基质金属蛋白酶
肺纤维化
博莱霉素
纤维化
基质金属蛋白酶3
病理
金属蛋白酶组织抑制剂
肺
金属蛋白酶
医学
基质金属蛋白酶抑制剂
细胞凋亡
转基因小鼠
特发性肺纤维化
癌症研究
免疫学
生物
转基因
内科学
基因
生物化学
化疗
作者
Ryo Inoue,Taro Yasuma,Valeria Fridman D’Alessandro,Masaaki Toda,Toshiyuki Ito,Atsushi Tomaru,Corina N. D’Alessandro-Gabazza,Tatsuki Tsuruga,Tomohito Okano,Atsuro Takeshita,Kota Nishihama,Hajime Fujimoto,Tetsu Kobayashi,Esteban C. Gabazza
摘要
Idiopathic pulmonary fibrosis is a progressive and fatal disease with a poor prognosis. Matrix metalloproteinase-2 is involved in the pathogenesis of organ fibrosis. The role of matrix metalloproteinase-2 in lung fibrosis is unclear. This study evaluated whether overexpression of matrix metalloproteinase-2 affects the development of pulmonary fibrosis. Lung fibrosis was induced by bleomycin in wild-type mice and transgenic mice overexpressing human matrix metalloproteinase-2. Mice expressing human matrix metalloproteinase-2 showed significantly decreased infiltration of inflammatory cells and inflammatory and fibrotic cytokines in the lungs compared to wild-type mice after induction of lung injury and fibrosis with bleomycin. The computed tomography score, Ashcroft score of fibrosis, and lung collagen deposition were significantly reduced in human matrix metalloproteinase transgenic mice compared to wild-type mice. The expression of anti-apoptotic genes was significantly increased, while caspase-3 activity was significantly reduced in the lungs of matrix metalloproteinase-2 transgenic mice compared to wild-type mice. Active matrix metalloproteinase-2 significantly decreased bleomycin-induced apoptosis in alveolar epithelial cells. Matrix metalloproteinase-2 appears to protect against pulmonary fibrosis by inhibiting apoptosis of lung epithelial cells.
科研通智能强力驱动
Strongly Powered by AbleSci AI