Role of immunoproteasome subunit β2i in DOCA/salt-induced vascular inflammation in mice
10.3969/j.issn.1000-4718.2017.05.027
- VernacularTitle:免疫蛋白酶体β2i亚基在DOCA/盐敏感小鼠血管炎症反应中的作用
- Author:
Nannan LI
;
Chunyu ZHOU
;
Lixin LIU
;
Cuiliu HOU
;
Hongxia WANG
;
Aili XU
;
Huihua LI
- Keywords:
Immuneproteasome subunit β2i;
Vascular inflammation;
Deoxycorticosterone acetate/salt
- From:
Chinese Journal of Pathophysiology
2017;33(5):930-934
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the role of immunoproteasome subunit β2i in deoxycorticosterone acetate (DOCA)/salt-induced vascular inflammation in mice.METHODS:Wild-type and β2i knockout male mice were used.The right kidney was removed and DOCA pellet was subcutaneously implanted in the mice.The mice were then received 1% NaCl as drinking water for 3 weeks.The total RNA and protein were isolated from thoracic aorta 3 weeks later.The aortic tissues were fixed in formalin, embedded in paraffin and sectioned.Western blot, real-time PCR and immunohistochemistry were performed to detect the expression of β2i, macrophage marker Mac-2, NF-κB, and proinflammatory cytokines IL-1β, IL-6 and TNF-α in thoracic aorta.RESULTS:Compared with sham group, DOCA/salt treatment significantly increased the expression of β2i at mRNA and protein levels, increased the infiltration of macrophages and expression of Mac-2, and upregulated the expression of NF-κB and proinflammatory cytokines including IL-1β, IL-6 and TNF-α in wild-type group, whereas theses effects were markedly attenuated in β2i knockout mice.CONCLUSION:Immuneproteasome subunit β2i is involved in DOCA/salt-induced vascular inflammation through activation of NF-κB signaling in the mice.
