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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Claro, Sandra [1] ; Miyamoto Oshiro, Maria Etsuko [1] ; Mortara, Renato Arruda [2] ; Paredes-Gamero, Edgar Julian [1] ; Silva Pereira, Gustavo Jose [3] ; Smaili, Soraya Soubhi [3] ; Ferreira, Alice Teixeira [1]
Total Authors: 7
Affiliation:
[1] Univ Fed Sao Paulo, Dept Biophys, BR-04023062 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Parasitol, BR-04023062 Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Pharmacol, BR-04023062 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: International Journal of Radiation Biology; v. 90, n. 10, p. 914-927, OCT 2014.
Web of Science Citations: 5
Abstract

Purpose: gamma-rays (IR) cause an increase in intracellular calcium {[}Ca2+], 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 Co-60 gamma-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. (AU)

FAPESP's process: 10/00106-5 - Study of differentiation of the mesenchymal and tumoural cells into muscular and neuronal cells emphasizing calciun signalling and markers cells expression after transplantation in a stroke animal model
Grantee:Alice Teixeira Ferreira
Support Opportunities: Regular Research Grants