GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin stimulates angiogenesis via GHSR1a-dependent MEK/ERK and PI3K/Akt signal pathways in rat cardiac microvascular endothelial cells.
Wang. Li L; Chen. Qingwei Q; Li. Guiqiong G; Ke. Dazhi D
Key Findings
- Ghrelin and its receptor GHSR1a are naturally present in rat cardiac microvascular endothelial cells.
- proliferation, migration, and in‑vitro tube formation (angiogenesis).",
Practical Outcomes
- For biohackers, this suggests that ghrelin‑based compounds (like GHRP‑6) might help promote heart vascular health or recovery, but the evidence is limited to rat cells in a lab setting. No human dosage or safety data are provided, so any use for cardiac angiogenesis remains speculative and should be approached with caution.
Summary
The study shows that the hormone ghrelin, which binds to the GHSR1a receptor, can make heart blood‑vessel cells (from rats) grow, move, and form new tiny vessels in a dish. This angiogenic effect needs two internal signaling routes – MEK/ERK and PI3K/Akt – and stopping either route weakens the effect, while blocking both stops it completely. Blocking the receptor itself also stops the whole process, proving ghrelin works through GHSR1a.
Abstract
Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor (GHSR), is thought to exert a protective effect on the cardiovascular system, specifically by promoting vascular endothelial cell function such as cell proliferation, migration, survival and angiogenesis. However, the effect of ghrelin on angiogenesis and the corresponding mechanisms have not yet been extensively studied in cardiac microvascular endothelial cells (CMECs) isolated from left ventricular myocardium of adult Sprague-Dawley (SD) rats. In our study, we found that ghrelin and GHSR are constitutively expressed in CMECs. Ghrelin significantly increases CMECs proliferation, migration, and in vitro angiogenesis. The ghrelin-induced angiogenic process was accompanied by phosphorylation of ERK and Akt. MEK inhibitor PD98059 abolished ghrelin-induced phosphorylation of ERK, but had no effect on Akt phosphorylation. PI3K inhibitor LY294002 abolished ghrelin-induced phosphorylation of Akt, but had no effect on ERK phosphorylation. Ghrelin-induced angiogenesis was partially blocked by treatment with PD98059 or LY294002. In addition, this angiogenic effect was almost completely inhibited by PD98059+LY294002. Pretreatment with GHSR1a blocker [D-Lys3]-GHRP-6 abolished ghrelin-induced phosphorylation of ERK, Akt and in vitro angiogenesis. In conclusion, this is the first demonstration that ghrelin stimulates CMECs angiogenesis through GHSR1a-mediated MEK/ERK and PI3K/Akt signal pathways, indicating that two pathways are required for full angiogenic activity of ghrelin. This study suggests that ghrelin may play an important role in myocardial angiogenesis.
Study Information
pubmed
2011
2011-11-07T00:00:00.000Z
10.1016/j.peptides.2011.11.001
63
33