Effect of Clofibric Acid on Desmin and Vimentin Contents in Rat Myocardiocytes

Abstract

The aim of this experimental study was to analyze in vitro effects of clofibric acid on vimentin and desmin contents in rat myocardiocytes, which was carried out in primary myocardiocyte cells that were treated only with clofibric acid at 0.1 mM. The measurement of vimentin and desmin were done by Western blotting and densitometry. This study showed that myocardiocytes exposed to clofibric acid exhibit a 26.3% decrease in vimentin and a 42.1% decrease in desmin. Considering the role that these intermediate filaments play in the anchorage and cellular organization of myocardiocytes, the decrease of desmin and vimentin observed in cells treated with clofibric acid may be partially responsible for the adverse effects observed in patients. In conclusion, the alteration of cytoskeletal proteins may be a cause of cardiopathy in patients treated with these compounds.

Assessment of Pep, Fndc5, C2c12, Pgc1α Pattern of Genes Expression during Differentiation of Human Embryonic Stem Cells into Heart Cells

“…Fibronectin type III domain-containing protein 5, the precursor of irisin, is a protein that is encoded by the FNDC5 gene [1]. Irisin is a cleaved version of FNDC5, named after the Greek messenger goddess Iris [2] (Figures 1 and 2).…”

“…The ectodomain was proposed to be cleaved to give a soluble peptide hormone named irisin. Separately it was proposed that irisin is secreted from muscle in response to exercise, and may mediate some beneficial effects of exercise in humans and the potential for generating weight loss and blocking diabetes has been suggested [2,[5][6][7][8][9][10][11]. Others questioned these findings [1,[12][13][14] (Figure 3).…”

“…The sequence of irisin, the cleaved and secreted portion of FNDC5, is highly conserved in mammals; the human and murine sequences are identical [2]. However, the start codon of human FNDC5 is mutated to ATA, which causes it to be expressed at only 1% the level of other animals with the normal ATG start -though its circulation levels are still on par with other key human hormones, such as insulin [15].…”

“…Exercise causes increased expression in muscle of peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1alpha), which is involved in adaptation to exercise. In mice, this causes production of the FNDC5 protein which is cleaved to give a new product irisin [2,7]. Due to its production through a mechanism initiated by muscular contraction, irisin has been classified as a myokine [16].…”

“…X-ray structures of PEPCK provide insight into the structure and the mechanism of PEPCK enzymatic activity. The mitochondrial isoform of chicken liver PEPCK complexed with Mn 2+ , Mn 2+ -phosphoenolpyruvate (PEP), and Mn 2+ -GDP provides information about its structure and how this enzyme catalyzes reactions [2]. Delbaere et al resolved PEPCK in E. coli and found the active site sitting between a C-terminal domain and an N-terminal domain.…”