scholarly journals Intercellular Adhesion Molecule 1 Regulates Left Ventricular Leukocyte Infiltration, Cardiac Remodeling, and Function in Pressure Overload–Induced Heart Failure

2016 ◽  
Vol 5 (3) ◽  
Author(s):  
Ane M. Salvador ◽  
Tania Nevers ◽  
Francisco Velázquez ◽  
Mark Aronovitz ◽  
Bonnie Wang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Adhesion Molecule ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Leukocyte Infiltration ◽  
Intercellular Adhesion Molecule 1 ◽  
And Function

scholarly journals Suppression of experimental glomerulonephritis by the interleukin-1 receptor antagonist: inhibition of intercellular adhesion molecule-1 expression.

1994 ◽  
Vol 4 (9) ◽  
pp. 1695-1700
Author(s):  
D J Nikolic-Paterson ◽  
H Y Lan ◽  
P A Hill ◽  
J L Vannice ◽  
R C Atkins
Keyword(s):  
Basement Membrane ◽  
Receptor Antagonist ◽  
Adhesion Molecule ◽  
Interleukin 1 ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Leukocyte Infiltration ◽  
Intercellular Adhesion Molecule 1 ◽  
Interleukin 1 Receptor Antagonist ◽  
Tubulointerstitial Damage

Interleukin-1 is a proinflammatory cytokine produced in glomerulonephritis. Blocking the action of interleukin-1 by the administration of the interleukin-1 receptor antagonist (IL-1ra) has been shown to prevent renal function impairment, reduce glomerular injury, inhibit leukocyte infiltration, and suppress tubulointerstitial damage in experimental antiglomerular basement membrane disease. A key mechanism in the entry of leukocytes into the kidney is the interaction between the interleukin-1 inducible intercellular adhesion molecule-1 (ICAM-1; CD54) and lymphocyte function-associated antigen-1 (CD11a/CD18). Therefore, this study investigated whether the inhibition of this mechanism was the means by which IL-1ra suppressed leukocyte infiltration in rat accelerated antiglomerular basement membrane glomerulonephritis. Disease was induced in two groups of six rats; animals were treated by constant sc infusion of recombinant human IL-1ra or saline from the initiation of disease until being euthanized 14 days later. In saline-treated animals, there was marked up-regulation of ICAM-1 in the glomerulus and interstitium, In which was associated with leukocyte infiltration. In particular, focal accumulation of CD11a+ and CD18+ cells was apparent in areas of tubulointerstitial damage exhibiting intense ICAM-1 expression. IL-1ra treatment partially reduced glomerular ICAM-1 expression and leukocyte infiltration. However, IL-1ra treatment resulted in a dramatic inhibition of interstitial ICAM-1 expression, interstitial leukocyte infiltration, and tubulointerstitial damage. In conclusion, this study has shown that interleukin-1 is a major inducer of ICAM-1 expression within the renal tubulo-interstitium--a process associated with focal leukocyte infiltration and tubulointerstitial damage.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ultrastructure and Function of Dimeric, Soluble Intercellular Adhesion Molecule-1 (ICAM-1)

2001 ◽  
Vol 276 (31) ◽  
pp. 29019-29027 ◽  
Author(s):  
Chang-Duk Jun ◽  
Christopher V. Carman ◽  
Sambra D. Redick ◽  
Motomu Shimaoka ◽  
Harold P. Erickson ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble Intercellular Adhesion Molecule ◽  
Ultrastructure And Function ◽  
And Function
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