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Titolo:
beta 2-microglobulin increases the expression of vascular cell adhesion molecule on human synovial fibroblasts
Autore:
Jaradat, MI; Schnizlein-Bick, CT; Singh, GK; Moe, SM;
Indirizzi:
Indiana Univ, Sch Med, Dept Med, Indianapolis, IN USA Indiana Univ Indianapolis IN USA Sch Med, Dept Med, Indianapolis, IN USA Richard Roudebush VAMC, Indianapolis, IN USA Richard Roudebush VAMC Indianapolis IN USA sh VAMC, Indianapolis, IN USA
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 5, volume: 59, anno: 2001,
pagine: 1951 - 1959
SICI:
0085-2538(200105)59:5<1951:B2ITEO>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCATION END-PRODUCTS; DIALYSIS-RELATED AMYLOIDOSIS; HEMODIALYSIS-ASSOCIATED AMYLOIDOSIS; LONG-TERM HEMODIALYSIS; RHEUMATOID-ARTHRITIS; BETA(2)-MICROGLOBULIN AMYLOIDOSIS; PATHOGENESIS; RECEPTOR; VCAM-1; SERUM;
Keywords:
amyloidosis; dialysis amyloid; advanced glycation end products; hemodialysis; articular disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Moe, SM Indiana Univ, Wishard Mem Hosp, Sch Med, 1001 W 10th St,OPW 526, Indianapolis, IN 46202 USA Indiana Univ 1001 W 10th St,OPW 526 Indianapolis IN USA 46202 USA
Citazione:
M.I. Jaradat et al., "beta 2-microglobulin increases the expression of vascular cell adhesion molecule on human synovial fibroblasts", KIDNEY INT, 59(5), 2001, pp. 1951-1959

Abstract

Background. beta (2)-Microglobulin (beta (2)m) amyloidosis is a destructive articular disease that affects patients on dialysis. The disease presentation is similar to ether forms of arthritis in which adhesion molecules arefelt to be pathogenic. Therefore, we hypothesized that beta (2)m directly increases the expression of vascular cell adhesion molecule-1 (VCAM-1) by synovial fibroblasts. We also examined the effect of alteration of beta (2)mby advanced glycation end products on this cellular response. Methods. Human synovial fibroblasts were isolated and incubated with beta (2)m with and without alteration with advanced glycation end products. VCAM-1 expression was determined by immunnhistochemistry, flow cytometry, and Western blot and Northern blot analyses. Results. beta (2)m increased the protein expression of VCAM-1 by synovial fibroblasts in a dose-dependent manner, beta (2)m altered with advanced glycation end products had no effect. However, all forms of beta (2)m increased VCAM-1 mRNA. beta (2)m also increased the adhesion of peripheral blood mononuclear cells to synovial fibroblasts. Conclusion. beta (2)m directly increases the expression of VCAM-1 by synovial fibroblasts, indicating that synovial fibroblasts may play a key role in the pathogenesis of beta (2)m amyloidosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 10:13:40