Leukocyte Integrins

Elices, Mariano J.

doi:10.1016/b978-0-08-091729-0.50012-7

Cited by 3 publications

(1 citation statement)

References 228 publications

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“…These data are in good agreement with the recently described upregulation of adhesive partners VLA4 and VCAM-1 in the vasculature of ApoE Ϫ/Ϫ mice 3-7 days after air desiccation injury to carotid arteries and a remarkable efficiency of a neutralizing monoclonal anti-VLA4 antibody, PS/2, in attenuating leukocyte recruitment and neointimal formation (2). The observed selectivity of the RGD effect (significant attenuation of macrophage infiltration of and lipid accumulation in glomeruli and injured carotid artery, with the lesser effect in the aorta) is in good agreement with the predominant distribution of ␣ 4 ␤ 1 -integrin (VLA4) to the renal vasculature and injured vessels (2,7). In addition to this distinction, we clearly appreciate that there are multiple other receptors participating in the monocyte-endothelial cell adhesion and transmigration, and their contribution to the process may be insensitive to cRGD peptide, thus reducing its efficacy.…”

Section: Discussionmentioning

confidence: 64%

Cyclic arginine-glycine-aspartic acid peptide inhibits macrophage infiltration of the kidney and carotid artery lesions in apo-E-deficient mice

Elitok

Brodsky

Patschan

et al. 2006

American Journal of Physiology-Renal Physiology

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Elitok, Saban, Sergey V. Brodsky, Daniel Patschan, Tatyana Orlova, Kenneth M. Lerea, Praveen Chander, and Michael S. Goligorsky. Cyclic arginine-glycine-aspartic acid peptide inhibits macrophage infiltration of the kidney and carotid artery lesions in apo-Edeficient mice. Am J Physiol Renal Physiol 290: F159 -F166, 2006. First published August 16, 2005 doi:10.1152/ajprenal.00227.2005Interactions of leukocytes with the vascular endothelium culminating in their diapedesis represent not only a crucial event in immune surveillance and defense but are also critically involved in the pathogenesis of many inflammatory diseases, including atherosclerosis. Our previous in vitro studies using atomic force microscopy measurement of monocyte-endothelial cell interaction have demonstrated that a cyclic arginine-glycine-aspartic acid peptide (cRGD) inhibited their adhesion through very late antigen (␣ 4␤1-integrin; VLA4)-vascular cell adhesion molecule-1 by 60% with the IC50 ϭ 100 nM. To elucidate the potential efficacy of this peptide in vivo in preventing atherogenesis, experiments were performed in apolipoprotein E (ApoE)-deficient (Ϫ/Ϫ) mice fed a Western diet and receiving chronic treatment with cRGD peptide for 2-4 wk. In addition, some animals were subjected to a temporary carotid artery ligation while receiving the above treatment. Formation of fatty streaks and infiltration of the vascular wall with macrophages were not affected by cRGD treatment. Infiltration of the carotid artery postligation was significantly reduced in the cRGD-treated animals, as was the lipid accumulation. Furthermore, cRGD-treated ApoE Ϫ/Ϫ mice exhibited significantly lesser macrophage infiltration and lipid accumulation in the kidneys, the site of the highest expression of VLA4. These data demonstrated that cRGD peptide is a potent inhibitor of monocyte/ macrophage infiltration of the injured macrovasculature and of the renal microvasculature, where it results in the attenuation of lipid accumulation. Formation of fatty streaks in the aortic root was not inhibitable by this treatment.atherosclerosis; apolipoprotein E; VLA-4; kidney; lipid accumulation INTERACTIONS OF LEUKOCYTES with the vascular endothelium culminating in their diapedesis represent not only a crucial event in immune surveillance and defense but are also critically involved in the pathogenesis of many inflammatory diseases, including atherosclerosis. The process of leukocyte egress has been tentatively subdivided into stages of rolling, cell activation, firm adhesion, and transendothelial migration (TEM), with each stage engaging a distinct set of adhesion molecules and their activation (5, 13, 26). These adhesion molecules include L-selectin; carbohydrate ligands of selectins; ␤ 1 -, ␤ 2 -, and ␤ 7 -integrins; and platelet endothelial cell adhesion molecule (PECAM)-1 on leukocytes, and P-and E-selectins, intercellular adhesion molecule (ICAM)-1 and ICAM-2, vascular cell adhesion molecule (VCAM)-1, mucosal addressin cell adhesion molecule-1 (MadCAM-1), PECAM-1 and ␤ 1 -integr...

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Section: Discussionmentioning

confidence: 64%

Cyclic arginine-glycine-aspartic acid peptide inhibits macrophage infiltration of the kidney and carotid artery lesions in apo-E-deficient mice

Elitok

Brodsky

Patschan

et al. 2006

American Journal of Physiology-Renal Physiology

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Cyclo-VEGI inhibits bronchial artery remodeling in a murine model of chronic asthma

Kim

Hur

Lee

et al. 2021

Experimental Lung Research

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A novel RGD-independent fibronectin assembly pathway initiated by α4β1 integrin binding to the alternatively spliced V region

Sechler

Cumiskey

Gazzola

et al. 2000

Journal of Cell Science

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Fibronectin (FN) matrix assembly is a multi-step process that involves binding to integrin receptors, FN-FN interactions and connections to the actin cytoskeleton. Ultimately, FN is converted into stable matrix fibrils that are detergent-insoluble. RGD-binding integrins such as alpha5beta1 play a major role in the assembly of fibrillar FN. Here we show that alpha4beta1 binding to the alternatively spliced V (IIICS) region of FN initiates an alternative assembly pathway. Activation of alpha4beta1 with exogenous agents such as Mn(2+) or a beta1-stimulatory antibody TS2/16 was sufficient to induce initiation of FN fibrillogenesis by Ramos B lymphoma cells and by CHO(B2)alpha4 cells. Using recombinant FNs lacking specific sequences, we show that assembly is independent of the RGD sequence but requires the V25/CS-1 segment. Previously, we have characterized an activated recombinant FN (FN III(1–7)) that rapidly forms detergent-insoluble multimers upon binding to alpha5beta1 integrin. Alpha4beta1 also formed FNdeltaIII(1–7) multimers without the aid of exogenous stimulants, suggesting that an activated form of FN can override the need for activation of the integrin. In contrast to assembly by alpha5beta1, actin filaments remained largely cortical and no change in cell growth rate was observed with alpha4beta1-mediated assembly. These results show that binding sites on FN other than the RGD sequence/synergy site and distant from the cell binding domain can promote FN assembly. Thus, there appear to be multiple, integrin-specific mechanisms for assembly of FN matrix.

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Leukocyte Integrins

Cited by 3 publications

References 228 publications

Cyclic arginine-glycine-aspartic acid peptide inhibits macrophage infiltration of the kidney and carotid artery lesions in apo-E-deficient mice

Cyclic arginine-glycine-aspartic acid peptide inhibits macrophage infiltration of the kidney and carotid artery lesions in apo-E-deficient mice

Cyclo-VEGI inhibits bronchial artery remodeling in a murine model of chronic asthma

A novel RGD-independent fibronectin assembly pathway initiated by α4β1 integrin binding to the alternatively spliced V region

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