Ai W.-W.,Jiangxi Peoples Hospital |
Zhang M.,Jiangxi Peoples Hospital |
Wu S.,Jiangxi Peoples Hospital |
Huang Q.,Jiangxi Peoples Hospital |
And 2 more authors.
Journal of Dalian Medical University | Year: 2015
Objective: To study the correlation between N - terminal brain natriuretic peptide (NT - proBNP) and left ventricular end diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) in diastolic heart failure (DHF) patients as well as the diagnostic value for patients with varying degrees of diastolic heart failure. Methods: The 30 hospitalized patients with normal cardiac function were classified into normal group. The 60 hospitalized patients with abnormal cardiac function were classified into abnormal group. Besides, based on NYHA cardiac functional grading (grade I to III), the 60 patients were divided into 3 subgroups with 20 patients in each subgroup. LVEDP was measured with 6F pigtail catheter, and PCWP was measured with Swan - ganz catheter. Electrochemical luminescence device RocheElecsys 2010 was applied to determine NT - proBNP. Correlation between NT - proBNP and LVEDP and PCWP was analyzed. Results: With the progress in cardiac function grade, the levels of NT - proBNP, LVEDP and PCWP increased significantly (P <0.01). According to linear correlation and regression analysis, there was significant positive correlation between LogNT - proBNP and LVEDP (r = 0. 793, P < 0.01) and between LogNT - proBNP and PCWP (r = 0. 657, P < 0. 01). Conclusions: Serum NT - proBNP quantitative detection is a sensitive indicator of impaired left ventricular diastolic function. NT - proBNP has definite diagnostic value for the severity of diastolic heart failure. Source
Ge Y.,Translational Medicine Program |
Ge Y.,Jiangxi Cardiovascular Research Institute |
Ge Y.,Nanjing Medical University |
Pan S.,Translational Medicine Program |
And 14 more authors.
Biochimica et Biophysica Acta - Molecular Basis of Disease | Year: 2013
Recent studies have identified important roles for microRNAs (miRNAs) in many cardiac pathophysiological processes, including the regulation of cardiomyocyte hypertrophy. However, the role of miR-350 in the cardiac setting is still unclear. The objective of this study is to determine whether miR-350 alone can induce pathological cardiac hypertrophy by repressing the SAPK pathway in cardiomyocytes. Here we report that miR-350 plays a key role in determining pathological cardiomyocyte hypertrophy and apoptosis. Comprehensive microarray profiling of miRs and qPCR showed that this unique miRNA was significantly up-regulated in rat hearts in response to late-stage transverse aortic constriction. Western blotting and luciferase assays confirmed that the target mRNAs of miR-350 are mitogen activated protein kinase (MAPK) 11/14 and MAPK8/9 gene transcripts. Gain-of-unction and loss-of-function approaches were used to investigate the functional roles of miR-350. The forced over-expression of miR-350 was sufficient to induce hypertrophy of cardiomyocytes through the posttranslational suppression of p38 and JNK protein synthesis. Moreover, miR-350 led to an increase in unphosphorylated NFATc3 and its nuclear translocation, resulting in the over-expression of pathological hypertrophy markers. As predicted, these effects could effectively be imitated by siR-JNK/p38 through the degeneration of p38 and JNK mRNAs. Conversely, antagomir-350 could lower the levels of miR-350, reverse the expression of target proteins and reduce cell size and apoptosis relative to the administration of mutant antagomir-350. Our data provide the first evidence that miR-350 is a critical regulator of pathological cardiac hypertrophy and apoptosis in rats. © 2012 Elsevier B.V. Source