ERK1/2磷酸化异常在慢性肾衰竭继发性甲状旁腺功能亢进发病机制中的作用被引量：2

Disorder of ERK1/2 phosphorylation pathway in the pathogenesis of secondary hyperparathyroidism resulted from chronic renal failure

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摘要目的探讨ERK1/2磷酸化异常在慢性肾衰竭继发性甲状旁腺功能亢进(SHPT)发病机制中的作用。方法选取在我院肾内科住院行甲状旁腺全切术的SHPT患者50例为SHPT组,尸体甲状旁腺供体8例为对照组,检测血磷、血钙、碱性磷酸酶、甲状旁腺激素(PTH)及成纤维细胞生长因子-23(FGF-23)水平,免疫组化测定甲状旁腺组织中ERK1/2、p-ERK1/2、Egr-1的表达。结果 (1)SHPT组患者血FGF-23与PTH(r=0.438,P=0.001)、血磷(r=0.421,P=0.002)、碱性磷酸酶(r=0.452,P=0.001)均呈正相关;(2)SHPT组患者术后3 d FGF-23较术前相比明显降低(t=8.150,P=0.000);(3)与对照组相比,SHPT组ERK1/2的表达无统计学差异(F=0.101,P=0.091),p-ERK1/2及Egr-1的表达显著低于对照组(F=9.798,P=0.001;F=27.568,P=0.000),腺瘤性增生组p-ERK1/2及Egr-1的表达显著低于弥漫性增生组(t=2.812,P=0.011;t=2.316,P=0.036);(4)SHPT组患者血PTH与甲状旁腺细胞中ERK1/2(r=-0.656,P=0.000)、p-ERK1/2(r=-0.696,P=0.000)、Egr-1(r=-0.439,P=0.001)均呈负相关。结论 SHPT患者甲状旁腺细胞中ERK1/2磷酸化的异常,可能参与了甲状旁腺细胞增生及高PTH的分泌的过程,ERK1/2信号转导通路异常在SHPT发病机制中可能发挥一定的作用。 Objective To investigate the role ofERK1/2 phosphorylation pathway in the pathogenesis of Secondary hyperparathyroidism （SHPT） resulted from chronic renal failure. Methods A total of 50 SHPT patients and 8 cadaver were selected and accepted parathyroidectomy. Serum phosphorus, calcium, alkaline phosphatase, parathyroid hormone and FGF-23 were detected. The expression of ERK1/2, p-ERK1/2, Egr-1 were detected by immunohistochemistry. Results （1）In SHPT group, serum FGF-23 was positively correlated with PTH （r=0.438, P=0.001）, serum phosphorus （r=0.421, P=0.002） and alkaline phosphates （r=0.452, P=0.001）; （2）Compared with FGF-23 before parathyroidectomy, the FGF-23 level significantly decreased in SHPT group after parathyroidectomy （t=8.150, P=0.000）; （3）Compared with control group, the expression of ERK1/2 in SHPT group had no difference（F=0.101, P=0.091）. The expression of p-ERK1/2 and Egr-1 in SHPT group decreased significantly （F=9.798, P=0.001; F=27.568, P=0.000）. Compared with diffusible hyperplasia group, the expression of p-ERK1/2 and Egr-1 in adenoma hyperplasia group decreased significantly （t=2.812, P=0.011; t= 2.316, P=0.036）; （4） In SHPT group, serum PTH was negatively correlated with the expression of ERK1/2 （r= - 0.656, P=0.000）, p-ERK1/2 （r=-0.696, P=0.000）, Egr-1 （r=-0.439, P=0.001） in parathyroid cells. Conclusion The down-regulation of ERK1/2 phosphorylafion pathway in parathyroid cells may play a role in hyperplasia of parathyroid cells and secretion of high PTH. The ERK1/2 signal pathway may be involved in the pathogenesis of SHPT.

作者孙长丽张建荣

机构地区新乡医学院武警总医院肾内科

出处《中华临床医师杂志（电子版）》 CAS 2013年第17期45-48,共4页 Chinese Journal of Clinicians(Electronic Edition)

关键词细胞外信号调节MAP激酶类肾功能衰竭慢性甲状旁腺功能亢进症继发性成纤维细胞生长因子-23 Extracellular signal-regulated MAP kinases Kidney failure, chronic Hyperparathyroidism,secondary Fibroblast growth factor-23

分类号 R692.5 [医药卫生—泌尿科学]

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