PMN stimulation by factors from IL-1-treated human synovial cell cultures

1989 ◽  
Vol 27 (3-4) ◽  
pp. 448-450 ◽  
Author(s):  
M. L. Watson ◽  
G. P. Lewis ◽  
J. Westwick
1982 ◽  
Vol 2 (4) ◽  
pp. 313-329 ◽  
Author(s):  
David Hamerman ◽  
Carol Smith ◽  
Harold D. Keiser ◽  
Rita Craig

1994 ◽  
Vol 53 (9) ◽  
pp. 601-607 ◽  
Author(s):  
H Shimada ◽  
K Eguchi ◽  
Y Ueki ◽  
M Nakashima ◽  
I Yamashita ◽  
...  

1983 ◽  
Vol 3 (2) ◽  
pp. 125-140 ◽  
Author(s):  
Elaine E. Golds ◽  
T. Derek Cooke ◽  
A. Robin Poole

2010 ◽  
Vol 12 (1) ◽  
pp. R15 ◽  
Author(s):  
Kristel B Van Landuyt ◽  
Elena A Jones ◽  
Dennis McGonagle ◽  
Frank P Luyten ◽  
Rik J Lories

1990 ◽  
Vol 269 (1) ◽  
pp. 265-268 ◽  
Author(s):  
P Nyirkos ◽  
E E Golds

By SDS/PAGE analysis we have observed that human synovial cell monolayers secrete a prominent 39 kDa protein which could not be detected in skin and lung fibroblasts. This protein was purified to homogeneity by heparin-Sepharose chromatography and reverse-phase h.p.l.c. The N-terminal sequence was found to be almost identical to that of a recently described bovine protein detected in the mammary secretions during the involutionary phase of the lactational cycle. Characterization of this 39 kDa protein may provide a useful marker for classification of connective tissue cells.


Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 2060-2064 ◽  
Author(s):  
Narine Hakobyan ◽  
Tamara Kazarian ◽  
Adnan A. Jabbar ◽  
Kausar J. Jabbar ◽  
Leonard A. Valentino

Abstract Hemophilia is a genetic disease caused by a deficiency of blood coagulation factor VIII or IX. Bleeding into joints is the most frequent manifestation of hemophilia. Hemarthrosis results in an inflammatory and proliferative disorder termed hemophilic synovitis (HS). In time, a debilitating, crippling arthritis, hemophilic arthropathy, develops. Although the clinical sequence of events from joint bleeding to synovitis to arthropathy is well documented, the component or components in blood and the molecular changes responsible for hemophilic synovitis are not known. Iron has long been suspected to be the culprit but direct evidence has been lacking. Previously, we showed that iron increased human synovial cell proliferation and induced c-myc expression. Here we show that bleeding into a joint in vivo and iron in vitro result in increased expression of the p53-binding protein, mdm2. Iron induced the expression of mdm2 by normal human synovial cells approximately 8-fold. In a murine model of human hemophilia A, hemarthrosis resulted in pathologic changes observed in human hemophilic synovitis and a marked increase in synovial cell proliferation. Iron, in vitro, induced the expression of mdm2. The molecular changes induced by iron in the blood may be the basis of the increase in cell proliferation and the development of hemophilic synovitis. (Blood. 2004;104:2060-2064)


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