The Expression of High Mobility Group Protein-B1 and Alpha-Smooth Muscle Actin in Lung Tissues of Pulmonary Fibrosis Mice_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

CAI Lin ¹ , LI Li ² ,  XU Jun ¹

Institute of Respiratory Disease, The First Affiliated Hospital, Guangzhou Medical College. Guangzhou, Guangdong, 510120, China;

Corresponding author：

XU Jun, Email: xufeili@vip.163.com

Keywords：

Pulmonary fibrosis; Bleomycin; High mobility group protein-B1; α-smooth muscle actin; Pathogenesis

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Objective To investigate the expression of high mobility group protein-B1( HMGB1)and α-smooth muscle actin( α-SMA) in Bleomycin induced pulmonary fibrosis in mice. Methods Twenty C57BL/ 6 male mice were randomly divided into a Bleomycin group and a control group. The Bleomycin group was treated with Bleomycin( 3 mg/kg) by endotracheally injection to induce pulmonary fibrosis. The control group were treated with normal saline( NS) . Then they were sacrificed by abdominal aortic bleeding 10 days after the injection. The right lung was stained with hematoxylin-eosin and Masson trichrome respectively for pathological examination. Immunohistochemistry and RT-PCR were performed to identify the protein and mRNA levels of α-SMA and HMGB1 respectively. Results The mRNA( 0. 89 ±0. 12, 0. 61 ±0. 08) and protein( 13. 66 ±1. 01, 13. 12 ±1. 33) expressions of α-SMA and HMGB1 in the Bleomycin group were all significantly higher than those of the control group( mRNA: 0. 60 ±0. 07, 0. 15 ±0. 02; protein: 8. 18 ±1. 33,7. 92 ±1. 10; all P lt; 0. 01) . Conclusions The expressions of HMGB1 and α-SMA are increased in Bleomycin induced pulmonary fibrosis. HMGB1 participates in the pathological process of pulmonary fibrosis probably by activation of the α-SMA expression.

Citation： CAI Lin ,LI Li,XU Jun. The Expression of High Mobility Group Protein-B1 and Alpha-Smooth Muscle Actin in Lung Tissues of Pulmonary Fibrosis Mice. Chinese Journal of Respiratory and Critical Care Medicine, 2009, 09(2): 181-185. doi: Copy

1.	蔡琳, 吴壮, 徐军. 博莱霉素诱导α平滑肌肌动蛋白Cre 重组酶转基因小鼠肺纤维化上皮细胞-间质转分化的研究. 中国呼吸与危重监护杂志, 2009, 8: 52-56.
2.	张敏, 徐军. MAPKs 通路在转化生长因子β1 诱导气道上皮细胞转化中的作用. 中国呼吸与危重监护杂志, 2007, 6: 440-443.
3.	Phan SH. The myofibroblast in pulmonary fibrosis. Chest, 2002 ,122: 286s-289s.
4.	Sadikot RT, Christman JW, Blackwell TS. Molecular targets for modulating lung inflammation and injury. Curr Drug Targets, 2004 ,5: 581-588.
5.	White ES, Atrasz RG, Hu B, et al. Negative regulation of myofibroblast differentiation by PTEN ( Phosphatase and Tensin Homolog Deleted on chromosome 10 ) . AmJ Respir Crit Care Med,2006, 173: 112-121.
6.	Lotze MT, Tracey KJ. High-mobility group box 1 protein( HMGB1) :nuclear weapon in the immune arsenal. Nat Rev Immunol, 2005, 5 :331-342.
7.	Bustin M. Regulation of DNA-dependent activities by the functional motifs of the high-mobility-group chromosomal proteins. Mol Cell Biol, 1999, 19 : 5237 -5246 .
8.	Kuhn C, McDonald JA. The roles of the myofibroblast in idiopathic pulmonary fibrosis. Ultrastructural and immunohistochemical features of sites of active extracellular matrix synthesis. Am J Pathol, 1991, 138: 1257-1265.
9.	Schissel SL, Layne MD. Telomerase, myofibroblasts, and pulmonary fibrosis. Am J Respir Cell Mol Biol, 2006, 34: 520-522.
10.	Gross TJ, Hunninghake GW. Idiopathic pulmonary fibrosis. N Engl J Med, 2001, 345: 517-525.
11.	Zhang HY, Gharaee-Kermani M, Zhang K, et al. Lung fibroblast alpha-smooth muscle actin expression and contractile phenotype in bleomycin-induced pulmonary fibrosis. Am JPathol, 1996, 148: 527-537.
12.	Darby I, Skalli O, Gabbiani G. Alpha-smooth muscle actin is transiently expressed by myofibroblasts during experimental wound healing. Lab Invest, 1990, 63: 21-29.
13.	Goodwin GH, Sanders C, Johns EW. A new group of chromatinassociated proteins with a high content of acidic and basic amino acids. Eur J Biochem, 1973, 38: 14-19.
14.	Scaffidi P, Misteli T, Bianchi ME. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature, 2002 , 418 :191-195.
15.	Wang H, Bloom O, Zhang M, et al. HMG-1 as a late mediator of endotoxin lethality in mice. Science, 1999, 285: 248-251.
16.	Yang H, Ochani J, Li J, et al. Reversing established sepsis with antagonists of endogenous high-mobility group box 1. Proc Natl Acad Sci USA, 2004, 101: 296-301.
17.	Andersson U, Wang H, Palmblad K, et al. High mobility group 1 protein( HMG-1 ) stimulates proinflammatory cytokine synthesis in human monocytes. J Exp Med, 2000, 192: 565-570.
18.	He M, Kubo H, Ishizawa K, et al. The role of the receptor for advanced glycation end-products in lung fibrosis. AmJ Physiol Lung Cell Mol Physiol, 2007, 293: L1427-L1436.

1. 蔡琳, 吴壮, 徐军. 博莱霉素诱导α平滑肌肌动蛋白Cre 重组酶转基因小鼠肺纤维化上皮细胞-间质转分化的研究. 中国呼吸与危重监护杂志, 2009, 8: 52-56.
2. 张敏, 徐军. MAPKs 通路在转化生长因子β1 诱导气道上皮细胞转化中的作用. 中国呼吸与危重监护杂志, 2007, 6: 440-443.
3. Phan SH. The myofibroblast in pulmonary fibrosis. Chest, 2002 ,122: 286s-289s.
4. Sadikot RT, Christman JW, Blackwell TS. Molecular targets for modulating lung inflammation and injury. Curr Drug Targets, 2004 ,5: 581-588.
5. White ES, Atrasz RG, Hu B, et al. Negative regulation of myofibroblast differentiation by PTEN ( Phosphatase and Tensin Homolog Deleted on chromosome 10 ) . AmJ Respir Crit Care Med,2006, 173: 112-121.
6. Lotze MT, Tracey KJ. High-mobility group box 1 protein( HMGB1) :nuclear weapon in the immune arsenal. Nat Rev Immunol, 2005, 5 :331-342.
7. Bustin M. Regulation of DNA-dependent activities by the functional motifs of the high-mobility-group chromosomal proteins. Mol Cell Biol, 1999, 19 : 5237 -5246 .
8. Kuhn C, McDonald JA. The roles of the myofibroblast in idiopathic pulmonary fibrosis. Ultrastructural and immunohistochemical features of sites of active extracellular matrix synthesis. Am J Pathol, 1991, 138: 1257-1265.
9. Schissel SL, Layne MD. Telomerase, myofibroblasts, and pulmonary fibrosis. Am J Respir Cell Mol Biol, 2006, 34: 520-522.
10. Gross TJ, Hunninghake GW. Idiopathic pulmonary fibrosis. N Engl J Med, 2001, 345: 517-525.
11. Zhang HY, Gharaee-Kermani M, Zhang K, et al. Lung fibroblast alpha-smooth muscle actin expression and contractile phenotype in bleomycin-induced pulmonary fibrosis. Am JPathol, 1996, 148: 527-537.
12. Darby I, Skalli O, Gabbiani G. Alpha-smooth muscle actin is transiently expressed by myofibroblasts during experimental wound healing. Lab Invest, 1990, 63: 21-29.
13. Goodwin GH, Sanders C, Johns EW. A new group of chromatinassociated proteins with a high content of acidic and basic amino acids. Eur J Biochem, 1973, 38: 14-19.
14. Scaffidi P, Misteli T, Bianchi ME. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature, 2002 , 418 :191-195.
15. Wang H, Bloom O, Zhang M, et al. HMG-1 as a late mediator of endotoxin lethality in mice. Science, 1999, 285: 248-251.
16. Yang H, Ochani J, Li J, et al. Reversing established sepsis with antagonists of endogenous high-mobility group box 1. Proc Natl Acad Sci USA, 2004, 101: 296-301.
17. Andersson U, Wang H, Palmblad K, et al. High mobility group 1 protein( HMG-1 ) stimulates proinflammatory cytokine synthesis in human monocytes. J Exp Med, 2000, 192: 565-570.
18. He M, Kubo H, Ishizawa K, et al. The role of the receptor for advanced glycation end-products in lung fibrosis. AmJ Physiol Lung Cell Mol Physiol, 2007, 293: L1427-L1436.

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The Expression of High Mobility Group Protein-B1 and Alpha-Smooth Muscle Actin in Lung Tissues of Pulmonary Fibrosis Mice

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