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Mol. Cells 2003; 15(1): 94-101

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Cell Proliferation Induced by Reactive Oxygen Species Is Mediated via Mitogen-activated Protein Kinase in Chinese Hamster Lung Fibroblast (V79) Cells

Min-Joon Han, Bu-Yeo Kim, Sang-Oh Yoon, An-Sik Chung

Abstract

Reactive oxygen species (ROS) are generated during cellular metabolism or by external factors. Recently, it was learned that ROS can stimulate cellular proliferation and act as a second messenger in cellular signaling. We previously reported that hydroxyl radicals might be the signaling molecules. In the present experiment, phenazine methosulfate (PMS) was used to generate superoxide anion intracellularly. Treatment with 3 mM PMS in V79 cells increased cellular proliferation by 50%. PMS also activated the c-Jun N-terminal kinase (JNK) and p38 MAPK, but not extracellular signal-regulated kinase (ERK) 1/2 and ERK5. In particular, increased proliferation was blocked by pretreatment with SB203580 (an inhibitor of p38 MAPK). At the transcriptional level, the phosphorylation of c-Jun and ATF-2, which are mediated by JNK and p38 MAPK, were also increased by treatment with PMS.

Keywords Cell Proliferation, Superoxide Anion, MAPK, ROS

Article

Research Article

Mol. Cells 2003; 15(1): 94-101

Published online February 28, 2003

Copyright © The Korean Society for Molecular and Cellular Biology.

Cell Proliferation Induced by Reactive Oxygen Species Is Mediated via Mitogen-activated Protein Kinase in Chinese Hamster Lung Fibroblast (V79) Cells

Min-Joon Han, Bu-Yeo Kim, Sang-Oh Yoon, An-Sik Chung

Abstract

Reactive oxygen species (ROS) are generated during cellular metabolism or by external factors. Recently, it was learned that ROS can stimulate cellular proliferation and act as a second messenger in cellular signaling. We previously reported that hydroxyl radicals might be the signaling molecules. In the present experiment, phenazine methosulfate (PMS) was used to generate superoxide anion intracellularly. Treatment with 3 mM PMS in V79 cells increased cellular proliferation by 50%. PMS also activated the c-Jun N-terminal kinase (JNK) and p38 MAPK, but not extracellular signal-regulated kinase (ERK) 1/2 and ERK5. In particular, increased proliferation was blocked by pretreatment with SB203580 (an inhibitor of p38 MAPK). At the transcriptional level, the phosphorylation of c-Jun and ATF-2, which are mediated by JNK and p38 MAPK, were also increased by treatment with PMS.

Keywords: Cell Proliferation, Superoxide Anion, MAPK, ROS

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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