Role of immunoproteasome subunit β2i in DOCA/salt-induced vascular inflammation in mice / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12): 930-934, 2017.
Artigo
em Chinês
| WPRIM
| ID: wpr-614108
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Journal of Pathophysiology
Ano de publicação:
2017
Tipo de documento:
Artigo
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