摘要
利用Tbx18谱系示踪小鼠模型及Tbx18条件性基因敲除小鼠模型,探讨转录因子Tbx18对小鼠心血管结构发育的影响.实验建立Tbx18-Cre/Rosa26R-EYFP和Tbx18-Cre/Rosa26R-Lac Z两种基因敲入谱系示踪小鼠模型和Tbx18:Cre/Cre基因敲除小鼠模型;通过免疫荧光及X-gal染色技术,示踪Tbx18在心血管系统结构形成中的命运;通过小鼠心脏整体血管免疫组化及切片HE染色、免疫组化、免疫荧光技术,比较Tbx18:Cre/Cre基因敲除小鼠与野生型对照小鼠心脏室壁结构及冠状血管结构发育情况.示踪结果提示,Tbx18参与小鼠冠状血管及室间隔结构的形成,并与冠脉平滑肌细胞共表达;对Tbx18基因敲除小鼠及野生型小鼠的心脏结构比较提示,Tbx18基因敲除后,仍能形成形态正常的冠状血管系统,小鼠心室肌及室间隔厚度较野生型无明显差异.结果表明,Tbx18参与小鼠心脏血管平滑肌及室间隔结构的形成,但其在小鼠心脏腔室结构及冠状血管结构形成过程中不是必需的.
Using Tbx18 lineage tracer mouse model and Tbx18 conditional knockout mouse model to explore the functions of Tbx 18 in the development of the structures of coronary vascular and ventricular wall. Two types of lineage tracer mouse models are established: Tbx18-Cre/Rosa26R-EYFP and Tbx18-Cre/Rosa26R-LacZ, and Tbxl8:Cre/Cre gene knockout mouse model are used in the experiment. We trace the fate of Tbxl8 in the formation of the vascular and myocardial structure in the cardiovascular system by immunofluorescence and X-gal staining techniques. And we compare the structure of coronary vascular and ventricular wall in Tbx18:Cre/Cre gene knockout mouse with wild-type mouse by whole-mount PECAM immunohistochemistry, HE staining, immunohistochemistry and immunofluorescence techniques. The trace of Tbx18 shows that Tbx18 contributes to the structure of the mouse coronary vessels and interventricular septum, and Tbxl8 expression co-locolize with smooth muscle cells. The comparison between Tbx18:Cre/Cre gene knockout mouse and wild-type mouse shows that the knockout mouse can form normal coronary vascular system, and there is no difference between the thickness of the ventricular wall and the interventricular septurn. The gene Tbx18 contributes to the heart vascular smooth muscle and interventricular septum, but it is not necessary in the formation of coronary vascular structure and the heart chamber structure.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2015年第4期348-355,共8页
Progress In Biochemistry and Biophysics
基金
国家自然科学基金(81270211
81100088)
高等学校博士学科点专项基金(20125503110009)
重庆教委科学技术研究(KJ130324)资助项目~~