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Effect of urotensin II on the proliferation of cardiac myofibroblasts and its intracellular signaling mechanism in new-born SD rats

Jing Yang

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Abstract

AIM: To explore the effects of urotensinⅡ (UⅡ) on the proliferation of the cardiac fibroblasts (CFs) and its intracellular signaling mechanism in new born SD rats. METHODS: CFs from new born SD rats were isolated and cultured. Cell number was observed by MTT assay. Cell cycle was evaluated by flow cytometry (FCM). RESULTS: With the treatment of 10 -10 , 10 -9 , 10 -8 mol/L UⅡ, the cell number, S phase cell percentage and the proliferation index (PI), were significantly higher than those of control group. G 0/G 1 phase cell percentage was significantly lower than that in control group ( P 0.01), but the indices in the 10 -7 mol/L UⅡ group were not significantly different from those of control( P 0.05). The OD values in 10 -6 mol/L Che+10 -8 mol/L UⅡ, 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups increased significantly compared with those in control group ( P 0.05), but decreased compared with those in 10 -8 mol/L UⅡ group ( P 0.05). Compared with those in control group, S phase cell percentage and PI increased, but G 0/G 1 phase cell percentage decreased in 10 -6 mol/L Che+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups ( P 0.05). No difference was found between 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and control groups ( P 0.05). Compared with those in 10 -8 mol/L UⅡ group, S phase cell percentage and the PI declined significantly ( P 0.01), while G 0/G 1 phase cell percentage rose remarkably in 10 -6 mol/L Che+10 -8 mol/L UⅡ, 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups ( P 0.01). CONCLUSION: UⅡ can stimulate the proliferation of CFs in new born SD rats and the UⅡ induced proliferation of CFs is probably mediated by PKC/MAPK/CaN.

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AIM: To explore the effects of urotensinⅡ (UⅡ) on the proliferation of the cardiac fibroblasts (CFs) and its intracellular signaling mechanism in new born SD rats. METHODS: CFs from new born SD rats were isolated and cultured. Cell number was observed by MTT assay. Cell cycle was evaluated by flow cytometry (FCM). RESULTS: With the treatment of 10 -10 , 10 -9 , 10 -8 mol/L UⅡ, the cell number, S phase cell percentage and the proliferation index (PI), were significantly higher than those of control group. G 0/G 1 phase cell percentage was significantly lower than that in control group ( P 0.01), but the indices in the 10 -7 mol/L UⅡ group were not significantly different from those of control( P 0.05). The OD values in 10 -6 mol/L Che+10 -8 mol/L UⅡ, 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups increased significantly compared with those in control group ( P 0.05), but decreased compared with those in 10 -8 mol/L UⅡ group ( P 0.05). Compared with those in control group, S phase cell percentage and PI increased, but G 0/G 1 phase cell percentage decreased in 10 -6 mol/L Che+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups ( P 0.05). No difference was found between 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and control groups ( P 0.05). Compared with those in 10 -8 mol/L UⅡ group, S phase cell percentage and the PI declined significantly ( P 0.01), while G 0/G 1 phase cell percentage rose remarkably in 10 -6 mol/L Che+10 -8 mol/L UⅡ, 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups ( P 0.01). CONCLUSION: UⅡ can stimulate the proliferation of CFs in new born SD rats and the UⅡ induced proliferation of CFs is probably mediated by PKC/MAPK/CaN.

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Available abstract

AIM: To explore the effects of urotensinⅡ (UⅡ) on the proliferation of the cardiac fibroblasts (CFs) and its intracellular signaling mechanism in new born SD rats. METHODS: CFs from new born SD rats were isolated and cultured. Cell number was observed by MTT assay. Cell cycle was evaluated by flow cytometry (FCM). RESULTS: With the treatment of 10 -10 , 10 -9 , 10 -8 mol/L UⅡ, the cell number, S phase cell percentage and the proliferation index (PI), were significantly higher than those of control group. G 0/G 1 phase cell percentage was significantly lower than that in control group ( P 0.01), but the indices in the 10 -7 mol/L UⅡ group were not significantly different from those of control( P 0.05). The OD values in 10 -6 mol/L Che+10 -8 mol/L UⅡ, 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups increased significantly compared with those in control group ( P 0.05), but decreased compared with those in 10 -8 mol/L UⅡ group ( P 0.05). Compared with those in control group, S phase cell percentage and PI increased, but G 0/G 1 phase cell percentage decreased in 10 -6 mol/L Che+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups ( P 0.05). No difference was found between 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and control groups ( P 0.05). Compared with those in 10 -8 mol/L UⅡ group, S phase cell percentage and the PI declined significantly ( P 0.01), while G 0/G 1 phase cell percentage rose remarkably in 10 -6 mol/L Che+10 -8 mol/L UⅡ, 10 -5 mol/L PD98059+10 -8 mol/L UⅡ and 5 mg/L CsA+10 -8 mol/L UⅡ groups ( P 0.01). CONCLUSION: UⅡ can stimulate the proliferation of CFs in new born SD rats and the UⅡ induced proliferation of CFs is probably mediated by PKC/MAPK/CaN.

Key concepts: Urotensin-II, Intracellular, Mole, Cell growth, Cell counting, Pi, Proliferation index, Cell

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Effect of urotensin II on the proliferation of cardiac myofibroblasts and its intracellular signaling mechanism in new-born SD rats — Research Paper | ScholarLens