Skip to search boxSkip to navigationSkip to main content

Upregulation of thrombospondin-1(TSP-1) and its binding partners, CD36 and CD47, in sporadic inclusion body myositis

  • Mohammad Salajegheh
    ,
  • Raghavan Raju
    ,
  • Jens Schmidt
    ,
  • Marinos C. Dalakas(corresponding author)
*Corresponding author for this work
  • Massachusetts General Hospital
    ,
  • 1670 University Blvd
    ,
  • Institute of Experimental and Clinical
    ,
  • National Institutes of Health
Scholary Output:
Contribution to journal
Article
 Peer-review

Abstract

The TSP1/CD36/CD47-complex is involved in T cell expansion and inflammatory responses to β-amyloid, both relevant to IBM. We report on the mRNA and protein expression of TSP1/ CD36 /CD47-complex in IBM muscles and in human myoblasts after cytokine stimulation. The TSP1/CD36 /CD47 was upregulated in IBM. TSP1 immunolocalized to the connective tissue contiguous to inflammation and CD36/CD47 on the myofibers and CD8+ cells. Further, TNF-α upregulated the production of TSP1 and CD47 by myoblasts. The TSP-complex is another inflammatory mediator associated with chronic inflammation in IBM that may perpetuate the immune responses to local antigens in response to TNF-α.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
 Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 166-174 (9 pages)

Journal (Volume, Issue Number)

Journal of Neuroimmunology (Volume 187, Issue 1-2)

Publication milestones

  • Published - 07/2007

Publication status

Published - 07/2007

ISSN

0165-5728

Publication IDs

  • Scopus: 34347345098
  • PubMed: 17572512

Access to documents

Publication metrics

Metrics

SciVal
FWCI
0.33
SciVal
Author count
4
SciVal
citations
18
SciVal
Paper percentile
71
Scopus
citations
21, opens in new tab
Fractional count
1
Fractional count
0.25
Fractional count
3
Fractional count
0.75
Fractional count
1
Fractional count
1

PlumX, opens in new tab

Captures
30
Citation count
24

Funding Details

This research was supported by the Intramural Research Program of NINDS, NIH. Mohammad Salajegheh thanks the Comprehensive Neuroscience Program (CNP) of The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc. (HJF) for their financial support. Jens Schmidt was supported by the Deutsche Forschungsgemeinschaft (DFG, Schm 1669/1-1) and the Myositis Association (TMA).
FundersFunding numbers
Comprehensive Neuroscience Program
-
NIH
-
NINDS
Z01NS002038
HJF
-
TMA
-
DFG
Schm 1669/1-1