Hypertension is a global health problem and ACE inhibitors are largely used to control this pathology. Recently, it has been shown that ACE can also act as a transducer signal molecule when its inhibitors or substrates bind to it. This new role of ACE could contribute to understanding some of the effects not explained by its catalytic activity only. In this study we investigated signaling pathways activation in Chinese hamster ovary (CHO) cells stably expressing ACE (CHO-ACE) under different treatments. We also investigated gene modulation after 4h and 24h captopril treatments. Our results demonstrated that CHO-ACE cells when stimulated with AngI, ramipril or captopril led to JNK and ERK1/2 phosphorylation. To verify any physiological role at endogenous level we made use of primary cultures of mesangial cells from spontaneously hypertensive rats (SHR) and Wistar rats. Our results showed that ERK1/2 activation occurred only in primary cultures of mesangial cells from SHR rats upon captopril stimulation suggesting that this signaling pathway is differentially regulated during hypertension. Our results also showed that captopril treatment leads to decrease of COX2, interleukin 1β and β-arrestin 2 gene expression level.Our findings strengthen the fact that in addition to the blockage of enzymatic activity, ACE inhibitors also trigger signaling pathways activation and this may contribute to their beneficial effects in the treatment of hypertension and other pathologies.
AJP - Cell Physiology – The American Physiological Society
Published: Jan 13, 2016
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