Abstract

Transforming growth factor-beta 1 (TGF-beta 1) is a cytokine with marked pro-fibrotic action on cardiac fibroblasts (CF). TGF-beta 1 induces CF-to-cardiac myofibroblast (CMF) differentiation, defined by an increase in alpha-smooth muscle cells (alpha-SMA), collagen secretion and it has a cytoprotective effect against stimuli that induce apoptosis. In the Endoplasmic Reticulum (ER) lumen, misfolded protein accumulation triggers ER stress and induces apoptosis, and this process plays a critical role in cell death mediated by Ischemia/Reperfusion (I/R) injury and by ER stress inducers, such as Tunicamycin (Tn). Here, we studied the regulation of CHOP, a proapoptotic ER-stress-related transcription factor in CF under simulated I/R (sI/R) or exposed to Tn. Even though TGF-beta 1 has been shown to participate in ER stress, its regulatory effect on CF apoptosis and ER stress-induced by sI/R or TN has not been evaluated yet.