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目的:结缔组织生长因子(connective tissue growth factor,CTGF)可诱导人肾小管上皮细胞HK-2表达整合素连接激酶(integrin-linked kinase,ILK),本研究观察脂氧素A4(lipoxinA4,LXA4)是否调节CTGF对合成ILK的作用,并探讨其作用机制。方法:对体外培养的人肾小管上皮细胞(HK-2细胞株),用不同浓度的LXA4预刺激,再加入CTGF共同孵育;或单用CTGF刺激HK-2细胞。应用RT-PCR和Westernblot方法测定ILKmRNA和蛋白表达,应用Westernblot法测定分裂原激活的蛋白激酶(p42/44mitogen-activated protein kinase,p42/44MAPK)(也称为ERK1/2)、磷脂酰肌醇3-激酶(phosphoinositide 3-kinase,PI3-K)。结果:CTGF刺激使HK-2细胞ILKmRNA表达和蛋白合成增加,磷酸化ERK1/2、磷酸化PI3-K的表达增加。LXA4呈剂量依赖性地抑制CTGF所致的上述变化。结论:LXA4可抑制CTGF引起的HK-2细胞表达ILK,其机制依赖于抑制ERK1/2、PI3-K的磷酸化。
OBJECTIVE: Connexin tissue growth factor (CTGF) induces the expression of integrin-linked kinase (ILK) in human renal tubular epithelial cells HK-2. Lipoxin A4 (LXA4) Whether to regulate CTGF on the role of ILK synthesis, and explore its mechanism of action. Methods: Human renal tubular epithelial cells (HK-2 cell line) cultured in vitro were preincubated with different concentrations of LXA4 and then added with CTGF for co-incubation. Alternatively, HK-2 cells were stimulated with CTGF alone. The expressions of ILK mRNA and protein were determined by RT-PCR and Western blotting. The p42 / 44mitogen-activated protein kinase (p42 / 44MAPK) (also called ERK1 / 2) and phosphatidylinositol 3 - kinase (phosphoinositide 3-kinase, PI3-K). Results: CTGF stimulated ILKmRNA expression and protein synthesis in HK-2 cells. The phosphorylation of ERK1 / 2 and phosphorylated PI3-K increased. LXA4 dose-dependently inhibited the above changes caused by CTGF. Conclusion: LXA4 can inhibit the expression of ILK induced by CTGF in HK-2 cells. The mechanism of LXA4 depends on the inhibition of phosphorylation of ERK1 / 2 and PI3-K.