Proteomic identification of the proteins related to cigarette smoke-induced cardiac hypertrophy in spontaneously hypertensive rats

Abstract

Smoking increases the risk of cardiovascular diseases. The present study was designed to determine the effects of 2-month exposure to cigarette smoke (CS) on proteins in the left ventricles of spontaneously hypertensive rats (SHR) and to identify the molecular targets associated with the pathogenesis/progression of CS-induced cardiac hypertrophy. SHR and Wistar Kyoto rats (WKY) were exposed to CS at low (2 puffs/min for 40 min) or high dose (2 puffs/min for 120 min), 5 days a week for 2 months. Using the two-dimensional fluorescence difference gel electrophoresis combined with MALDI-TOF/TOF tandem mass spectrometry, we compared differences in the expression levels of proteins in the whole left ventricles induced by long-term smoking. High-dose CS mainly caused cardiac hypertrophy in SHR, but not WKY, but no change in blood pressure. Proteomic analysis identified 30 protein spots with significant alterations, with 14 up-regulated and 16 down-regulated proteins in the left ventricles of CS-exposed SHR, compared with control SHR. Among these proteins, two members of the heat shock proteins (HSP70 and HSP20) showed significant up-regulation in the left ventricles of CS high-dose SHR, and the results were confirmed by western blot analysis. Our findings suggested that HSPs play an important role in regulation of CS-induced cardiac hypertrophy.

Proteomics analysis in myocardium of spontaneously hypertensive rats

“…Adult SHR is an ideal animal model of compensatory LVH, as supported by increased left ventricle relative mass, elevated left ventricular end-systolic pressure in combined with greater + dp/dt max in SHR. As expected, more DEPs were found in this study than previous study possible due to the adoption of LC–MS/MS 2 . It is noteworthy that a great number of DEPs were located in mitochondria, implying the vital role of mitochondrial dysfunction in hypertension-related LVH.…”

“…As a complicated pathological process, LVH may result from the changes of numerous proteins. Proteomics analysis is a potential approach to identify, characterize and quantify global changes in protein profile, and the approach has been applied to examine protein profiles in myocardium of spontaneously hypertensive rats (SHRs), an inbred homozygous rodent model of human essential hypertension 2 . However, the sample separation technologies used in previous studies are almost all two-dimensional polyacrylamide gel electrophoresis (2D PAGE).…”

Analysis of the Serum Peptidomics Profile for Cats With Sarcomeric Gene Mutation and Hypertrophic Cardiomyopathy

“…HCM can be characterized by an increase in left ventricular myocardial mass. However, other causes of cardiac hypertrophy, such as hyperthyroidism, systemic hypertension, and aortic stenosis, are the primary differential diagnosis for this disease (5)(6)(7).…”

Relationship between HSPA1A-regulated gene expression and alternative splicing in mouse cardiomyocytes and cardiac hypertrophy

“…It has been reported to participate in cellular regulation of apoptosis and proliferation, as well as the activation of transcription factors and protein degradation. It has been reported that hypertrophic stimulation can induce Hsp70 expression, which consequently causes cardiac dysfunction and the development of cardiac hypertrophy by activating JNK, p38-MAPK, Raf-1, and ERK (41). Studies have also revealed Hsp70 induction under conditions of different hypertrophic stress responses and subsequent activation of HDAC2 to trigger cardiac hypertrophy (42).…”