Resistin does not down-regulate the transcription of insulin receptor promoter

Objective: To detect the effect of resistin on the transcription of insulin receptor promoter. Methods: Luciferase reporter gene was fused downstream of human insulin receptor promoter and the enzymatic activity of luciferase was determined in the presence or absence of resistin. The resistin expressed with plasmid was stained with antibody against Myc tag which was in frame fused with resistin coding sequence, and then imaged with confocal microscopy. Results: The treatment of pIRP-LUC transfected cells with recombinant resistin did not result in significant difference in the enzymatic activity of luciferase compared to the untreated cells. Cell staining showed that green fluorescence could be observed in the cytoplasm, but not in the nucleus. Conclusion: The results suggest that the endogenous resistin may functionally locate in the cytoplasm, but does not enter the nucleus and not down-regulate the transcription of insulin receptor promoter.

Relationship between resistin level in serum and acute coronary syndrome or stable angina pectoris

Objective： To investigate the relationship between serum resistin level and acute coronary syndrome （ACS） or stable angina pectoris （SAP）. Methods： Sixty-five patients, with coronary artery disease, were enrolled and divided into three subgroups： acute myocardial infarction （AMI）, unstable angina pectoris （UAP） and SAP, and 26 healthy people were recruited as controls in the cross-sectional study. Serum resistin levels were determined by ELISA （enzyme-linked immunosorbent assay）, and WBC （white blood cell count）, hsCRP （high sensitive C-reaction protein）, CKmax （maximum of creatinkinase）, CK-MBmax （maximum of isozyme of creatinkinase） and cTnImax （maximum of troponin） were measured by standard laboratory methods. Results： The serum resistin levels were 4 folds higher in AMI patients, 2.43 folds in UAP patients and I. 12 folds in SAP patients than in the healthy controls （P〈0.05）. The resistin levels were also significantly different between AMI [（8.16±0.79） ng/ml], UAP [（5.59±0.75） ng/ml] and SAP [（3.45±0.56） ng/ml] groups （P〈0.01）; WBC, hsCRP, CK CK-MBmax and cTnlmax were significantly increased in AMI patients over UAP and SAP patients. Spearman analysis showed that serum resistin levels were positively correlated with WBC （r=0.412, P=0.046）, hsCRP （r=0.427,p=0.037）, CK CK-MBmax and cTnImax （r=0.731, 0.678, 0.656; P〈0.01）. Conclusion： Serum resistin levels increased with inflammatory factors and myocardial impairment. The results suggest that human resistin might play an important role in the pathogenesis of atherosclerosis and AMI as an inflammatory factor.

Molecular analysis for diagnosis of Marfan syndrome and Marfan-associated disorders

Marfan syndrome is a systemic disorder of connective tissue, caused by mutations in the FBN1, TGFBR1 or TGFBR2 genes. This syndrome is characterized by involvement of three major systems, skeletal, ocular, and cardiovascular. The continuing improvements in molecular biology and increasing availability of molecular diagnosis in clinical practice allow recognition of Marfan syndrome in patients with incomplete phenotypes. Additionally, molecular analyses could also be used for preimplantation genetic diagnosis. The identification of a mutation allows for early diagnosis, prognosis, genetic counseling, preventive management of carriers and reassurance for unaffected relatives. The importance of knowing in advance the location of the putative family mutation is highlighted by its straightforward application to prenatal and postnatal screening.