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Mol. Cells 2008; 25(1): 78-85

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

The Fast Skeletal Muscle Myosin Light Chain Is Differentially Expressed in Smooth Muscle Cells of OVA-challenged Mouse Expressed in Smooth Muscle Cells of OVA-challenged Mouse

Ho-Young Kim, TaiYoun Rhim, Mi-Hyun Ahn, Pyoung-Oh Yoon, Soo-Ho Kim, Sang-Han Lee and Choon-Sik Park

Abstract

In a search for new molecular pathways associated with asthma, we performed an mRNA differential display analysis using total RNA extracted from the tracheal tissues of ovalbumin (OVA)-challenged mice and sham controls. cDNAs corresponding to mRNAs for which expression levels were altered by OVA-challenge were isolate and sequenced. Twenty-eight genes differentially expressed in sham and OVA challenged mice were identified. A GenBank BLAST homology search revealed that they were related to cytoskeleton remodeling, transcription, protein synthesis and modification, energy production, and cell growth and differentiation. Two were selected for further characterization. Up-regulation of both the perinatal skeletal myosin heavy chain (skMHC) and fast skeletal muscle myosin light chain (skMLC) genes was confirmed by RT-PCR of trachea tissue from OVA challenged mice. Overexpression of skMLC protein was observed in the smooth muscle layers of OVA-challenged mice by immunohis-tochemistry, and the surface areas stained with skMLC antibody increased in the OVA-challenged mice. The overexpression of skMLC in murine asthma may be associated with the changes of bronchial smooth muscle.

Keywords DD-PCR, OVA Induced Asthma, skMLC, Smooth Muscle

Article

Research Article

Mol. Cells 2008; 25(1): 78-85

Published online February 29, 2008

Copyright © The Korean Society for Molecular and Cellular Biology.

The Fast Skeletal Muscle Myosin Light Chain Is Differentially Expressed in Smooth Muscle Cells of OVA-challenged Mouse Expressed in Smooth Muscle Cells of OVA-challenged Mouse

Ho-Young Kim, TaiYoun Rhim, Mi-Hyun Ahn, Pyoung-Oh Yoon, Soo-Ho Kim, Sang-Han Lee and Choon-Sik Park

Abstract

In a search for new molecular pathways associated with asthma, we performed an mRNA differential display analysis using total RNA extracted from the tracheal tissues of ovalbumin (OVA)-challenged mice and sham controls. cDNAs corresponding to mRNAs for which expression levels were altered by OVA-challenge were isolate and sequenced. Twenty-eight genes differentially expressed in sham and OVA challenged mice were identified. A GenBank BLAST homology search revealed that they were related to cytoskeleton remodeling, transcription, protein synthesis and modification, energy production, and cell growth and differentiation. Two were selected for further characterization. Up-regulation of both the perinatal skeletal myosin heavy chain (skMHC) and fast skeletal muscle myosin light chain (skMLC) genes was confirmed by RT-PCR of trachea tissue from OVA challenged mice. Overexpression of skMLC protein was observed in the smooth muscle layers of OVA-challenged mice by immunohis-tochemistry, and the surface areas stained with skMLC antibody increased in the OVA-challenged mice. The overexpression of skMLC in murine asthma may be associated with the changes of bronchial smooth muscle.

Keywords: DD-PCR, OVA Induced Asthma, skMLC, Smooth Muscle

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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