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作 者:彭媛媛 刘海波 张瑞霖 PENG Yuanyuan;LIU Haibo;ZHANG Ruilin(Experimental Research Center,Qingpu Branch of Zhongshan Hospital,Fudan University,Shanghai 201700,China;Department of Cardiology,Qingpu Branch of Zhongshan Hospital,Fudan University,Shanghai 201700,China;School of Basic Medical Sciences,Wuhan University,Wuhan Hubei 430071,China)
机构地区:[1]复旦大学附属中山医院青浦分院实验研究中心,上海201700 [2]复旦大学附属中山医院青浦分院心血管内科,上海201700 [3]武汉大学基础医学院,湖北武汉430071
出 处:《复旦学报(自然科学版)》2024年第4期502-508,518,共8页Journal of Fudan University:Natural Science
基 金:复旦大学附属中山医院青浦分院院级面上基金(QYM2022-04)。
摘 要:心脏发育异常会导致先天性心脏疾病。转化生长因子(TGF-β)信号通路在心脏发育中发挥重要作用。使用转基因斑马鱼并结合免疫荧光和原位杂交技术,研究抑制TGF-β信号通路不同靶点对心肌细胞增殖、细胞大小和肌小梁发育的作用。结果显示:抑制TGFBR1不影响心肌细胞增殖,抑制TGFBR1和TGFBR2能够促进心肌细胞的增殖和肌小梁的生成,抑制Smad3对细胞大小和肌小梁发育无影响。研究结果将为TGF-β作为心脏发育缺陷的潜在干预靶点奠定理论基础。Defects in heart development can lead to congenital heart diseases.The transforming growth factor-β(TGF-β)signaling pathway plays a crucial role in heart development.Several zebrafish reporter lines were utilized,along with immunofluorescence and in situ hybridization technology,to investigate the impact of suppressing different target sites of the TGF-βsignaling pathway on cardiomyocyte(CM)proliferation,cell size and trabecular development.The results showed that blocking TGFBR1 had no effect on CM proliferation.However,suppressing TGFBR1 and TGFBR2 promoted CM proliferation and trabecular development.On the other hand,impairing Smad3 resulted in cell cycle arrest and did not affect cell size and trabecular development.These findings provide a theoretical basis for considering TGF-βas a potential intervention target for heart development defects.
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