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2018 ; 38
(3
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness
and inflammatory response via suppressing NF-?B pathway
#MMPMID29784872
Li G
; Xia Z
; Liu Y
; Meng F
; Wu X
; Fang Y
; Zhang C
; Liu D
Biosci Rep
2018[Jun]; 38
(3
): ä PMID29784872
show ga
Rheumatoid arthritis (RA) is an autoimmune disease of the joints characterized by
synovial hyperplasia and chronic inflammation. Fibroblast-like synoviocytes (FLS)
play a central role in RA initiation, progression, and perpetuation. Prior
studies showed that sirtuin 1 (SIRT1), a deacetylase participating in a broad
range of transcriptional and metabolic regulations, may impact cell proliferation
and inflammatory responses. However, the role of SIRT1 in RA-FLS was unclear.
Here, we explored the effects of SIRT1 on the aggressiveness and inflammatory
responses of cultured RA-FLS. SIRT1 expression was significantly lower in
synovial tissues and FLS from RA patients than from healthy controls.
Overexpression of SIRT1 significantly inhibited RA-FLS proliferation, migration,
and invasion. SIRT1 overexpression also significantly increased RA-FLS apoptosis
and caspase-3 and -8 activity. Focusing on inflammatory phenotypes, we found
SIRT1 significantly reduced RA-FLS secretion of TNF-?, IL-6, IL-8, and IL-1?.
Mechanistic studies further revealed SIRT1 suppressed NF-?B pathway by reducing
p65 protein expression, phosphorylation, and acetylation in RA-FLS. Our results
suggest SIRT1 is a key regulator in RA pathogenesis by suppressing aggressive
phenotypes and inflammatory response of FLS. Enhancing SIRT1 expression or
function in FLS could be therapeutic beneficial for RA by inhibiting synovial
hyperplasia and inflammation.
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