Increased Expression of Intercellular Adhesion Molecule 1, CD11/CD18 Cell Surface Adhesion Glycoproteins and α4β1 Integrin in a Rat Model of Chronic Interstitial Lung Fibrosis

Pathobiology ◽  
1996 ◽  
Vol 64 (4) ◽  
pp. 187-192 ◽  
Author(s):  
Nora Barquín ◽  
Pauline Chou ◽  
Carlos Ramos ◽  
Martha Montaño ◽  
Annie Pardo ◽  
...  
1992 ◽  
Vol 118 (5) ◽  
pp. 1223-1234 ◽  
Author(s):  
O Carpén ◽  
P Pallai ◽  
D E Staunton ◽  
T A Springer

We have studied the cytoskeletal association of intercellular adhesion molecule-1 (ICAM-1, CD54), an integral membrane protein that functions as a counterreceptor for leukocyte integrins (CD11/CD18). A linkage between ICAM-1 and cytoskeletal elements was suggested by studies showing a different ICAM-1 staining pattern for COS cells transfected with wild-type ICAM-1 or with an ICAM-1 construct that replaces the cytoplasmic and transmembrane domains of ICAM-1 with a glycophosphatidylinositol (GPI) anchor. Wild-type ICAM-1 appeared to localize most prominently in microvilli whereas GPI-ICAM-1 demonstrated a uniform cell surface distribution. Disruption of microfilaments with cytochalasin B (CCB) changed the localization of wild-type ICAM-1 but had no effect on GPI-ICAM-1. Some B-cell lines demonstrated a prominent accumulation of ICAM-1 into the uropod region whereas other cell surface proteins examined were not preferentially localized. CCB also induced redistribution of ICAM-1 in these cells. For characterization of cytoskeletal proteins interacting with ICAM-1, a 28-residue peptide that encompasses the entire predicted cytoplasmic domain (ICAM-1,478-505) was synthesized, coupled to Sepharose-4B, and used as an affinity matrix. One of the most predominant proteins eluted either with soluble ICAM-1,478-505-peptide or EDTA, was 100 kD, had a pI of 5.5, and in Western blots reacted with alpha-actinin antibodies. A direct association between alpha-actinin and ICAM-1 was demonstrated by binding of purified alpha-actinin to ICAM-1,478-505-peptide and to immunoaffinity purified ICAM-1 and by a strict colocalization of ICAM-1 with alpha-actinin, but not with the cytoskeletal proteins talin, tensin, and vinculin. The region of ICAM-1,478-505 interacting with alpha-actinin was mapped to the area close to the membrane spanning region. This region contains several positively charged residues and appears to mediate a charged interaction with alpha-actinin which is not highly dependent on the order of the residues.


1998 ◽  
Vol 274 (3) ◽  
pp. F580-F586 ◽  
Author(s):  
Jeremiah J. Morrissey ◽  
Saulo Klahr

Ureteral obstruction causes infiltration of the kidney by monocytes/macrophages. This infiltrate is significantly reduced by administration of an angiotensin-converting enzyme (ACE) inhibitor but not by a specific angiotensin II type 1 receptor (AT1 receptor) antagonist. Chemoattractants and cell surface adhesive molecules mediate monocyte/macrophage infiltration. Rats with unilateral ureteral obstruction (UUO) of 1, 3, or 5 days duration were untreated or given enalapril or SC-51316 in the drinking water. We measured the mRNA levels of monocyte chemoatactic peptide 1 (MCP-1), a chemoattractant, and levels of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), two cell surface adhesion proteins. MCP-1 mRNA increased significantly after 1 day of UUO and increased further through 5 days of UUO in the obstructed kidney. ICAM-1 mRNA also increased significantly after 1 day but steadily declined through 5 days of UUO in the obstructed kidney. VCAM-1 mRNA did not increase significantly until after 3 days of UUO and increased further through 5 days of obstruction. Enalapril or SC-51316 treatment had no significant effect on ICAM-1 mRNA levels. MCP-1 mRNA levels were reduced but remained significantly elevated. Enalapril significantly blunted the increase in VCAM-1 mRNA levels and VCAM-1 protein determined by immunocytochemistry; SC-51316 had no significant effect. Thus changes in VCAM-1 levels may account for the differential effect of enalapril and SC-51316 on monocyte/macrophage infiltration of the kidney during ureteral obstruction.


2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Monika Mauliūtė ◽  
Rita Rugienė ◽  
Vytautas Žėkas ◽  
Loreta Bagdonaitė

AbstractObjectivesEndothelin-1 (ET-1) has been implicated in the pathogenesis of inflammatory and fibrotic diseases, including systemic sclerosis. In addition to modulating vascular tone and extracellular matrix turnover, ET-1 up-regulates cell surface adhesion molecules–intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).The aim of the study was to evaluate the diagnostic value of the detection of ET-1, VCAM-1 and ICAM-1 in the diagnosis of systemic sclerosis.MethodsA total of 30 patients with systemic sclerosis from Vilnius University Hospital Santaros Clinics were included in the study. Serum levels of ICAM-1, VCAM-1 and ET-1 were assessed by enzyme immunoassay.ResultsET-1 concentration was associated with VCAM-1 concentration (r=0.687; p<0.001). No associations between ET-1 and ICAM-1 concentrations were detected. Depending on the duration of the disease no significant differences in the concentrations of ET-1, ICAM-1 and VCAM-1 were detected.ConclusionsThe results of this study indicated that ET-1 and VCAM-1 may be assessed together as markers of inflammation and the identification of patients at high risk for disease progression.


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