2012Huanjing yu zhiye yixueRequires access

Expression and Potential Role of Relaxin in Lung Tissue of Rats Developing Silicosis

Ailin Liu

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Abstract

[Objective] To investigate the potential role of relaxin in the development of silica-induced silicosis.[Methods] Both in vitro and in vivo models of silicosis were established.Relaxin gene and protein expression in rat lung tissues were determined by real-time quantitative polymerase chain reaction(PCR) and immunohistochemical staining,respectively.Type I collagen in human fetal lung fibroblasts(HFL-I) supernatants was measured by enzyme-linked immunosorbent assay(ELISA).[Results] Slight expression of relaxin was observed in the normal control rat lung tissues and the signal intensities were primarily located in pulmonary alveolar type I cells.The relaxin protein and gene expression in the lungs of silica-treated(Dorentrup quartz,DQ12) rats showed a tendency of increasing first and then decreasing and was primarily located in pulmonary alveolar macrophages and type I cells.Compared with the controls,the relaxin protein expression reached maximum at 7 d(P 0.05),then went down at 14 d(P 0.05),and decreased markedly at 28 d(P 0.05).The levels of type I collagen in HFL-I cells in the relaxin group was significantly lower than that in the DQ12 group(P 0.05).[Conclusion] Relaxin can inhabit the formation of silica-induced type I collagen in lung fibroblasts,which may affect the development of silica-induced silicosis.

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[Objective] To investigate the potential role of relaxin in the development of silica-induced silicosis.[Methods] Both in vitro and in vivo models of silicosis were established.Relaxin gene and protein expression in rat lung tissues were determined by real-time quantitative polymerase chain reaction(PCR) and immunohistochemical staining,respectively.Type I collagen in human fetal lung fibroblasts(HFL-I) supernatants was measured by enzyme-linked immunosorbent assay(ELISA).[Results] Slight expression of relaxin was observed in the normal control rat lung tissues and the signal intensities were primarily located in pulmonary alveolar type I cells.The relaxin protein and gene expression in the lungs of silica-treated(Dorentrup quartz,DQ12) rats showed a tendency of increasing first and then decreasing and was primarily located in pulmonary alveolar macrophages and type I cells.Compared with the controls,the relaxin protein expression reached maximum at 7 d(P 0.05),then went down at 14 d(P 0.05),and decreased markedly at 28 d(P 0.05).The levels of type I collagen in HFL-I cells in the relaxin group was significantly lower than that in the DQ12 group(P 0.05).[Conclusion] Relaxin can inhabit the formation of silica-induced type I collagen in lung fibroblasts,which may affect the development of silica-induced silicosis.

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Available abstract

[Objective] To investigate the potential role of relaxin in the development of silica-induced silicosis.[Methods] Both in vitro and in vivo models of silicosis were established.Relaxin gene and protein expression in rat lung tissues were determined by real-time quantitative polymerase chain reaction(PCR) and immunohistochemical staining,respectively.Type I collagen in human fetal lung fibroblasts(HFL-I) supernatants was measured by enzyme-linked immunosorbent assay(ELISA).[Results] Slight expression of relaxin was observed in the normal control rat lung tissues and the signal intensities were primarily located in pulmonary alveolar type I cells.The relaxin protein and gene expression in the lungs of silica-treated(Dorentrup quartz,DQ12) rats showed a tendency of increasing first and then decreasing and was primarily located in pulmonary alveolar macrophages and type I cells.Compared with the controls,the relaxin protein expression reached maximum at 7 d(P 0.05),then went down at 14 d(P 0.05),and decreased markedly at 28 d(P 0.05).The levels of type I collagen in HFL-I cells in the relaxin group was significantly lower than that in the DQ12 group(P 0.05).[Conclusion] Relaxin can inhabit the formation of silica-induced type I collagen in lung fibroblasts,which may affect the development of silica-induced silicosis.

Key concepts: Relaxin, Silicosis, Lung, Immunohistochemistry, Gene expression, Molecular biology, Messenger RNA, Fetus

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