The endoplasmic reticulum (ER) is physically connected to mitochondria through the specific sub-domain,called mitochondria-associated endoplasmic reticulum membranes (MAMs). These contacts are involved in calcium signaling,lipid transferring,mitochondrial fission and fusion and energy metabolism. Recently,MAMs alterations have been identified to associate with some diseases,including neurodegenerative diseases,obesity,cardiovascular diseases and cancer. Therefore,in this paper,we introduce the structure,function and detection methods of MAMs. Besides,we also summarize the potential role of MAMs in these diseases. In any case,the signaling at the MAMs might be a promising pharmacological target for several diseases.
This study aims to investigate the role of calreticulin in (CRT) pressure overload induced cardiac hypertrophy. In our study, cardiac hypertrophy was induced by left ventricular pressure overload in male SD rats subjected to transverse aortic constriction (TAC) operation. Expression of gene and protein of calreticulin, markers of cardiac hypertrophy and endoplasmic reticulum stress (ERS) were measured with real-time qPCR and Western blot respectively. Meanwhile, atorvastatin (a known ERS inhibitor) and calreticulin-specific small interference ribonucleic acid (siRNA) were used to inhibit the expression of ERS and calreticulin respectively. The experimental data demonstrated that the gene and protein levels of calreticulin, hypertrophic and ERS markers were increased significantly in the heart tissues of TAC rat models after 4 weeks. Moreover, atorvastatin administration improved the cardiac function and reduced the expression of calreticulin and ERS markers in TAC rats. In addition, cultured primary neonatal rat cardiomyocytes (NCMs) were treated with norepinephrine (NE), angiotensionⅡ (AngⅡ) or isoprenaline (ISO) to induce hypertrophic phenotype and ERS. The expression of hypertrophic markers was reduced in NCMs transfected with calreticulin-siRNA. The results suggested that calreticulin might be a promising target for the treatment of cardiac hypertrophy.
