Immortalized Human Endometrial Stromal Cells (HESC)
Cat.No.: CSC-I9213L
Species: Homo sapiens
Source: Endometria
Morphology: Fibroblast-like
Culture Properties: Adherent
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Note: Never can cells be kept at -20 °C.
2) ELISA and RT-PCR were performed to detect IGFBP-1, FN, PRL and PAI-1 secretion and mRNA expression;
3) Western blot and densitometry were conducted to determine the expression of TF and Fas/Fas ligand.
The endometrium undergoes dynamic cyclic remodeling, in which endometrial stromal cells (ESCs) differentiate into secretory decidual cells under the influence of ovarian steroids-a process essential for embryo implantation and pregnancy establishment. However, primary human ESCs present considerable experimental limitations: they are hampered by the scarcity of adequate human tissue and possess a limited proliferative capacity, undergoing rapid dedifferentiation and senescence after only a finite number of passages. These constraints severely restrict long-term, high-throughput mechanistic investigations. To circumvent these obstacles, immortalized human ESC lines have been established through the stable transduction of human telomerase reverse transcriptase (hTERT).
These immortalized human ESC lines offer the following distinct advantages: (1) maintenance of a normal diploid karyotype without clonal chromosomal structural or numerical abnormalities; (2) preservation of classical decidualization responsiveness to estradiol and medroxyprogesterone acetate, including the secretion of prolactin (PRL), insulin-like growth factor binding protein-1 (IGFBP-1), tissue factor (TF), and plasminogen activator inhibitor-1 (PAI-1); (3) retention of stromal lineage markers (vimentin, CD90) while remaining negative for epithelial markers; (4) phenotypic and functional stability sustained for many passages (e.g., >150 passages for St-T1b); and (5) absence of tumorigenic potential, as demonstrated in nude mouse models.
Collectively, immortalized human ESCs provide a consistent, reproducible, and phenotypically faithful in vitro model for investigating endometrial physiology, hormone-mediated decidualization, the pathogenesis of endometriosis and endometrial cancer, and drug screening, while circumventing the material limitations and passage constraints inherent to primary cell cultures.
Impact of Vitamin D and Vitamin D Receptor (VDR) on Defective Endometrial Decidualization
Identifying the factors that regulate female reproduction is crucial to understanding how the environment affects female reproductive health. The vitamin D receptor (VDR) and its ligands (primarily 1,25(OH)2D3) have a recognized role in calcium homeostasis; however, their broader impact on female reproduction remains underexplored. We demonstrate that the VDR and its ligands are involved in the hormonal induction of uterine decidualization. Mice fed a vitamin D-deficient diet displayed an impaired hormonally induced decidual response. In a human telomerase reverse transcriptase-immortalized human endometrial stromal cell line (T-HESC), VDR decreased during in vitro decidualization. Small interfering RNA (siRNA) knockdown of VDR in T-HESC enhanced in vitro decidualization, while overexpression of VDR inhibited it. Chromatin accessibility and histone modification analyses revealed that VDR functions as a chromatin regulator, restricting accessibility and repressing transcription in specific genomic regions. Transcriptomic analyses confirmed that VDR broadly modulates gene expression, with most ligand-mediated effects occurring through the VDR. These findings identify VDR as a key regulator of transcriptional and chromatin landscapes in human endometrial stromal cells, offering novel insights into vitamin D signaling in reproduction.


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