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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Baker Medical Research Institute, Alfred Hospital, Prahran, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1996 Jun-Jul;23(6-7):573-5. doi: 10.1111/j.1440-1681.1996.tb02783.x.

This study examined the role of protein kinase C (PKC) on the action of transforming growth factor-beta 1 (TGF-beta 1) to regulate the proliferation of vascular smooth muscle cells (VSMC) isolated from the aorta of the spontaneously hypertensive rat (SHR). 2. Down-regulation of PKC by prolonged exposure to phorbol 12-myristate 13-acetate (PMA) completely inhibited the ability of TGF-beta 1 to potentiate epidermal growth factor-stimulated proliferation of VSMC. 3. In contrast, the inhibitory effect of TGF-beta 1 on serum-stimulated proliferation of VSMC was not altered by PMA action. 4. These results suggest that PKC-dependent signalling pathways involved in the regulation of growth by TGF-beta 1 may be important in any proliferative component of vascular hypertrophy that develops in the SHR.

本研究检测了蛋白激酶C（PKC）在转化生长因子-β1（TGF-β1）调节自发性高血压大鼠（SHR）主动脉分离的血管平滑肌细胞（VSMC）增殖作用中的角色。2. 长期暴露于佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）导致的PKC下调完全抑制了TGF-β1增强表皮生长因子刺激的VSMC增殖的能力。3. 相反，PMA作用并未改变TGF-β1对血清刺激的VSMC增殖的抑制作用。4. 这些结果表明，参与TGF-β1生长调节的PKC依赖性信号通路可能在SHR发生的血管肥厚的任何增殖成分中都很重要。

Baker Medical Research Institute, Alfred Hospital, Prahran, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1996 Jun-Jul;23(6-7):573-5. doi: 10.1111/j.1440-1681.1996.tb02783.x.

This study examined the role of protein kinase C (PKC) on the action of transforming growth factor-beta 1 (TGF-beta 1) to regulate the proliferation of vascular smooth muscle cells (VSMC) isolated from the aorta of the spontaneously hypertensive rat (SHR). 2. Down-regulation of PKC by prolonged exposure to phorbol 12-myristate 13-acetate (PMA) completely inhibited the ability of TGF-beta 1 to potentiate epidermal growth factor-stimulated proliferation of VSMC. 3. In contrast, the inhibitory effect of TGF-beta 1 on serum-stimulated proliferation of VSMC was not altered by PMA action. 4. These results suggest that PKC-dependent signalling pathways involved in the regulation of growth by TGF-beta 1 may be important in any proliferative component of vascular hypertrophy that develops in the SHR.

本研究检测了蛋白激酶C（PKC）在转化生长因子-β1（TGF-β1）调节自发性高血压大鼠（SHR）主动脉分离的血管平滑肌细胞（VSMC）增殖作用中的角色。2. 长期暴露于佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）导致的PKC下调完全抑制了TGF-β1增强表皮生长因子刺激的VSMC增殖的能力。3. 相反，PMA作用并未改变TGF-β1对血清刺激的VSMC增殖的抑制作用。4. 这些结果表明，参与TGF-β1生长调节的PKC依赖性信号通路可能在SHR发生的血管肥厚的任何增殖成分中都很重要。