血小板源性生长因子D抗体制备及其在人心脏纤维化组织中的表达

目的制备血小板源性生长因子D,探讨血小板源性生长因子D在人心肌纤维化组织中的表达及其对I型胶原表达的影响,从而初步明确血小板源性生长因子D与人心肌纤维化的关系。方法通过原核表达系统表达并纯化血小板源性生长因子D融合蛋白,免疫新西兰大白兔,获取血小板源性生长因子D抗体。应用免疫组化的方法观察血小板源性生长因子D在人心脏室壁瘤纤维化组织及正常心肌组织的表达情况,利用细胞转染及细胞免疫组化的方法观察转染血小板源性生长因子D后成纤维细胞系NIH3T3细胞中I型胶原的表达水平改变。结果血小板源性生长因子D在人心脏室壁瘤纤维化组织中的表达与周围正常心肌组织相比,显著升高。转染血小板源性生长因子D后,NIH3T3细胞中的I型胶原表达显著增加。结论血小板源性生长因子D可以通过增加I型胶原表达从而促进人心肌纤维化。

PDGF-D promoted myocardial fibrosis byupregulation of collagen I

Objective To investigate the role of PDGF-D in the myocardial fibrosis by detect its effect on collagen I expression. Methods Polyclonal antibody against PDGF-D was raised in rabbits by using purified recombinant PDGF-D-GST fusion protein, the immunobistoehemistry was used to determine whether PDGF-D is overexpressed in left ventricular aneurysm and the expression of collagen I in the NIH3T3 cell transfected with PDGF-D or empty vector, respectively. Results Our study demonstrated that PDGF-D was significantly upregnlated in the left ventricular aneu- rysm and PDGF-D stimulated the production of collagen I in NIH3T3 cells. Conclusions The PDGF-D may promote myocardial fibrosis by upregula- tion of collagen I.