Establishment and genotype identification of vascular endothelial cell specific Traf2 gene knockout mouse
- VernacularTitle:血管内皮细胞特异性Traf2基因敲除小鼠的制备及鉴定
- Author:
Zhuo CHEN
1
;
Jia-jie KUAI
1
;
Feng-ling WANG
1
;
Ju HE
1
;
Wei WEI
1
Author Information
- Publication Type:Journal Article
- Keywords: vascular endothelial cell; Traf2; specific gene knockout; thoracic aortic vessel; Cre-loxP; vascular dysfunction
- From: Chinese Pharmacological Bulletin 2025;41(8):1592-1598
- CountryChina
- Language:Chinese
- Abstract: Aim To construct a model of vascular endothelial cell(EC)-specific gene knockout mice of tumor necrosis factor receptor-associated factor 2(Traf2)by using Cre-loxP technolo-gy,thus to provide basis for the research of vascular dysfunction-related diseases related to the regulation of vascular EC activity through TRAF2.Methods The Cre-loxP system was used to construct a mouse model with EC-specific knockout of Traf2 gene(Traf2flox/flox Tek-iCre+).The mouse genotype was identi-fied through PCR and gel electrophoresis.Primary vascular ECs were isolated from the mice using flow cytometry.The knockout efficiency of Traf2 in vascular ECs was validated by Western blot and immunofluorescence.The pathological changes in blood ves-sels and major organs of the mice were examined using hematox-ylin-eosin(HE)staining.The tube-forming ability of primary vascular EC was assessed using Matrigel tube formation.Results The knockout mice met the required genetic criteria.Flow cy-tometry results demonstrated the successful isolation of primary vascular EC,and TRAF2 expression in vascular EC of knockout mice was significantly reduced(P＜0.01).Histological results showed that TRAF2 expression in the vessel of knockout mice decreased,and the morphology had no significant changes in their blood vessels and major organs.The Matrigel tube forma-tion demonstrated that the tube-forming ability of primary vascu-lar EC from knockout mice was reduced.Conclusion Traf2 specific knockout mouse model in vascular ECs is successfully constructed,providing a reliable animal model for research into the regulatory mechanisms of TRAF2 on vascular ECs in vascular dysfunction related diseases.
