Abstract
Radiation pulmonary injury is related to the accumulation of extracellular matrix proteins in the alveolar interstitial space. Matrilin-2 as a component of extracellular filamentous networks, present higher level in the lung tissue from irradiated mice and irradiated pulmonary epithelial cell line, HPAEpiC cells. Knockdown of endogenous matrilin-2 prevents the apoptosis of HPAEpiC cell induced by the irradiation injury. Consistently, over-expression of matrilin-2 reduced the proliferation and induced apoptosis of HPAEpiC cells. Matrilin-2 promotes the expression of p21 via increasing the transcriptional activity of p53, by which induces the G1 phase arresting in HPAEpiC cells. In summary, matrilin-2, increased by irradiation, reduced the proliferation and induces apoptosis of pulmonary epithelial cells via p53/p21 pathway.
Keywords:
Apoptosis; Cell cycle; Matrilin-2; Proliferation; Radiation pulmonary injury.
Copyright © 2016 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / genetics*
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Apoptosis / radiation effects
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Blotting, Western
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Cell Proliferation / genetics*
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Cell Proliferation / radiation effects
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Cells, Cultured
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Cyclin-Dependent Kinase Inhibitor p21 / genetics
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism
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Epithelial Cells / metabolism*
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Epithelial Cells / radiation effects
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G1 Phase Cell Cycle Checkpoints / genetics*
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G1 Phase Cell Cycle Checkpoints / radiation effects
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Gene Expression / radiation effects
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Humans
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Lung / metabolism
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Lung / radiation effects
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Male
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Matrilin Proteins / genetics*
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Matrilin Proteins / metabolism
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Mice, Inbred C57BL
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Pulmonary Alveoli / cytology
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RNA Interference
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction / genetics
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Signal Transduction / radiation effects
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
Substances
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Cyclin-Dependent Kinase Inhibitor p21
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Matrilin Proteins
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Tumor Suppressor Protein p53