Conclusion
Collectively, in this study, we demonstrated that Cav-1 acts as a protective regulator of MI injury through maintaining endothelial homeostasis. These findings implied that Cav-1 may be a potential therapeutic target for MI injury.
Methods
To elucidate the role of Cav-1 in MI in vivo, we generated the global knockout Cav-1 (Cav-1-KO) mice. And we manipulated the expression of Cav-1 by siRNA in vitro to evaluate the effects apoptosis, inflammatory response and oxidative stress as well as autophagy flux under the hypoxic model of endothelial cells (ECs).
Objective
Caveolin-1 (Cav-1) plays a crucial role in maintaining the homeostasis of vascular endothelium. Endothelial dysfunction is involved in many ischemic diseases. However, the role of Cav-1 in myocardial infarction (MI) has not been fully elucidated. Here, this study aims to delineate the function of Cav-1 in MI injury and its impact on endothelial homeostasis.
Results
Initially, we found that Cav-1 was mainly expressed in vascular endothelial cells of myocardium. Interestingly, we found that Cav-1 deficiency significantly amplified the size of myocardial infarction areas, alongside the deteriorated cardiac function in vivo. Consistently in vitro, siRNA-mediated knockdown of Cav-1 exacerbated the endothelial apoptosis, inflammatory response and oxidative stress as well as eliminated autophagy flux. However, pretreatment with β-cyclodextrin (β-CD), which depletes membrane-bound cholesterol and disrupts lipid rafts, markedly mitigated the effects induced by downregulation of Cav-1, respectively.