Nitrite circumvents canonical cGMP signaling to enhance proliferation of myocyte precursor cells
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- 作者：Matthias Totzeck (1)
Andreas Schicho (1)
Pia Stock (1)
Malte Kelm (1)
Tienush Rassaf (1)
Ulrike B. Hendgen-Cotta (1)
1. Division of Cardiology ; Pulmonology and Vascular Medicine ; Department of Medicine ; Medical Faculty ; University Hospital Duesseldorf ; Moorenstrasse 5 ; 40225 ; D眉sseldorf ; Germany - 关键词：Nitrite ; Nitric oxide ; Myoblast ; Cyclic GMP
- 刊名：Molecular and Cellular Biochemistry
- 出版年：2015
- 出版时间：March 2015
- 年：2015
- 卷：401
- 期：1-2
- 页码：175-183
- 全文大小：900 KB
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- 刊物主题：Life Sciences
Biochemistry
Medical Biochemistry
Oncology
Cardiology - 出版者：Springer Netherlands
- ISSN：1573-4919
文摘
Skeletal muscle tissue has a remarkable high regenerative capacity. The underlying cellular events are governed by complex signaling processes, and the proliferation of skeletal myoblasts is a key initial event. The role of nitric oxide (NO) in cell cycle regulation is well-appreciated. Nitrite, an NO oxidation product, is a stable source for NO-like bioactivity particularly in cases when oxygen shortage compromises NO-synthases activity. Although numerous studies suggest that nitrite effects are largely related to NO-dependent signaling, emerging evidence also implicates that nitrite itself can activate protein pathways albeit under physiological, normoxic conditions. This includes a recently demonstrated cyclic guanosine monophosphate-(cGMP)-independent enhancement of endothelial cell proliferation. Whether nitrite itself has the potential to affect myoblast proliferation and metabolism with or without activation of the canonical NO/cGMP pathway to subsequently support muscle cell regeneration is not known. Here we show that nitrite increases proliferation and metabolic activity of murine cultured myoblasts dose-dependently. This effect is not abolished by the NO scavenger 2-(4-carboxy-phenyl)-4,4,5,5-tetramethylimida-zoline-1-oxyl-3 oxide and does not affect intracellular cGMP levels, implicating a cGMP-independent mechanism. Nitrite circumvents the rapamycin induced attenuation of myoblast proliferation and enhances mTOR activity. Our results provide evidence for a novel potential physiological and therapeutic approach of nitrite in skeletal muscle regeneration processes under normoxia independent of NO and cGMP.