HSPA12B attenuates cardiac dysfunction and remodelling after myocardial infarction through an eNOS-dependent mechanism

Abstract

These data demonstrate for the first time that the overexpression of HSPA12B attenuates cardiac dysfunction and remodelling after MI. This action of HSPA12B was mediated, at least in part, by prevention of cardiomyocyte apoptosis and promotion of myocardial angiogenesis via an eNOS-dependent mechanism. HSPA12B could be a novel target for the management of patients with post-MI cardiac dysfunction and remodelling.

NOD2 Deficiency Protects against Cardiac Remodeling after Myocardial Infarction in Mice

“…MI was induced by permanent ligation of the left coronary artery as described [7,15]. In sham-operated animals, the suture was placed under the artery and removed without ligating the artery.…”

Expression of HSPA12B in acute cardiac allograft rejection in rats

“…Others showed that overexpression of HSPA12B attenuated LPS-induced cardiac dysfunction by limiting LPS-induced expression of VCAM-1/ICAM-1, iNOS, and leucocytes infiltration in the myocardium [29]. More recently, several studies confirmed the attenuation on heart and brain apoptosis by overexpression of HSPA12B in experimental models [32][33][34]. These studies suggest that HSPA12B might be closely associated with apoptosis and inflammation, which are regarded as major part of the hallmarks of cardiac allograft rejection [5].…”

“…In 2013, some studies show that overexpression of HSPA12B could significantly decrease apoptosis in mice cerebral ischemia/reperfusion (I/R) injury [32]. In the same year, another study proved that overexpression of HSPA12B attenuates cardiac dysfunction and remodeling after myocardial infarction, at least in part, by prevention of cardiomyocyte apoptosis [34]. In addition, others demonstrated that HSPA12B is involved in apoptosis in rat middle cerebral artery occlusion experimental models and they also confirmed that HSPA12B inhibited the expression of active caspase-3 in vitro [33].…”

Impact of microRNA-134 on neural cell survival against ischemic injury in primary cultured neuronal cells and mouse brain with ischemic stroke by targeting HSPA12B

“…2C and D, n Po0.05, n¼ 5 per group). It is worth mentioning that HSPA12B expression was strongly inducible by ischemia or heat shocks both in vivo and in vitro experiments Li et al, 2013;Ma et al, 1832), and other control factors together made HSPA12B highly expressed against brain injury at 12 h after ischemic stroke. Also, the opposite trend between miR-134 and HSPA12B protein levels suggests that perhaps there is a modulation of HSPA12B protein levels by miR-134 under ischemic conditions.…”