Kisspeptin-10 inhibits angiogenesis in human placental vessels ex vivo and endothelial cells in vitro.
Ramaesh. Thayalini T; Logie. James J JJ; Roseweir. Antonia K AK; Millar. Robert P RP; Walker. Brian R BR; Hadoke. Patrick W F PW; Reynolds. Rebecca M RM
Key Findings
- Kisspeptin‑10 stops new vessel sprouting from placental arteries in a dose‑dependent way
- It prevents endothelial cells from forming tube‑like structures in vitro
- It does not kill the cells but reduces their proliferation and migration
Practical Outcomes
- The findings are mainly of scientific interest for understanding placental biology and tumor spread. There are no clear dosage guidelines or protocols for everyday use, so biohackers have little to apply directly from this study.
Summary
Kisspein‑10, a short form of the hormone kisspeptin, was shown to block the growth of new blood vessels in human placental tissue and in cultured endothelial cells, without killing the cells but slowing their growth and movement. This effect was seen in lab experiments and depends on the amount used.
Abstract
Recent studies suggest that kisspeptin (a neuropeptide central to the regulation of gonadotrophin secretion) has diverse roles in human physiology, including a putative role in implantation and placental function. Kisspeptin and its receptor are present in human blood vessels, where they mediate vasoconstriction, and kisspeptin is known to inhibit tumor metastasis and trophoblast invasion, both processes involving angiogenesis. We hypothesized that kisspeptin contributes to the regulation of angiogenesis in the reproductive system. The presence of the kisspeptin receptor was confirmed in human placental blood vessels and human umbilical vein endothelial cells (HUVEC) using immunochemistry. The ability of kisspeptin-10 (KP-10) (a shorter biologically active processed peptide) to inhibit angiogenesis was tested in explanted human placental arteries and HUVEC using complementary ex vivo and in vitro assays. KP-10 inhibited new vessel sprouting from placental arteries embedded in Matrigel and tube-like structure formation by HUVEC, in a concentration-dependent manner. KP-10 had no effect on HUVEC viability or apoptosis but induced concentration-dependent inhibition of proliferation and migration. In conclusion, KP-10 has antiangiogenic effects and, given its high expression in the placenta, may contribute to the regulation of angiogenesis in this tissue.
Study Information
pubmed
2010
2010-10-06T00:00:00.000Z
10.1210/en.2010-0565
56
38