Ghrelin mediated cardioprotection using in vitro models of oxidative stress

Ghrelin is commonly known as the 'hunger hormone' due to its role in stimulating food intake in humans. However, the roles of ghrelin extend beyond regulating hunger. Our aim was to investigate the ability of ghrelin to protect against hydrogen peroxide (H O ), a reactive oxygen species co...

Full description

Saved in:
Bibliographic Details
Published in:Gene therapy 2024-03, Vol.31 (3-4), p.165-174
Main Authors: Kok, Cindy Y, Ghossein, George, Igoor, Sindhu, Rao, Renuka, Titus, Tracy, Tsurusaki, Shinya, Chong, James Jh, Kizana, Eddy
Format: Article
Language:English
Subjects:
Animal models
Animals
Apoptosis
Cardiomyocytes
Cell viability
Food intake
Ghrelin
Ghrelin - genetics
Ghrelin - metabolism
Ghrelin - pharmacology
Hormones
Humans
Hunger
Hydrogen peroxide
Hydrogen Peroxide - pharmacology
In vitro
Myocytes, Cardiac - metabolism
Oxidative Stress
Proprotein convertases
Rats
Reactive oxygen species
Reactive Oxygen Species - metabolism
Reactive Oxygen Species - pharmacology
Signal Transduction
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Ghrelin is commonly known as the 'hunger hormone' due to its role in stimulating food intake in humans. However, the roles of ghrelin extend beyond regulating hunger. Our aim was to investigate the ability of ghrelin to protect against hydrogen peroxide (H O ), a reactive oxygen species commonly associated with cardiac injury. An in vitro model of oxidative stress was developed using H O injured H9c2 cells. Despite lentiviral ghrelin overexpression, H9c2 cell viability and mitochondrial function were not protected following H O injury. We found that H9c2 cells lack expression of the preproghrelin cleavage enzyme prohormone convertase 1 (encoded by PCSK1), required to convert ghrelin to its active form. In contrast, we found that primary rat cardiomyocytes do express PCSK1 and were protected from H O injury by lentiviral ghrelin overexpression. In conclusion, we have shown that ghrelin expression can protect primary rat cardiomyocytes against H O , though this effect was not observed in other cell types tested.
ISSN:0969-7128
1476-5462
DOI:10.1038/s41434-023-00435-9