also attenuated in the presence of conditioned media obtained from miR-145-transfected decidualizing cells. In conclusion, the study demonstrated the role of miR-145 in regulation of progression of decidualization which is mediated through inhibition of Smad1. KEY MESSAGES: MiR-145 expression is downregulated during decidualization in the rat uterus. Overexpression of miR-145 inhibited the decidualization progression. MiR-145 suppressed the migration and invasion of HUVECs. MiR-145 downregulated Smad1 which suppresses Smad1/5/8, Wnt-4, MMP-9, Cox-2, and VEGF.
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http://dx.doi.org/10.1007/s00109-019-01744-6 | DOI Listing |
Gynecol Endocrinol
December 2024
Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Objective: To investigate the effectiveness of gelatin/polycaprolactone (GT/PCL) membranes for restoring endometrial structure and function and fertility in a rat model of endometrial injury.
Methods: We randomized 125 female Sprague-Dawley (SD) rats to the sham, natural repair (NR), estrogen (E), GT/PCL, and E-GT/PCL groups. Except for the sham group, all rats underwent uterine curettage.
Comb Chem High Throughput Screen
November 2024
Nanjing University of Chinese Medicine, Nanjing Jiangsu 210023, China.
Background: Reproductive endocrine disorder can impair endometrial receptivity, preventing embryo implantation and increasing miscarriage risk. Impaired endometrial receptivity contributes significantly to female infertility. Inflammatory signaling pathways including the IL-6/STAT3 pathway help embryos implant.
View Article and Find Full Text PDFReprod Toxicol
November 2024
Division of Toxicology, Wageningen University and Research, Stippeneng 4, Wageningen 6708 WE, the Netherlands.
Placenta
November 2024
Universidad de Buenos Aires (UBA). Facultad de Medicina, Argentina; CONICET - UBA. Laboratory of Reproduction and Metabolism, Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Buenos Aires, Argentina. Electronic address:
Mol Nutr Food Res
November 2024
Institute of Applied Anatomy and Reproductive Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan, 421001, China.
Scope: Polycystic ovary syndrome (PCOS) is a common endocrine disorder that can lead to insulin resistance (IR) and dysregulation of glucose metabolism, resulting in an imbalance in the endometrial environment, which is unfavorable for embryo implantation of PCOS. This study aims to investigate whether nicotinamide mononucleotide (NMN) improves the stability of the endometrium in a rat model of PCOS and identifies whether it is related to reduce IR and increase glycolysis levels and its potential signaling pathway.
Methods And Results: Female Sprague-Dawley (SD) rats are fed letrozole and a high-fat diet (HFD) to form the PCOS model, then the model rats are treated with or without NMN.
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