GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin promotes differentiation of human embryonic stem cells into cardiomyocytes.
Yang. Jin J; Liu. Guo-qiang GQ; Wei. Rui R; Hou. Wen-fang WF; Gao. Mei-juan MJ; Zhu. Ming-xia MX; Wang. Hai-ning HN; Chen. Gui-an GA; Hong. Tian-pei TP
Key Findings
- Ghrelin (0.1‑1 nmol/L) increased the percentage of beating embryoid bodies and raised cardiac markers (cTnI, α‑MHC).
- The boost in heart‑cell formation grew over time (days 6‑18) with continuous ghrelin exposure.
- Blocking the GHS‑R1α receptor with D‑[lys(3)]‑GHRP‑6 did not stop ghrelin’s effect, indicating a different pathway.
Practical Outcomes
- The results are interesting for stem‑cell research but offer no actionable protocol for self‑experimentation or supplementation. There’s no guidance on safe human doses, timing, or expected performance benefits, so biohackers should treat this as a basic science finding rather than a usable technique.
Summary
In lab-grown stem cells, adding the peptide ghrelin helped more cells turn into beating heart cells, but this effect didn't work through the usual ghrelin receptor and the study didn't test any real‑world dosing or benefits for people.
Abstract
Ghrelin is involved in regulating the differentiation of mesoderm-derived precursor cells. The aim of this study was to investigate whether ghrelin modulated the differentiation of human embryonic stem (hES) cells into cardiomyocytes and, if so, whether the effect was mediated by growth hormone secretagogue receptor 1α (GHS-R1α). Cardiomyocyte differentiation from hES cells was performed according to an embryoid body (EB)-based protocol. The cumulative percentage of beating EBs was calculated. The expression of cardiac-specific markers including cardiac troponin I (cTnI) and α-myosin heavy chain (α-MHC) was detected using RT-PCR, real-time PCR and Western blot. The dispersed beating EBs were examined using immunofluorescent staining. The percentage of beating EBs and the expression of cTnI were significantly increased after ghrelin (0.1 and 1 nmol/L) added into the differentiation medium. From 6 to 18 d of differentiation, the increased expression of cTnI and α-MHC by ghrelin (1 nmol/L) was time-dependent, and in line with the alteration of the percentages of beating EBs. Furthermore, the dispersed beating EBs were double-positively immunostained with antibodies against cTnI and α-actinin. However, blockage of GHS-R1α with its specific antagonist D-[lys(3)]-GHRP-6 (1 μmol/L) did not alter the effects of ghrelin on cardiomyocyte differentiation. Our data show that ghrelin enhances the generation of cardiomyocytes from hES cells, which is not mediated via GHS-R1α.
Study Information
pubmed
2011
2011-08-01T00:00:00.000Z
10.1038/aps.2011.79
16
29