Telomerase reverse transcriptase (TERT) is an enzyme required for the proliferative capacity and survival of cells. It is an RNA-dependent DNA polymerase responsible for de novo elongation of telomere repeats at the chromosome termini, by adding telomeric repeats to the 3’ end of the telomeric strand, through copying of the selleck compound template sequence present in Inhibitors,research,lifescience,medical its RNA moiety (21, 22). Low level of telomerase activity has been discovered in mitotically active cells, including skin, lymphocytes, and endometrium and stem cells (23). In the present study we find significantly decreased levels in telomerase activity among DMD patients compared to controls. Evidence support that, a correlation

Inhibitors,research,lifescience,medical is observed between the level of induced telomerase activity and change in telomere length, such that telomere lengthening rather than telomere loss was found in cells when telomerase activity reached relatively high levels; conversely, telomere loss was evident when telomerase activity was low (24). The decrease in telomerase activity observed in DMD

patients compared to controls can be attributed to the fact that increased oxidative stress induces a decrease Inhibitors,research,lifescience,medical in telomerase activity (25). Bax genes expresses a Bax, a pro-apoptotic Bcl-2 family member, can heterodimerize with either Bcl-2 or Bcl-xL to nullify their anti-apoptotic properties (26). Increased Bax mRNA expression has been observed in ageing human lymphocytes (27, 28). Exercise loading caused an increased expression in Bax localization in muscular dystrophy animal model (29). Meaning that oxidative stress due to exercise in DMD brings damage similar to that observed in aging, which coincide with our results. An aging hypothesis states that aged tissues are Inhibitors,research,lifescience,medical characterized by the accumulation of a variety of types of advanced glycation end products (AGEs), which are the products of nonenzymatic glycation and oxidation of proteins and lipids and DNA (30, 31). RAGE is a multiligand receptor

of the immunoglobulin superfamily expressed in almost all body cells including endothelial cells, Inhibitors,research,lifescience,medical monocytes, neutrophils, myoblasts and vascular smooth muscle cells (32). RAGE has been identified as receptor, which binds β-sheet fibrils characteristic of amyloid; proinflammatory cytokine-like mediators of the S100/calgranulin out family. Engagement of RAGE by these ligands activates key signal transduction pathways, such as p21ras, erk 1/2 kinases and nuclear factor-κB in endothelial cells, monocytes, and vascular smooth muscle cells (33). This cascade of events leads to RAGE-mediated-enhanced expression of proinflammatory mediators. Evidence support that RAGE mediate the effects of AGEs by both ligand engagement and signal transduction (34). There was a significant increase in RAGEs mRNA expression in peripheral blood mononuclear cells of DMD compared to controls.