Cachectin/tumor necrosis factor stimulates collagenase and prostaglandin E2 production by human synovial cells and dermal fibroblasts.
Cachectin/tumor necrosis factor stimulates collagenase and prostaglandin E2 production by human synovial cells and dermal fibroblasts.
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DOI：
10.1084/jem.162.6.2163
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发表时间：
1985-12-01
期刊：
影响因子：
--
通讯作者：
Cerami A
中科院分区：
文献类型：
--
作者：
Dayer JM;Beutler B;Cerami A
恶病质/TNF（肿瘤坏死因子）是一种内毒素诱导的鼠巨噬细胞激素，与恶病质和休克的发病机制有关，已被发现能够刺激分离的人滑膜细胞和真皮成纤维细胞产生胶原酶和前列腺素 E2 (PGE2)。这种与恶病素相关的生物活性与单核白细胞介素 1 (IL-1) 观察到的生物活性相当，此前认为单核白细胞介素 1 (IL-1) 是蛋白水解的主要介质。恶病素/TNF 刺激胶原酶和 PGE2 产生的能力表明，它可能在组织破坏和重塑中发挥作用，因为这些过程发生在炎症性疾病中。
Cachectin/TNF (tumor necrosis factor), an endotoxin-induced murine macrophage hormone implicated in the pathogenesis of cachexia and shock, has been found capable of stimulating collagenase and prostaglandin E2 (PGE2) production by isolated human synovial cells and dermal fibroblasts. This bioactivity associated with cachectin is comparable to that observed with the monokine interleukin 1 (IL-1), previously suggested as the major mediator of proteolysis. The ability of cachectin/TNF to stimulate collagenase and PGE2 production suggests that it may play a role in tissue destruction and remodelling, as these processes occur in inflammatory diseases.