Houyou Yu

Serum adropin levels are decreased in patients with acute myocardial infarction.

OBJECTIVE Adropin is a recently identified bioactive protein that is important for energy homeostasis and maintaining insulin sensitivity. We sought to detect serum adropin levels in acute myocardial infarction (AMI) patients. METHODS We enrolled 138 AMI patients, 114 stable angina pectoris (SAP) patients and 75 controls. Adropin levels were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS Serum adropin levels were significantly lower in patients with AMI compared with SAP patients or controls (P<0.01). Multivariate logistic regression demonstrated that lower adropin was the independent predictor for the presence of AMI in coronary artery disease (CAD) patients (P<0.01). Serum adropin levels were negatively associated with body mass index (BMI) (P<0.01) and triglyceride levels (P<0.05) in AMI patients. CONCLUSION Decreased serum adropin levels are associated with the presence of AMI in CAD patients. These results revealed that adropin might represent as a novel biomarker for predicting AMI onset in CAD patients.

Neuroprotective Effects of Viral Overexpression of microRNA‐22 in Rat and Cell Models of Cerebral Ischemia‐Reperfusion Injury

Several studies have reported that microRNA (MIR) is involved in the pathogenesis and progression of ischemic diseases, including cerebral ischemia, and that MIR‐22 may inhibit the inflammatory response and cell apoptosis, which contribute to ischemia/reperfusion (I/R) injury. However, the specific function of MIR‐22 in cerebral I/R injury remains far from clear. This study aimed to examine the potential protective effect of MIR‐22 against cerebral I/R injury and its mechanism. As predicted, adenovirus‐mediated MIR‐22 overexpression markedly reduced the neurological score and infarct size (P < 0.05). We demonstrated that MIR‐22 overexpression resulted in a reduction in inflammatory cytokines TNF‐α, IL‐6, COX‐2, and iNOS, whereas the level of IL‐10 was enhanced. MIR‐22 overexpression significantly inhibited NF‐κB activity by decreasing NF‐κB coactivator NCOA1 expression. Furthermore, we found that MIR‐22 could reduce the apoptotic rate of cortical neurons. Caspase‐3 activity was inhibited by MIR‐22, and the expression of the anti‐apoptosis gene Bcl‐2 in neurons was increased and that of the pro‐apoptosis gene Bax decreased following MIR‐22 overexpression. Our results suggest that MIR‐22 could be used to treat cerebral I/R injury and that its neuroprotective effect may be attributed to a reduction in inflammation and apoptosis. J. Cell. Biochem. 116: 233–241, 2015.

Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer's disease and the cerebral ischemia model.

Alzheimer’s disease (AD) and ischemic brain injury are two major neurodegenerative diseases. Mitochondrial dysfunction commonly occurs in AD and ischemic brain injury. Currently, little attention has been paid to the glycans on mitochondrial glycoproteins, which may play vital roles during the process of mitochondrial dysfunction. The aim of this study was to illustrate and compare the glycopattern alterations of mitochondrial glycoproteins extracted from the cerebral cortex of the rat models of these two diseases using High-throughput lectin microarrays. The results shown that the number of lectins with significant differences compared to normal brains was nine for the rat sporadic Alzheimer’s disease (SAD) model and eighteen for the rat middle cerebral artery occlusion (MCAO) model. Interestingly, five lectins showed opposite expression patterns between the SAD and MCAO rat models. We conclude that glycopattern alterations of mitochondrial glycoproteins in the cerebral cortex may provide vital information to help understand mitochondrial dysfunction in AD and ischemic brain injury. In addition, glycans recognized by diverse lectins with opposite expression patterns between these two diseases hints at the different pathomechanisms of mitochondrial dysfunction in AD and ischemic brain injury.