17β-Estradiol Promotes Goat Granulosa Cell Proliferation via the ERα/NO/Wnt/β-Catenin Signaling Axis

Clicks: 17
ID: 333694
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #256 of 847 articles by views in italian journal of animal science

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 847 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
Abstract Ovarian granulosa cells (GCs) are central to follicular development in goats, and their proliferation is tightly regulated by estrogen, yet the downstream signaling cascade mediating this effect in ruminants remains undefined. This study aimed to investigate whether estrogen regulates goat ovarian GC proliferation through the nitric oxide (NO) signaling pathway and to further elucidate the molecular mechanisms by which NO modulates GC proliferation. Primary goat GCs were treated with 17β-estradiol (17β-E2), the NO donor sodium nitroprusside (SNP), the NOS inhibitor NG-monomethyl-L-arginine (L-NMMA), the Wnt inhibitor FH535, and the Wnt agonist SKL2001. Cell viability, proliferation, and protein expression were assessed by CCK‑8, EdU, and Western blotting. 17β-E2 at concentrations of 1, 2, and 10 μg/mL all promoted GC viability (P < 0.05), with maximal effect at 1 μg/mL (P < 0.01), and simultaneously upregulated inducible NOS (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS) protein expression via estrogen receptor α (ERα). The NO donor SNP enhanced GC proliferation, whereas the NOS inhibitor L‑NMMA suppressed it; co‑treatment with SNP partially rescued the L‑NMMA‑induced inhibition. Mechanistically, SNP increased β‑catenin and proliferating cell nuclear antigen (PCNA) protein levels, an effect reversed by FH535, whereas L‑NMMA‑induced NO depletion reduced their expression, which was restored by SKL2001, positioning NO upstream of the Wnt/β‑catenin pathway. Collectively, these findings establish that 17β-E2 promotes goat GC proliferation through a signaling cascade involving ERα, NOS, NO, and the Wnt/β‑catenin pathway, providing the functional evidence for this axis in a ruminant model and offering a mechanistic framework for understanding ovarian follicular dynamics with implications for improving reproductive efficiency in goats.
Reference Key
openalex_W7223375200 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors
Journal italian journal of animal science
Year 2026
DOI
10.1093/jas/skag342
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.