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Objective:To investigate the correlation between telomere dysfunction of human gastric mucosa and chronic atrophic gastritis (CAG).Methods:From February 12, 2019 to July 10, 2020, at Endoscopy Center, Guang′anmen Hospital, China Academy of Chinese Sciences, 30 patients received endoscopy and pathological diagnosed with CAG (CAG group) were collected, and 30 patients with chronic non-atrophic gastritis (CNAG) were collected at the same time (CNAG group). The relative telomere length was detected by real time fluorescent quantitative polymerase chain reaction. The expression of telomere repeat binding factor (TRF) 1, TRF2 and protection of telomere (POT) 1 at protein level were detected by immunohistochemical staining and semi-quantitative analysis. Spearman analysis was used to analyze the correlation between the relative telomere length of gastric mucosa and the protein expression levels of TRF1, TRF2 and POT1. Mann-Whitney U test and independent sample t test were used for statistical analysis. Results:The relative telomere length of the gastric mucosa in the CAG group was shorter than that in the CNAG group (0.67 (0.51 to 1.17) vs. 1.06(0.69 to 1.37)), and the difference was statistically significant ( U=297.00, P=0.024). The protein expression levels of TRF1, TRF2, and POT1 in the CAG group were all higher than those in the CNAG group, respectively (4.26±2.49 vs. 1.86±1.34, 10.12±2.76 vs. 8.78±2.81, 4.22±2.48 vs. 2.53±1.62), and the differences were statistically significant ( t=8.05, 3.23, 5.39; P<0.001, =0.001, and <0.001). In the CAG group, the protein expression levels of TRF2 and POT1 in gastric mucosa were negatively correlated with the relative telomere length ( r=-0.477 and -0.417, P=0.008 and 0.022). Conclusions:The telomere dysfunction is related to the pathogenesis of CAG. The change of telomere binding protein expression level is involved in the shortening of telomere and pathological process of CAG patients.
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Objective To observe the mRNA expression levels of POT1 in peripheral blood mononuclear cells of acquired aplastic anemia patients with different syndrome, and explore its relationship with acquired aplastic anemia and its TCM syndrome. Methods Peripheral blood mononuclear cells of 52 cases with acquired aplastic anemia and 20 cases as control group were collected to detect mRNA expression of POT1 by using real-time quantitative polymerase chain reaction (RT-qPCR), and its relation with TCM syndrome was analyzed. Results The expression levels of POT1 mRNA in patients with acquired aplastic anemia were lower significantly than control group (P<0.05). The expression levels of POT1 mRNA in patients with deficiency of kidney-yin were lower than patients with deficiency of kidney-yang, and it was lowest in patients with kidney deficiency of both yin and yang. There was significant correlation between the expression levels of POT1 mRNA and age (r=0.374, P=0.038). Conclusion The changes in expression levels of POT1 play a role in the pathogenesis of acquired aplastic anemia. There is correlation between mRNA expression level of POT1 in peripheral blood mononuclear cells and TCM syndrome.
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Objective To characterize the effects of TPP1 knockdown on Pot1a and Pot1b localization at telomeres and on the telomere end protection.Methods Knockdown of endogenous TPP1 in mouse embryonic fibroblasts(MEFs) with the retrovirus vector encoding shRNA targeting TPP1,IF/PNA-FISH was performed to determine the localization of Pot1a and Pot1b at telomeres,and TdT-FITC was applied to characterize the effects on the function of telomere end protection,cellular senescence was analyzed by SA-beta gal staining,and phosphorylated p53ser18 and p21 were examined by Western blotting.Results Pot1a and Pot1b were unable to localize at telomeres in about 65% of MEFs with TPP1 knockdown,while that was found in less than 5% of MEFs without TPP1 knockdown(t=10.96,P