Kp-10 promotes bovine mammary epithelial cell proliferation by activating GPR54 and its downstream signaling pathways.
Li. Yanwei Y; Cao. Yu Y; Wang. Jiaxin J; Fu. Shoupeng S; Cheng. Ji J; Ma. Lijun L; Zhang. Qing Q; Guo. Wenjin W; Kan. Xingchi X; Liu. Juxiong J
Key Findings
- 100 nM kisspeptin‑10 increased proliferation of bovine mammary epithelial cells.
- Kisspeptin‑10 pushed cells from the G1 phase into S and G2 phases, raising Cyclin D1/D3 and lowering p21.
- Blocking GPR54, AKT, mTOR, or ERK1/2 reduced the kisspeptin‑10‑driven cell growth.
Practical Outcomes
- For self‑directed health optimizers, this research doesn’t provide a ready‑to‑use protocol because it’s limited to cow cells and milk production. It does suggest that kisspeptin can activate growth pathways (GPR54‑AKT‑mTOR‑ERK), but any benefits for human muscle, metabolism, or longevity remain untested and speculative.
Summary
The study shows that a tiny protein called kisspeptin‑10 can make cow breast cells grow faster by turning on a receptor (GPR54) and several cell‑growth pathways. The effect was seen at a concentration of 100 nM in lab dishes, but the work was done only in cow cells, not in people.
Abstract
It has been reported that the proliferation and apoptosis of mammary epithelial cells affect milk production. Therefore, ensuring adequate mammary epithelial cells is expected to enhance milk production. This study is devoted to studying the effects of kisspeptin-10 (Kp-10), a peptide hormone composed of 10 amino acids, on bovine mammary epithelial cell (bMEC) proliferation and exploring the underlying mechanism of its action. bMECs were treated with various concentrations of Kp-10 (1, 10, 100, and 1,000 nM), and 100 nM Kp-10 promoted the proliferation of the bMECs. Kp-10 promoted the cell cycle transition from G1 to the S and G2 phases, increased the protein levels of Cyclin D1 and Cyclin D3, and reduced the expression levels of the p21 gene. This study also showed that inhibition of G protein-coupled receptor 54 (GPR54), AKT, mTOR, and ERK1/2 reduced the proliferation of the bMECs that had been induced by Kp-10. In addition, Kp-10 decreased the complexes formed by Rb and E2F1 and increased the expression levels of the E2F1 target genes. These results indicate that Kp-10 promotes bMEC proliferation by activating GPR54 and its downstream signaling pathways.
Study Information
pubmed
2019
2019-10-17T00:00:00.000Z
10.1002/jcp.29325
21
64