Endothelial cell surface alkaline phosphatase activity is induced by IL-6 released during wound repair
Endothelial cell surface alkaline phosphatase activity is induced by IL-6 released during wound repair
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DOI：
10.1111/1523-1747.ep12337529
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发表时间：
1997-10-01
影响因子：
6.5
通讯作者：
Bernfield, M
中科院分区：
文献类型：
--
作者：
Gallo, RL;Dorschner, RA;Bernfield, M
内皮细胞表面上的磷酸酶活性部分地负责腺苷核苷酸转化为腺苷，腺苷是一种有效的血管扩张剂和抗炎介质，可以保护组织免受由损伤引起的缺血性损伤。为了评估磷酸酶是否被损伤后释放的可溶性因子主动诱导，在内皮细胞的原代培养物上测试了从猪或人皮肤伤口收集的组织液的作用。磷酸酶活性增加了约50倍，48小时的文化在伤口液的存在下。诱导活性仅存在于伤口修复炎症阶段收集的液体中。磷酸酶活性将腺苷一磷酸代谢为游离磷酸盐，是肝/骨/肾碱性磷酸酶同工酶：活性对温度和左旋咪唑敏感，耐1-苯丙氨酸，并通过磷脂与细胞表面相连，并以与该同工酶相同的大小迁移。白细胞介素-6被鉴定为伤口液中的磷酸酶诱导因子，相关细胞因子白血病抑制因子和制瘤素M引起类似程度的碱性磷酸酶诱导。因此，在损伤后，白细胞介素-6的积累可导致腺苷的碱性磷酸酶的产生和随后的缺血性损伤的保护。
Phosphatase activity on endothelial cell surfaces is responsible, in part, for the conversion of adenosine nucleotides to adenosine, a potent vasodilator and anti-inflammatory mediator that can protect tissues from the ischemic damage that results from injury. To evaluate whether phosphatases are actively induced by a soluble factor released following injury, the effect of tissue fluids collected from porcine or human skin wounds was tested on primary cultures of endothelial cells. Phosphatase activity increased approximate to 50-fold following 48-h culture in the presence of wound fluid. Inductive activity was present only in fluids collected during the inflammatory phase of wound repair. The phosphatase activity metabolized adenosine monophosphate to free phosphate and was the liver/bone/kidney alkaline phosphatase isoenzyme: activity was temperature- and levamisole-sensitive, 1-phenylalanine-resistant, and linked to the cell surface via phospholipid, and migrated at a size identical to this isozyme. interleukin-6 was identified as the phosphatase-inducing factor in wound fluid and the related cytokines, leukaemia inhibiting factor and oncostatin M, caused a similar degree of alkaline phosphatase induction. Therefore, following injury, accumulation of interleukin-6 can lead to production by alkaline phosphatase of adenosine and subsequent protection from ischemic injury.