Protein kinase C mRNA and protein expressions in hypobaric hypoxia‐induced cardiac hypertrophy in rats

Aim:  Protein kinase C (PKC), cloned as a serine/threonine kinase, plays key roles in diverse intracellular signalling processes and in cardiovascular remodelling during pressure overload or volume overload. We looked for correlations between changes in PKC isoforms (levels and/or subcellular distributions) and cardiac remodelling during experimental hypobaric hypoxic environment (HHE)-induced pulmonary hypertension. Methods:  To study the PKC system in the heart during HHE, 148 male Wistar rats were housed for up to 21 days in a chamber at the equivalent of 5500 m altitude level (10% O2). Results:  At 14 or more days of exposure to HHE, pulmonary arterial pressure (PAP) was significantly increased. In the right ventricle (RV): (1) the expression of PKC-α protein in the cytosolic and membrane fractions was increased at 3–14 days and at 5–7 days of exposure respectively; (ii) the cytosolic expression of PKC-δ protein was increased at 1–5, 14 and 21 days of exposure; (3) the membrane expressions of the proteins were decreased at 14–21 (PKC-βII), 14–21 (PKC-γ), and 0.5–5 and 21 (PKC-e) days of exposure; (4) the expression of the active form of PKC-α protein on the plasma membrane was increased at 3 days of exposure (based on semiquantitative analysis of the immunohistochemistry). In the left ventricle, the expressions of the PKC mRNAs, and of their cytosolic and membrane proteins, were almost unchanged. The above changes in PKC-α, which were strongly evident in the RV, occurred alongside the increase in PAP. Conclusion:  PKC-α may help to modulate the right ventricular hypertrophy caused by pulmonary hypertension in HHE.