Expression of matrix-degrading enzymes in pulmonary vascular remodeling in the rat.
Expression of matrix-degrading enzymes in pulmonary vascular remodeling in the rat.
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基质降解酶在大鼠肺血管重塑中的表达。
DOI：
10.1152/ajplung.1998.275.2.l398
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Riley,DJ
中科院分区：
文献类型：
--
作者：
Thakker-Varia,S;Tozzi,CA;Poiani,GJ;Babiarz,JP;Tatem,L;Wilson,FJ;Riley,DJ
大鼠暴露在低氧环境中会导致肺动脉重塑，这种重塑在回到空气中后部分可逆。我们推测，在缺氧后，重塑的肺动脉中过量的胶原降解是由内源性基质金属蛋白酶(MMPs)介导的。大鼠常氧暴露10天后，测定总的蛋白分解、胶原酶和明胶溶解活性、基质分解酶-1和金属蛋白酶组织抑制因子-1(TIMP-1)的水平以及基质分解素-1在大鼠主肺动脉中的免疫定位。我们观察到，在停止低氧暴露的3天内，总蛋白水解酶、胶原酶和明胶水解酶的活性以及∼72、68和60 kDa明胶酶的表达都有短暂的增加。TIMP-1水平随着基质分解素-1水平的升高而升高。基质分解素-1免疫反应主要定位于正常和高血压肺动脉的管腔区域。这些结果与内源性MMPs可能在缺氧后早期介导重塑的肺动脉中过量的胶原分解的观点是一致的。
Exposure of rats to hypoxia causes pulmonary arterial remodeling, which is partly reversible after return to air. We hypothesized that degradation of excess collagen in remodeled pulmonary arteries in the posthypoxic period is mediated by endogenous matrix metalloproteinases (MMPs). Total proteolytic, collagenolytic, and gelatinolytic activities, levels of stromelysin-1 and tissue inhibitor of metalloprotease-1 (TIMP-1), and immunolocalization of stromelysin-1 in main pulmonary arteries were determined after exposure of rats to 10% O2for 10 days followed by normoxia. We observed transient increases in total proteolytic, collagenolytic, and gelatinolytic activities and expression of ∼72-, 68-, and 60-kDa gelatinases by zymography within 3 days of cessation of hypoxic exposure. The level of TIMP-1 increased as the stromelysin-1 level increased. Immunoreactive stromelysin-1 was localized predominantly in the luminal region of normal and hypertensive pulmonary arteries. These results are consistent with the notion that endogenous MMPs may mediate the breakdown of excess collagen in remodeled pulmonary arteries during the early posthypoxic period.