Effect of ghrelin on protein kinase C-ε and protein Kinase C-δ gene expression in the pulmonary arterial smooth muscles of chronic hypoxic rats

Abstract

Protein kinase C (PKC), can be activated in pulmonary arterial smooth muscle cells during hypoxia, leading to hypoxic pulmonary vasoconstriction (HPV). Studies are going on to detect the strict PKC isoform involved in the phenomenon. It has been shown that ghrelin, a 28-amino-acid peptide, may protect lungs from HPV side effects, to some extent. The aim of study was to evaluate the effect of exogenous ghrelin on PKC-? and PKC-? gene expression during chronic hypoxia. Twenty-four adult male Wistar rats were divided randomly in 3 groups. Hypoxic rats with saline or ghrelin treatment were placed in a normobaric hypoxic chamber for 2 weeks. Controls remained in room air. PKC-? and PKC-? gene expression was measured by real-time RT-PCR. Morphometric analysis showed that ghrelin reversed the hypoxia induced pulmonary artery wall thickness. In hypoxic animals, there was a 2- and 4-fold increment in PKC-? and PKC- ? gene expression, respectively. Ghrelin treatment reduced the overexpression of PKC-? and PKC-? to control animals' value. Ghrelin by decreasing the expression of PKC-? and PKC-? in hypoxic animals reduces the HPV. Although more studies are needed, it could be an honest deduction that ghrelin affects HPV in a multifunctional manner and might be used as a therapeutic agent in the future.