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2015 ; 7
(311
): 311ra173
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Inflammation activation and resolution in human tendon disease
#MMPMID26511510
Dakin SG
; Martinez FO
; Yapp C
; Wells G
; Oppermann U
; Dean BJ
; Smith RD
; Wheway K
; Watkins B
; Roche L
; Carr AJ
Sci Transl Med
2015[Oct]; 7
(311
): 311ra173
PMID26511510
show ga
Improved understanding of the role of inflammation in tendon disease is required
to facilitate therapeutic target discovery. We studied supraspinatus tendons from
patients experiencing pain before and after surgical subacromial decompression
treatment. Tendons were classified as having early, intermediate, or advanced
disease, and inflammation was characterized through activation of pathways
mediated by interferon (IFN), nuclear factor ?B (NF-?B), glucocorticoid receptor,
and signal transducer and activator of transcription 6 (STAT-6). Inflammation
signatures revealed expression of genes and proteins induced by IFN and NF-?B in
early-stage disease and genes and proteins induced by STAT-6 and glucocorticoid
receptor activation in advanced-stage disease. The proresolving proteins FPR2/ALX
and ChemR23 were increased in early-stage disease compared to intermediate- to
advanced-stage disease. Patients who were pain-free after treatment had tendons
with increased expression of CD206 and ALOX15 mRNA compared to tendons from
patients who continued to experience pain after treatment, suggesting that these
genes and their pathways may moderate tendon pain. Stromal cells from diseased
tendons cultured in vitro showed increased expression of NF-?B and IFN target
genes after treatment with lipopolysaccharide or IFN? compared to stromal cells
derived from healthy tendons. We identified 15-epi lipoxin A4, a stable lipoxin
isoform derived from aspirin treatment, as potentially beneficial in the
resolution of tendon inflammation.
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