Increased Synovial Expression of Transforming Growth Factor (TGF)-β Receptor Endoglin and TGF-β1 in Rheumatoid Arthritis: Possible Interactions in the Pathogenesis of the Disease

Z. Szekanecz, G. Kenneth Haines, Lisa A. Harlow, Manisha R. Shah, Timothy W. Fong, Rebekah Fu, Samuel J W Lin, Ghazi Rayan, Alisa E. Koch

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Abstract

The ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST) plays a role in the pathogenesis of this disease. Transforming growth factor β (TGF-β) may play a role in this process. We have investigated the distribution of endoglin, a newly described receptor for TGF-β1 and -β3, in RA compared to osteoarthritis (OA) or normal ST. Immunohistochemical analysis was carried out using an anti-TGF-β1 monoclonal antibody (mAb) as well as 10 mAbs raised against various epitopes of endoglin. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. TGF-β1 expression was significantly up-regulated on RA compared to OA and normal ST lining cells, interstitial macrophages, and endothelial cells (P <0.05). All anti-endoglin mAbs uniformly reacted with endothelial cells in RA, OA, and normal STs. However, 3 out of 10 anti-endoglin mAbs reacted with significantly more RA versus normal ST lining cells (P <0.05), as well as RA compared to OA and normal macrophages (P <0.05). There was a positive correlation between TGF-β1 and endoglin reactivity on the synovial lining layer and subsynovial macrophages (P <0.05). These results indicate that TGF-β1 and certain epitopes of endoglin, a TGF-β1 and -β3 receptor, are up-regulated on myeloid elements in RA compared to normal ST. Endoglin is also present on ST endothelia, and its expression may also be increased on OA compared to normal ST lining cells. These findings implicate endoglin in the pathogenesis of RA.

Original languageEnglish
Pages (from-to)187-194
Number of pages8
JournalClinical Immunology and Immunopathology
Volume76
Issue number2
DOIs
Publication statusPublished - Aug 1995

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Growth Factor Receptors
Transforming Growth Factors
Rheumatoid Arthritis
Osteoarthritis
Macrophages
Epitopes
Endothelial Cells
Endoglin
Endothelium
Monoclonal Antibodies

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Immunology and Allergy
  • Immunology

Cite this

Increased Synovial Expression of Transforming Growth Factor (TGF)-β Receptor Endoglin and TGF-β1 in Rheumatoid Arthritis : Possible Interactions in the Pathogenesis of the Disease. / Szekanecz, Z.; Haines, G. Kenneth; Harlow, Lisa A.; Shah, Manisha R.; Fong, Timothy W.; Fu, Rebekah; Lin, Samuel J W; Rayan, Ghazi; Koch, Alisa E.

In: Clinical Immunology and Immunopathology, Vol. 76, No. 2, 08.1995, p. 187-194.

Research output: Contribution to journalArticle

Szekanecz, Z. ; Haines, G. Kenneth ; Harlow, Lisa A. ; Shah, Manisha R. ; Fong, Timothy W. ; Fu, Rebekah ; Lin, Samuel J W ; Rayan, Ghazi ; Koch, Alisa E. / Increased Synovial Expression of Transforming Growth Factor (TGF)-β Receptor Endoglin and TGF-β1 in Rheumatoid Arthritis : Possible Interactions in the Pathogenesis of the Disease. In: Clinical Immunology and Immunopathology. 1995 ; Vol. 76, No. 2. pp. 187-194.
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abstract = "The ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST) plays a role in the pathogenesis of this disease. Transforming growth factor β (TGF-β) may play a role in this process. We have investigated the distribution of endoglin, a newly described receptor for TGF-β1 and -β3, in RA compared to osteoarthritis (OA) or normal ST. Immunohistochemical analysis was carried out using an anti-TGF-β1 monoclonal antibody (mAb) as well as 10 mAbs raised against various epitopes of endoglin. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. TGF-β1 expression was significantly up-regulated on RA compared to OA and normal ST lining cells, interstitial macrophages, and endothelial cells (P <0.05). All anti-endoglin mAbs uniformly reacted with endothelial cells in RA, OA, and normal STs. However, 3 out of 10 anti-endoglin mAbs reacted with significantly more RA versus normal ST lining cells (P <0.05), as well as RA compared to OA and normal macrophages (P <0.05). There was a positive correlation between TGF-β1 and endoglin reactivity on the synovial lining layer and subsynovial macrophages (P <0.05). These results indicate that TGF-β1 and certain epitopes of endoglin, a TGF-β1 and -β3 receptor, are up-regulated on myeloid elements in RA compared to normal ST. Endoglin is also present on ST endothelia, and its expression may also be increased on OA compared to normal ST lining cells. These findings implicate endoglin in the pathogenesis of RA.",
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