γ-Rays-generated ROS induce apoptosis via mitochondrial and cell cycle alteration in smooth muscle cells.

Autor: Claro S; Department of Biophysics, Federal University of São Paulo , São Paulo , Brazil., Oshiro ME, Mortara RA, Paredes-Gamero EJ, Pereira GJ, Smaili SS, Ferreira AT
Jazyk: angličtina
Zdroj: International journal of radiation biology [Int J Radiat Biol] 2014 Oct; Vol. 90 (10), pp. 914-27. Date of Electronic Publication: 2014 May 02.
DOI: 10.3109/09553002.2014.911988
Abstrakt: Purpose: γ-rays (IR) cause an increase in intracellular calcium [Ca(2+)], alters contractility and triggers apoptosis via the activation of protein kinase C in intestinal guinea pig smooth muscle cells. The present study investigated the role of the mitochondria in these processes and characterized proteins involved in IR-induced apoptosis.
Materials and Methods: Intestinal smooth muscle cells were exposed to 10-50 Gy from a (60)Co γ-source. Reactive oxygen species (ROS) levels were measured by colourimetry with a fluorescente probe. Protein expression was analyzed by immunoblotting and immunofluorescence.
Results: Apoptosis was inhibited by glutathione, possible by inhibiting the generation or scavenging ROS. Apoptosis was mediated by the mitochondria releasing cytochrome c leading to caspase 3 activation. IR increased the expression of the cyclins A, B2 and E and led to unbalanced cellular growth in an absorption dose-dependent manner. However, radiation did not induce alterations in the mitochondrial ultrastructure or in transmembrane electric potential. In contrast, IR increased the nuclear expression of cytoplasmic proteins and cyclins A and E.
Conclusion: Smooth muscle cells subjected to IR undergo mitochondrial-mediated apoptosis that involves oncoproteins activation and preserves mitochondrial structure. IR also cause alterations in the expression and localization of both pro- and anti-apoptotic proteins.
Databáze: MEDLINE
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