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作 者:周冬冬[1] 姜亦瑶[2] 袁超[2] 施超[1] ZHOU Dong - dong JIANG Yi - yao YUAN Chao SHI Chao(Department of Cardiovascular Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233000, Anhui, Chin)
机构地区:[1]蚌埠医学院第一附属医院心脏外科,安徽蚌埠233000 [2]南开大学生命科学院,天津300071
出 处:《广东医学》2017年第14期2147-2150,共4页Guangdong Medical Journal
基 金:天津市企业博士后创新项目择优资助计划(编号:2015-001);天津市滨海新区卫生局基金项目(编号:2014BHKY010);安徽省高校优秀青年人才支持计划重点项目(编号:gxyq ZD2016167);安徽省学术和技术带头人及后备人选学术科研活动资助项目(编号:2015H070)
摘 要:目的探讨胶原纤维在风湿性心脏瓣膜病心房颤动(房颤)患者中的异常表达以及与房颤发生的相关性。方法 33例风湿性心脏病接受换瓣患者分为窦性心律组与房颤组。于手术中获取右心耳组织。采用转录组学进行差异表达基因的功能分析;RT-PCR检测Ⅰ~Ⅳ型胶原纤维RNA在右心房组织中的表达;免疫组化观察心肌组织各型胶原纤维的表达与分布。结果与窦性心律组相比,房颤组左心房内径明显扩大。转录组学分析显示COL1A2、COL2A1、COL3A1以及COL4A3与COL5A2、COL6A3、COL11A1等胶原纤维存在相互关联之外,与多种细胞因子也存在相互作用;RT-PCR结果示COL1A2、COL2A1、COL3A1和COL4A3均在房颤患者右心房组织中上调表达,其中COL3A1、COL4A3上调表达显著(P<0.05)。免疫组化结果显示Ⅰ型胶原纤维分布在血管内皮细胞及血管基底膜;Ⅱ型胶原纤维分布在心肌细胞肌节;Ⅲ型胶原纤维分布在间皮细胞及心肌细胞浆;Ⅳ型胶原纤维分布在心肌细胞外膜。结论心房组织中COL3A1与COL4A3表达异常,与多种细胞因子相互作用引发房颤的发生和发展。Objective To investigate the expression and distribution of collagens in patients with rheumatic valvular heart disease, Methods Thirty -three patients with rheumatic heart disease, who accepted valve surgery, were divided into sinus rhythm group and atrial fibrillation group. Right atrial appendage tissues were obtained during operation. Functional analysis of differentially expressed genes was performed by transcriptomics. By RT- PCR, we detected the expression of type Ⅰ - Ⅳ collagen mRNA in myocardial tissue. The distribution of collagen in myocardium was observed by immunohistoehemistry. Results Compared to sinus rhythm group, the left atrial diameter was significantly expanded. Transcriptomies showed that COL1A2, COL2A1, COL3A1 and COL4A3 interacted with COL5A2, COL6A3, COLIlA1, and various cytokines. The results of RT -PCR showed that COL1A2, COL2A1, COL3A1, and COL4A3 were up -regulated in atrial fibrillation group. Furthermore, COL3A1 and COL4A3 were significantly up -regulated (P 〈 0. 05 ). Posi- tive type Ⅰ collagen staining was predominantly on the basement membrane beneath the vascular endothelial and partially in the intereellular space. Myocardial collagen fiber was stained with type Ⅱ collagen. Type Ⅲ collagen was positive on capillary endothelial and vascular basement membrane. Type Ⅳ collagen was detected around myoeyte, lipocyte, vaseular smooth muscle and the vascular endothelial basement membrane. Conclusion Abnormal expression of COL3A1 and COIAA3 is revealed in atrial myocytes, interacting with various cytokines. It is related with the occurrence and develop- ment of atrial fibrillation.
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