Activation of IGF-I Survival Signaling and Its Compensative Inhibition of the Cardiac Apoptosis on Carotid Arteries Balloon-Injured Rat Hearts

Abstract

In this study, a rat carotid balloon injury-animal model was used to elucidate the temporal relation of hypertrophy in the progression of cardiac damage and the role of insulin-like growth factor (IGF)-I survival pathway on course of the cardiac damage. Rats were subjected to carotid balloon-injury and examined at different time points. We further studied the heart-weight/body-weight-ratio, histology and protein expression to understand the pathological events associated with percutaneous transluminal coronary angioplasty (PTCA) induced damages. Protein expression analysis showed increased levels of IGF-I signaling pathway and mitogen-activated protein kinase (MAPK) signaling pathway after 2 h and after 2 d of carotid balloon injury. On the other hand, apoptosis signaling pathways were enhanced after 14 d of carotid balloon injury. According to the results, rat carotid balloon injury significantly induced IGF-I survival signaling and compensated hypertrophy pathway during the initial period of injury however after 14 d the proteins involved in apoptotic cell death were elevated and the proteins of the survival pathway and compensatory hypertrophy were significantly reduced.

Exercise training restores IGFIR survival signaling in d-galactose induced-aging rats to suppress cardiac apoptosis

“…When the mitochondrial membrane potential is lost, the mitochondrial cytochrome c is released to cytosol which subsequently results in cellular apoptosis [14] . Further, circulating insulin-like growth factor I (IGF-1) levels are negatively correlated with cardiovascular risks and is considered as a prognostic indicator in conditions such as ischemic heart disease but most importantly, reduced levels of IGF-1 in aged persons increases the risk for heart failure [15] , [16] , [17] . IGF-1 signaling is transduced by its transmembrane tyrosine kinase receptor IGF1R.…”

Pheretima aspergillum extract attenuates high‐KCl‐induced mitochondrial injury and pro‐fibrotic events in cardiomyoblast cells

“…In this regard, IGF1 survival signaling is seen as a compensatory mechanism to attenuate the apoptosis initiation in various cardiac conditions . Alterations in the activation levels of IGFI‐receptor (IGFI‐R), phosphatidylinositol 3‐kinase (PI3K), and protein kinase B (Akt) affect IGF‐1 cell survival and trigger apoptosis . Cardiac damages normally trigger cardiac remodeling processes like myofibroblast proliferation, migration and their invasion, and cardiac fibrosis .…”