Matrix metalloproteinase‐2 is not active in the diaphragm during mechanical ventilation
Abstract
Prolonged mechanical ventilation (MV) results in diaphragmatic atrophy and contractile dysfunction, which occurs, in part, due to the activation of several proteolytic systems. New evidence shows matrix metalloproteinase‐2 (MMP‐2) can contribute to muscle fiber atrophy and contractile dysfunction in animal models of muscle disuse. Therefore, this experiment determined if prolonged MV alters mRNA expression and protein abundance of MMP‐2 and its regulators, TIMP‐2 and MT1‐MMP. Our results reveal that prolonged MV (12 hours) did not alter MMP‐2 mRNA expression or protein abundance in the diaphragm. Furthermore, prolonged MV did not promote an increase in mRNA expression of TIMP‐2 in the diaphragm. However, prolonged MV did result in a small increase in MT1‐MMP mRNA expression, but this increase may not be physiologically significant (<2‐fold). Finally, MV did not result in a significant change in diaphragmatic protein abundance for TIMP‐2 or MT1‐MMP. Collectively, our results demonstrate that MV does not activate MMP‐2 or its regulators. Supported by NIH RO1 HL087839 (SKP) and MRMC (MLU).
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2013
- Source ID
- 10.1096/fasebj.27.1_supplement.lb779
Entities
People
- Ashley J Smuder
- Christopher T. Carrigan
- Kurt J Sollanek
- Maria L. Urso
- Matthew B Hudson
- Scott K Powers
- W Bradley Nelson
Organizations
- National Institutes of Health
- United States Army Medical Research and Development Command
- University of Florida