NDLI: Metabolic Reprogramming Is Required for Myofibroblast Contractility and Differentiation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mitra, Kasturi Liu, Gang Zmijewski, Jaroslaw W. Persons, Benjamin P. Bernard, Karen Logsdon, Naomi J. Rangarajan, Sunad Darley-usmar, Victor M. Ravi, Saranya Thannickal, Victor J. Xie, Na
Description	Author Affiliation: Bernard K ( From the Division of Pulmonary, Allergy and Critical Care Medicine, kbernard@uab.edu.); Logsdon NJ ( From the Division of Pulmonary, Allergy and Critical Care Medicine.); Ravi S ( Departments of Pathology and Center for Free Radicals Biology and Medicine, University of Alabama, Birmingham, Alabama 35294.); Xie N ( From the Division of Pulmonary, Allergy and Critical Care Medicine.); Persons BP ( From the Division of Pulmonary, Allergy and Critical Care Medicine.); Rangarajan S ( From the Division of Pulmonary, Allergy and Critical Care Medicine.); Zmijewski JW ( From the Division of Pulmonary, Allergy and Critical Care Medicine.); Mitra K ( Genetics, and.); Liu G ( From the Division of Pulmonary, Allergy and Critical Care Medicine.); Darley-Usmar VM ( Departments of Pathology and Center for Free Radicals Biology and Medicine, University of Alabama, Birmingham, Alabama 35294.); Thannickal VJ ( From the Division of Pulmonary, Allergy and Critical Care Medicine.)
Abstract	Contraction is crucial in maintaining the differentiated phenotype of myofibroblasts. Contraction is an energy-dependent mechanism that relies on the production of ATP by mitochondria and/or glycolysis. Although the role of mitochondrial biogenesis in the adaptive responses of skeletal muscle to exercise is well appreciated, mechanisms governing energetic adaptation of myofibroblasts are not well understood. Our study demonstrates induction of mitochondrial biogenesis and aerobic glycolysis in response to the differentiation-inducing factor transforming growth factor ß1 (TGF-ß1). This metabolic reprogramming is linked to the activation of the p38 mitogen-activated protein kinase (MAPK) pathway. Inhibition of p38 MAPK decreased accumulation of active peroxisome proliferator-activated receptor Î³ coactivator 1 in the nucleus and altered the translocation of mitochondrial transcription factor A to the mitochondria. Genetic or pharmacologic approaches that block mitochondrial biogenesis or glycolysis resulted in decreased contraction and reduced expression of TGF-ß1-induced -smooth muscle actin and collagen -2(I) but not of fibronectin or collagen -1(I). These data indicate a critical role for TGF-ß1-induced metabolic reprogramming in regulating myofibroblast-specific contractile signaling and support the concept of integrating bioenergetics with cellular differentiation.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	42
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-10-16
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Energy Metabolism Myofibroblasts Metabolism Cell Line Electron Transport Glycolysis Lung Cytology Mitochondria Oxygen Consumption Transforming Growth Factor Beta1 Physiology P38 Mitogen-Activated Protein Kinases Research Support, N.I.H., Extramural Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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