Coexpression of HSP47 gene and type I and type III collagen genes in LPS-induced pulmonary fibrosis in rats.
Coexpression of HSP47 gene and type I and type III collagen genes in LPS-induced pulmonary fibrosis in rats.
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发表时间：
2007
期刊：
影响因子：
5
通讯作者：
S. Hagiwara;H. Iwasaka;Shigekiyo Matsumoto;T. Noguchi;H. Yoshioka
中科院分区：
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作者：
S. Hagiwara;H. Iwasaka;Shigekiyo Matsumoto;T. Noguchi;H. Yoshioka
弥漫性肺泡损伤是急性呼吸窘迫综合征（ARDS）的组织病理学标志。相当比例的ARDS幸存者有残余肺纤维化和受损的肺功能。另一方面，热休克蛋白47（HSP 47）是一种胶原结合应激蛋白，被认为在活细胞中前胶原的生物合成和分泌期间充当胶原特异性分子伴侣。据报道，在几种细胞系中，HSP 47的合成与胶原蛋白的合成相关。本研究观察了内毒素（LPS）诱导的大鼠急性呼吸窘迫综合征（ARDS）肺组织中热休克蛋白47（HSP 47）mRNA和蛋白的表达。将雄性Wistar大鼠随机分为对照组和LPS组，对照组仅滴入0.9%NaCl溶液，LPS组滴入溶于0.9%NaCl溶液中的LPS（10 mg/kg）。LPS处理组大鼠出现组织学改变。北方印迹分析显示，在肺损伤的进展过程中，与I型和III型胶原mRNA平行，HSP 47 mRNA的表达被显著诱导。提示HSP 47和胶原蛋白表达上调在LPS诱导的ARDS肺纤维化过程中可能起重要作用。
Diffuse alveolar damage is the histopathologic hallmark of acute respiratory distress syndrome (ARDS). A significant proportion of ARDS survivors have residual pulmonary fibrosis and compromised pulmonary function. On the other hand, heat shock protein 47 (HSP47) is a collagen-binding stress protein that is assumed to act as a collagen-specific molecular chaperone during the biosynthesis and secretion of procollagen in living cells. The synthesis of HSP47 has been reported to correlate with that of collagen in several cell lines. We examined the expression of HSP47 mRNA and protein during the progression of lipopolysaccharide (LPS)-induced ARDS in rat lung. Male Wistar rats were randomly divided into two groups: a control group with instillation of 0.9% NaCl solution alone, and a LPS group with instillation of LPS dissolved in 0.9% NaCl solution (10 mg/kg). Histologic changes thereafter appeared in the LPS-treated rats. Northern blot analysis revealed the expression of HSP47 mRNA to be markedly induced during the progression of lung damage in parallel with type I and type III collagen mRNA. These results suggest that the upregulation of HSP47 and collagen may play an important role in the fibrotic process of LPS-induced ARDS lung.