Extragonadal function of follicle-stimulating hormone: Evidence for a role in endothelial physiology and dysfunction
Maria Santa Rocca1, Micaela Pannella2, Erva Bayraktar3
1University Hospital of Padua, Unit of Andrology and Reproductive Medicine, Padua, Italy.
Molecular and Cellular Endocrinology
|September 27, 2024
Summary
High concentrations of follicle-stimulating hormone (FSH) impact endothelial cell function, increasing permeability and potentially affecting the endothelial barrier. This suggests a role for FSH beyond reproduction, possibly linked to cardiovascular risks.
Area of Science:
- Endocrinology
- Cell Biology
- Reproductive Biology
Background:
- Follicle-stimulating hormone (FSH) is crucial for reproductive functions like folliculogenesis and spermatogenesis.
- The FSH receptor (FSHR) is present in extra-gonadal tissues, suggesting roles beyond fertility.
- Previous research on FSH's effect on endothelial cells yielded conflicting results.
Purpose of the Study:
- To investigate the role of FSH in endothelial cell function.
- To examine FSH's effects on Human Umbilical Vein Endothelial Cells (HUVECs).
Main Methods:
- Stimulation of HUVECs with recombinant human FSH (rhFSH).
- Measurement of endothelial nitric oxide synthase (eNOS) expression, phosphorylation, and nitric oxide (NO) production.
- Assessment of calcium release, IP3 production, NFAT1 localization, and wound healing assays.
- Analysis of cellular permeability and VE-cadherin distribution.
Main Results:
- rhFSH stimulation increased eNOS expression, eNOS phosphorylation, and NO production in HUVECs.
- Increased calcium release and IP3 production were observed following rhFSH stimulation.
- Wound healing assays showed significant differences in cell migration at various rhFSH concentrations and time points.
- rhFSH elevated cellular permeability and altered VE-cadherin distribution and actin filaments.
Conclusions:
- High concentrations of FSH can compromise the endothelial membrane by affecting VE-cadherin.
- Altered VE-cadherin and increased membrane permeability suggest a compromised endothelial barrier.
- Excessive NO production due to FSH may impact endothelial functionality and potentially contribute to cardiovascular risks in specific conditions.
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