受外源性因素或内源性病理学影响的 c-kit 免疫阳性胰腺 beta 细胞的动态变化

IF 0.1 Q4 MEDICINE, GENERAL & INTERNAL
T. V. Ivanenko, Y. Kolesnyk, A. Abramov
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引用次数: 0

摘要

涉及c-kit的β-内分泌细胞分化机制可能与信号通路和调控机制等多个过程有关。c-kit信号通路的激活、细胞增殖和存活的增加或减少、分化基因程序和干细胞的调节等因素在控制自我保存和调节细胞数量和类型方面具有重要作用,而细胞分化受到间歇性缺氧缺血、高血压和糖尿病的影响。这项工作的目的是确定在外源性影响(间歇性缺氧缺血)和内源性病理影响(动脉高血压和糖尿病)下,β细胞中 c-kit 增殖因子的动态变化。研究使用 15 只白色 Wistar 大鼠和 5 只自发性高血压大鼠(SHR),将其分为 4 组,每组 5 只。第 1 组--对照组(完好无损)大鼠,第 2 组--实验性糖尿病动物,第 3 组--遗传性动脉高血压大鼠(SHR),第 4 组--暴露于间歇性低氧缺氧影响下的动物。实验结束后,动物被安乐死,器官被收获和处理,5 µm 厚的连续胰腺组织切片被去石蜡和取回。使用抗体免疫荧光法检测胰岛素和 c-kit+ β祖细胞。使用 AxioImager-M2 荧光显微镜对免疫荧光反应进行研究。糖尿病大鼠的β细胞定量指标几乎下降了 6 倍。该组动物体内的胰岛素浓度比正常动物有所增加,增殖活性标志物有所下降,但 c-kit 免疫阳性 beta 细胞的百分比没有变化。与完好无损组和实验性糖尿病组的动物相比,SHR在患遗传性动脉高血压的过程中,每1平方厘米β细胞的数量减少了8倍,β细胞中的胰岛素增加了。在暴露于低氧缺血的实验组动物中,每个测量单位的β细胞数量明显增加,β细胞中的胰岛素浓度与完整动物相比有所增加,但低于糖尿病和高血压大鼠。增殖活性标志物 c-kit 与完整动物和糖尿病动物相比均有所下降。至于c-kit免疫阳性β细胞的数量,与完整动物和糖尿病动物相比没有统计学差异,但高于SHR。Wistar大鼠患实验性糖尿病和SHR患遗传性高血压会导致胰腺中β细胞的特异性密度显著降低,而多天缺氧训练则会刺激胰岛素合成内分泌细胞的密度增加。在糖尿病、高血压和适应缺氧等实验条件下,胰岛素会增加,β细胞中的 c-kit 表达会减少。然而,只有在出现遗传性动脉高血压时,胰岛中 c-kit 免疫阳性 beta 细胞的数量才会明显减少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dynamics of c-kit immunopositive pancreatic beta cells influenced by exogenous factors or endogenous pathology
Mechanisms of beta-endocrinocyte differentiation involving c-kit may be associated with a number of processes, including signaling pathways and regulatory mechanisms. Such factors as activation of the c-kit signaling pathway, an increase or decrease in cell proliferation and survival, regulation of differentiation gene programs and stem cells are important in controlling self-preservation and regulating the cellular number and types, that are differentiated being impacted by intermittent hypoxic hypoxia, hypertension and diabetes mellitus. The aim of the work is to determine the dynamics of c-kit proliferative factor in beta cells under an exogenous influence (intermittent hypoxic hypoxia) and endogenous pathology (arterial hypertension and diabetes mellitus). Materials and methods. The study was conducted using 15 white Wistar rats and 5 spontaneously hypertensive rats (SHR), which were divided into 4 groups of 5 animals each. Group 1 – control (intact) rats, group 2 – animals with experimental diabetes mellitus, group 3 – rats with hereditary arterial hypertension (SHR), group 4 – animals exposed to the effect of intermittent hypoxic hypoxia. At the end of the experiment, the animals were euthanized, organs were harvested and processed, serial histological pancreatic sections 5 µm thick were deparaffinized and retrieved. Insulin and c-kit+ beta progenitor cells were detected by the immunofluorescence method using antibodies. Immunofluorescent reactions were studied using an AxioImager-M2 fluorescence microscope. Results. The quantitative indicator of beta cells was almost 6 times decreased in rats with diabetes mellitus. Concentrations of insulin in animals of this group were increased compared to intact animals and the marker of proliferative activity was decreased without changes in the percentage of c-kit-immunopositive beta cells. The course of hereditary arterial hypertension in SHR was accompanied by an 8-fold decrease in the number of beta cells per 1 cm2, an increase in insulin in beta cells as compared to the animals of both intact and experimental diabetes groups. Regarding the c-kit expression in beta cells, it was significantly reduced only in the group of intact animals and the number of c-kit-immunopositive beta cells was almost 2.8 times decreased. In the experimental group of animals exposed to hypoxic hypoxia, the number of beta cells per measurement unit was significantly increased, the concentration of insulin in beta cells was increased as compared to the intact animals, but lower than that in rats with diabetes and hypertension. The marker of proliferative activity c-kit was decreased compared to both intact and diabetic animals. As for the number of c-kit-immunopositive beta cells, it did not differ statistically from that in intact and diabetic animals, but was higher than that in SHR. Conclusions. The development of experimental diabetes in Wistar rats and hereditary hypertension in SHR results in a significant decrease in the specific density of beta cells in the pancreas in contrast to the effect of multiple-day hypoxic training, which stimulates an increase in the density of insulin-synthesizing endocrinocytes. Experimental conditions, diabetes mellitus, hypertension and adaptation to hypoxia, are accompanied by an increase in insulin and a decrease in the c-kit expression in beta cells. However, the number of c-kit-immunopositive beta cells in the pancreatic islets significantly decreases only with the development of hereditary arterial hypertension.
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来源期刊
Zaporozhye Medical Journal
Zaporozhye Medical Journal MEDICINE, GENERAL & INTERNAL-
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