miR-494 promotes islet β cell proliferation, inhibits apoptosis and increases insulin secretion by activating Wnt/β-catenin signaling pathway
Objective To investigate the relation between the miR-494 expression with pancreatic islets β cell function and gestational diabetes mellitus. Methods Twenty patients with gestational diabetes mellitus and healthy subjects were enrolled. The content of miR-494 in peripheral blood was measured by reverse transcription PCR. INS-1 cells were cultured and treated with low glucose (3.3 mmol/L) and high glucose (16.7 mmol/L), respectively. The insulin concentration was tested by ELISA to evaluate the insulin secretion of islet cells stimulated by high glucose. Cells were collected, after treated with miR-494 mimics control, miR-494 mimics, miR-494 inhibitor control and miR-494 inhibitor for 24 hours, 48 hours and 72 hours, respectively. The activity of INS-1 cells was detected by MTT assay; Apoptosis was detected by flow cytometry. Reverse transcription PCR and Western blot analysis were used to detect the mRNA and protein expression of Wnt3a, β-catenin, cyclin D1 and c-Myc, respectively. Results Compared with the normal control, fasting insulin, fasting blood glucose, 1 hour-blood glucose and 2 hour-blood glucose in patients with gestational diabetes mellitus increased significantly. The content of miR-494 in peripheral blood decreased. The insulin concentration in the supernatant of INS-1 cells overexpressing miR-494 increased. When high glucose was given, the overexpression of miR-494 further promoted insulin secretion. Overexpression of miR-494 significantly promoted INS-1 cell activity and inhibited INS-1 cell apoptosis. miR-494 significantly promoted the protein expression of Wnt3a, β-catenin, cyclin D1 and c-Myc. miR-494 inhibitor treatment showed the opposite results. Conclusion miR-494 promotes islet β cell proliferation, inhibits apoptosis and increases insulin secretion by activating Wnt/β-catenin signaling pathway.
Medienart: |
Artikel |
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Erscheinungsjahr: |
2021 |
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Erschienen: |
2021 |
Enthalten in: |
Zur Gesamtaufnahme - volume:37 |
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Enthalten in: |
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology - 37(2021), 11 vom: 23. Nov., Seite 1003-1009 |
Sprache: |
Chinesisch |
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Beteiligte Personen: |
Song, Shanshan [VerfasserIn] |
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Themen: |
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Anmerkungen: |
Date Completed 24.11.2021 Date Revised 31.05.2022 published: Print Citation Status MEDLINE |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM333470524 |
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520 | |a Objective To investigate the relation between the miR-494 expression with pancreatic islets β cell function and gestational diabetes mellitus. Methods Twenty patients with gestational diabetes mellitus and healthy subjects were enrolled. The content of miR-494 in peripheral blood was measured by reverse transcription PCR. INS-1 cells were cultured and treated with low glucose (3.3 mmol/L) and high glucose (16.7 mmol/L), respectively. The insulin concentration was tested by ELISA to evaluate the insulin secretion of islet cells stimulated by high glucose. Cells were collected, after treated with miR-494 mimics control, miR-494 mimics, miR-494 inhibitor control and miR-494 inhibitor for 24 hours, 48 hours and 72 hours, respectively. The activity of INS-1 cells was detected by MTT assay; Apoptosis was detected by flow cytometry. Reverse transcription PCR and Western blot analysis were used to detect the mRNA and protein expression of Wnt3a, β-catenin, cyclin D1 and c-Myc, respectively. Results Compared with the normal control, fasting insulin, fasting blood glucose, 1 hour-blood glucose and 2 hour-blood glucose in patients with gestational diabetes mellitus increased significantly. The content of miR-494 in peripheral blood decreased. The insulin concentration in the supernatant of INS-1 cells overexpressing miR-494 increased. When high glucose was given, the overexpression of miR-494 further promoted insulin secretion. Overexpression of miR-494 significantly promoted INS-1 cell activity and inhibited INS-1 cell apoptosis. miR-494 significantly promoted the protein expression of Wnt3a, β-catenin, cyclin D1 and c-Myc. miR-494 inhibitor treatment showed the opposite results. Conclusion miR-494 promotes islet β cell proliferation, inhibits apoptosis and increases insulin secretion by activating Wnt/β-catenin signaling pathway | ||
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700 | 1 | |a He, Jing |e verfasserin |4 aut | |
700 | 1 | |a Tang, Junfeng |e verfasserin |4 aut | |
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