# Ghrelin mediated cardioprotection using in vitro models of oxidative stress

## TL;DR

Ghrelin, known as the 'hunger hormone', protects rat heart cells from oxidative stress but not in other cell types due to missing enzymes.

## Contribution

Demonstrated that ghrelin's cardioprotective effect depends on the presence of PCSK1 in primary rat cardiomyocytes.

## Key findings

- H9c2 cells lack PCSK1 and do not benefit from ghrelin overexpression against H2O2 injury.
- Primary rat cardiomyocytes express PCSK1 and are protected by ghrelin overexpression from oxidative stress.
- Ghrelin's protective effect is cell-type dependent, highlighting the importance of PCSK1 in its activation.

## Abstract

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 (H2O2), a reactive oxygen species commonly associated with cardiac injury. An in vitro model of oxidative stress was developed using H2O2 injured H9c2 cells. Despite lentiviral ghrelin overexpression, H9c2 cell viability and mitochondrial function were not protected following H2O2 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 H2O2 injury by lentiviral ghrelin overexpression. In conclusion, we have shown that ghrelin expression can protect primary rat cardiomyocytes against H2O2, though this effect was not observed in other cell types tested.