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首页> 外文期刊>Journal of Cellular Physiology >Effects of FGF‐23‐mediated ERK/MAPK signaling pathway on parathyroid hormone secretion of parathyroid cells in rats with secondary hyperparathyroidism
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Effects of FGF‐23‐mediated ERK/MAPK signaling pathway on parathyroid hormone secretion of parathyroid cells in rats with secondary hyperparathyroidism

机译：FGF的影响还是23介导ERK / MAPK信号甲状旁腺激素的分泌途径甲状旁腺细胞有二次的老鼠甲状旁腺功能亢进

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摘要

This study is supposed to investigate the effect of FGF‐23 on parathyroid hormone (PTH) secretion through ERK/MAPK signaling pathway in secondary hyperparathyroidism (SHPT) rat model. Thirty rats were equally served as the normal and SHPT groups. After transfection, parathyroid cells was assigned into blank, NC, pcDNA3.1‐FGF‐23, siRNA‐FGF‐23, U0126, and siRNA‐FGF‐23?+?U0126 groups. The serum levels of Calcium (Ca), Phosphorus (P), alkaline phosphatase (ALP), and PTH were detected. HE and immunohistochemical (IHC) staining were used for the histopathological changes and the FGF‐23, EKR1/2, and pEKR1/2 expressions. qRT‐PCR and Western blotting were performed to determine the mRNA and protein expression of FGF‐23, PTH, MAPK, EKR1/2, and Klotho. The proliferation, apoptosis, and cell cycle were all measured for parathyroid cells by CCK‐8 assay, TUNEL staining and Flow cytometry. Compared with the normal group, the SHPT group showed increased serum levels PTH, P, ALP, and FGF‐23 and mRNA and protein expressions of FGF‐23 and PTH, whereas declined Ca and p‐ERK1/2 expression, mRNA and protein expression of Klotho, cell apoptosis rate was reduced. Furthermore, compared to the blank and NC groups, the pcDNA3.1‐FGF‐23 and U0126 groups had a decreased mRNA expression of Klotho, protein expression of EKR1/2 and Klotho, and cell apoptosis rate was down‐regulated, whereas the RNA and protein expressions of FGF‐23 and PTH were up‐regulated, and cell proliferation was elevated. The opposite results were observed in the siRNA‐FGF‐23 group. Our study demonstrated that FGF‐23 could inhibit signaling transduction of ERK/MAPK pathway and accelerate the secretion of PTH in rats with SHPT.
机译：这项研究应该调查效果FGF 23应承担的甲状旁腺素分泌通过ERK / MAPK信号通路在次要的甲状旁腺功能亢进(船期)大鼠模型。同样作为正常和船期吗组。分为空白,数控,pcDNA3.1必经FGF高23siRNA‐FGF‐23、U0126 and siRNA‐FGF‐23 + ?组。磷(P)、碱性磷酸酶(ALP)、和甲状旁腺素被发现。(包含IHC)用于染色EKR1/2组织病理学变化和FGF检测——23日,和pEKR1/2表达式。信使rna印迹进行确定甲状旁腺素蛋白表达的FGF还是23日,MAPK, EKR1/2,和克罗索。细胞周期都是测量甲状旁腺细胞,CCK 8化验,TUNEL染色法和流动血细胞计数。船期组显示血清甲状旁腺素增加,P,高山,FGF 23和信使rna和蛋白质表达FGF 23和甲状旁腺素,而拒绝Ca和p量ERK1/2表达式,mRNA和蛋白表达克罗索,细胞凋亡率降低。此外,与空白和NC组相比,pcDNA3.1检测FGF 23和U0126组就这种基因mRNA的表达减少,蛋白质表达EKR1/2克罗索,细胞细胞凋亡率下降量调节,而RNA和蛋白质FGF 23和甲状旁腺素的表达上升量调节,细胞增殖是吗升高。核检测FGF 23组。FGF必经23可以抑制信号转导ERK / MAPK通路和加速分泌甲状旁腺素的老鼠和船期。

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