[Effect of palmitate on proliferation and apoptosis of INS-1 pancreatic beta-cell].
Wei Cui, Ting Huang, Jun‐Li Liu, Bingyin Shi
Abstract
Wei Cui, Ting Huang, Jun‐Li Liu, Bingyin Shi
Abstract
AIM: To investigate the effect of saturated fatty acid palmitate (PA) on cell viability of MIN6 beta-cell and the possible cell cycle pathways affected by PA. METHODS: MIN6 cells were synchronized at G(0); phase by serum deprivation for 36 h, and further MIN6 cells were exposed to different concentrations of PA(0.25-1.0 mmol/L, 45 min-24 h)compared with control cell treated with BSA.Cell viability was assessed by MTT colorimetric assay. The cell cycle was measured by FACS analysis, and cell cycle proteins were further detected using Western blot. RESULTS: (1)PA significantly affected the cell viability of MIN6 cells. (2)The G(0);/G(1); cell cycle arrest (n=6, P<0.05) also induced by PA, whereas MIN6 cells in S and G(2);/M phase were decreased. (3) For cell cycle proteins, PA treatment caused significant reductions in cyclin D1 and CDK4 levels, which was consistent to the cell cycle delay. CONCLUSION: The findings thus suggest that increased PA directly affects pancreatic beta-cell proliferation, possibly by reducing the levels of cyclin D1/CDK4 in the cells, which results in arresting in progression through the G(1); phase to the S phase of the cell cycle.
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AIM: To investigate the effect of saturated fatty acid palmitate (PA) on cell viability of MIN6 beta-cell and the possible cell cycle pathways affected by PA. METHODS: MIN6 cells were synchronized at G(0); phase by serum deprivation for 36 h, and further MIN6 cells were exposed to different concentrations of PA(0.25-1.0 mmol/L, 45 min-24 h)compared with control cell treated with BSA.Cell viability was assessed by MTT colorimetric assay. The cell cycle was measured by FACS analysis, and cell cycle proteins were further detected using Western blot. RESULTS: (1)PA significantly affected the cell viability of MIN6 cells. (2)The G(0);/G(1); cell cycle arrest (n=6, P<0.05) also induced by PA, whereas MIN6 cells in S and G(2);/M phase were decreased. (3) For cell cycle proteins, PA treatment caused significant reductions in cyclin D1 and CDK4 levels, which was consistent to the cell cycle delay. CONCLUSION: The findings thus suggest that increased PA directly affects pancreatic beta-cell proliferation, possibly by reducing the levels of cyclin D1/CDK4 in the cells, which results in arresting in progression through the G(1); phase to the S phase of the cell cycle.
Key concepts: Cell cycle, Viability assay, Cell growth, Apoptosis, Cyclin D1, Cell, Cell cycle checkpoint, Chemistry