Increased expression of collagen-binding heat shock protein 47 in murine bleomycin-induced pneumopathy
Increased expression of collagen-binding heat shock protein 47 in murine bleomycin-induced pneumopathy
复制标题
DOI：
10.1152/ajplung.00305.2002
复制
发表时间：
2003-10-01
影响因子：
4.9
通讯作者：
Kohno, S
中科院分区：
文献类型：
--
作者：
Ishii, H;Mukae, H;Kohno, S
47kda热休克蛋白47 （HSP47）是一种胶原特异性分子伴侣，已被证明在前胶原的加工和/或分泌过程中发挥重要作用。据报道，在各种纤维化模型的进展过程中，HSP47的表达与胶原的表达平行增加。本研究的目的是探讨在博来霉素（BLM）诱导的小鼠纤维化中HSP47的表达与胶原积累之间的关系。我们采用免疫组织化学和半定量RT-PCR方法研究了HSP47蛋白和mRNA在blm诱导的小鼠肺纤维化中的表达。免疫组织化学分析显示，与对照组相比，blm诱导的肺纤维化中HSP47蛋白的表达更高。HSP47主要定位于α -平滑肌肌动蛋白阳性的肌成纤维细胞、F4/80阴性、表面活性蛋白a阳性的II型肺细胞和F4/80阳性的巨噬细胞。RTPCR还显示，在blm处理的肺中，HSP47 mRNA表达增加。HSP47 mRNA相对表达量与肺羟脯氨酸含量呈显著相关（r = 0.406, P < 0.05）。我们的研究结果表明，这些细胞可能通过上调HSP47在blm治疗的肺纤维化过程中发挥作用。
The 47-kDa heat shock protein 47 (HSP47) is a collagen-specific molecular chaperone that has been shown to play a major role during the processing and/or secretion of procollagen. Expression of HSP47 has been reported to increase in parallel with expression of collagens during the progression of various fibrosis models. The aim of the present study was to investigate the association between HSP47 expression and collagen accumulation in bleomycin (BLM)-induced murine fibrosis. We investigated the expression of HSP47 protein and mRNA using immunohistochemical analysis and semiquantitative RT-PCR in murine BLM-induced pulmonary fibrosis. Immunohistochemical analysis showed that higher expression of HSP47 protein was present in BLM-induced pulmonary fibrosis compared with controls. HSP47 was localized predominantly in alpha-smooth muscle actin-positive myofibroblasts, F4/80 negative, surfactant protein-A-positive type II pneumocytes, and F4/80-positive macrophages. RTPCR also demonstrated an increase of HSP47 mRNA expression in BLM-treated lungs. Moreover, the relative amounts of HSP47 mRNA correlated significantly with the lung hydroxyproline content as an indicator of pulmonary fibrosis in BLM-treated lungs (r = 0.406, P < 0.05). Our results suggest that these cells may play a role in the fibrotic process of BLM-treated lungs through upregulation of HSP47.