Kisspeptin-10 inhibits OHSS by suppressing VEGF secretion.
Zhai. Junyu J; Liu. Jiansheng J; Zhao. Shigang S; Zhao. Han H; Chen. Zi-Jiang ZJ; Du. Yanzhi Y; Li. Weiping W
Key Findings
- Injecting kisspeptin‑10 into OHSS rats reduced vascular permeability and VEGF levels while increasing KISS1R expression in ovary and lung tissue.
- High estradiol (E2) levels, typical of OHSS, suppress KISS1R and raise VEGF and nitric oxide via estrogen receptor ESR2 in endothelial cells.
- Human luteinized granulosa cells from high‑risk OHSS patients also showed lower KISS1R mRNA, matching the animal and cell findings.
Practical Outcomes
- At this stage kisspeptin‑10 is not a ready‑to‑use supplement or protocol for the biohacking community; it is a candidate for future fertility‑related drug development. For most enthusiasts focused on longevity or performance, the findings have limited direct application.
Summary
The study shows that a short peptide called kisspeptin‑10 can lower the leakiness of blood vessels and the amount of VEGF (a protein that makes vessels leaky) in a rat model of ovarian hyperstimulation syndrome (OHSS), a side effect of fertility drugs. It works by boosting the kisspeptin receptor (KISS1R) and blocking the estrogen‑driven rise in VEGF.
Abstract
The aim of the present study was to elucidate the effects of kisspeptin-10 (Kp-10) on ovarian hyperstimulation syndrome (OHSS) and its related mechanism in OHSS rat models, human umbilical vein endothelial cells (HUVECs) and human luteinized granulosa cells. OHSS is a systemic disorder with high vascular permeability (VP) and ovarian enlargement. KISS1R (KISS1 receptor) is the specific receptor of kisspeptin. The kisspeptin/KISS1R system inhibits the expression of vascular endothelial growth factor (VEGF), which is the main regulator of VP. In our study, decreased expression of Kiss1r was observed in both ovaries and lung tissue of OHSS rats. Injection of exogenous Kp-10 inhibited the increase of VP and VEGF while promoting the expression of Kiss1r in both the ovarian and lung tissue of OHSS rats. Using HUVECs, we revealed that a high level of 17-β estradiol (E<sub>2</sub>), a feature of OHSS, suppressed the expression of KISS1R and increased VEGF and nitric oxide (NO) through estrogen receptors (ESR2). Furthermore, <i>KISS1R</i> mRNA also decreased in the luteinized human granulosa cells of high-risk OHSS patients, and was consistent with the results in rat models and HUVECs. In conclusion, Kp-10 prevents the increased VP of OHSS by the activation of KISS1R and the inhibition of VEGF.
Study Information
pubmed
2017
2017-07-04T00:00:00.000Z
10.1530/rep-17-0268