β1 integrin activation on human neutrophils promotes β2 integrin-mediated adhesion to fibronectin

Berg, J.M. van den; Mul, Frederik P. J.; Schippers, Esther; Weening, Jan J.; Roos, Dirk; Kuijpers, Taco W.

doi:10.1002/1521-4141(200101)31:1<276::aid-immu276>3.0.co;2-d

Cited by 56 publications

(23 citation statements)

References 36 publications

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“…Circulating granulocytes expressed high levels of L-selectin and b 2 , and to a lesser extent a 4 (Figure 1a-c), in line with other studies (Tamatani et al, 1991;Issekutz TB et al, 1996;van den Berg et al, 2001). In inflamed paws, CD45 þ cells expressed high levels of b 2 and low levels of L-selectin (Figure 1e and f).…”

Section: Coexpression Of Selectins Integrins and Pecam-1 With Opioidssupporting

confidence: 89%

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Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Machelska

Brack

Mousa

et al. 2004

British J Pharmacology

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1 Control of inflammatory pain can result from activation of opioid receptors on peripheral sensory nerves by opioid peptides secreted from leukocytes in response to stress (e.g. experimental swim stress or surgery). The extravasation of immunocytes to injured tissues involves rolling, adhesion and transmigration through the vessel wall, orchestrated by various adhesion molecules. 2 Here we evaluate the relative contribution of selectins, integrins a 4 and b 2 , and platelet-endothelial cell adhesion molecule-1 (PECAM-1) to the opioid-mediated inhibition of inflammatory pain. 3 We use flow cytometry, double immunofluorescence and nociceptive (paw pressure) testing in rats with unilateral hind paw inflammation induced by complete Freund's adjuvant. 4 In inflamed tissue, 43-58% of hematopoietic cells (CD45 þ ) expressed opioid peptides. L-selectin and b 2 were coexpressed by 7 and 98% of opioid-containing leukocytes, respectively. Alpha 4 integrin was expressed in low levels by the majority of leukocytes. Opioid-containing cells, vascular P-and E-selectin and PECAM-1 were simultaneously upregulated. 5 Swim stress produced potent opioid-mediated antinociception in inflamed tissue, unaffected by blockade of PECAM-1. However, blockade of L-and P-selectins by fucoidin, or of a 4 and b 2 by monoclonal antibodies completely abolished peripheral stress-induced antinociception. This coincided with a 40% decrease in the migration of opioid-containing leukocytes to inflamed tissue. 6 These findings establish selectins and integrins a 4 and b 2 , but not PECAM-1, as important molecules involved in stress-induced opioid-mediated antinociception in inflammation. They point to a cautious use of anti-inflammatory treatments applying anti-selectin, anti-a 4 and anti-b 2 strategies because they may impair intrinsic pain inhibition.

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Section: Coexpression Of Selectins Integrins and Pecam-1 With Opioidssupporting

confidence: 89%

“…Specificity was documented by the lack of staining with control Abs (Figure 1g-i). Because of the relatively low expression of a 4 by granulocytes van den Berg et al, 2001) and technical difficulties resulting therefrom, we did not examine coexpression of a 4 with opioids in paws.…”

Section: Coexpression Of Selectins Integrins and Pecam-1 With Opioidsmentioning

confidence: 99%

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Machelska

Brack

Mousa

et al. 2004

British J Pharmacology

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“…Thus, platelet-MSC interaction may also be facilitated by the tant to keep in mind that platelet activation plays pivotal roles in the pathogenesis of PAH (30). Platelets are concerted action of platelet integrin GPIIb/IIIa, fibronectin (38), and α4 and β1 integrins (very late antigen 4; therefore a double-edged sword; the intricate regulation of their activation status to minimize their influence on VLA-4) (34) on MSCs. In addition, chemokines expressed by platelets such as stromal cell-derived facthrombosis and inflammation, and to amplify the functions of promoting MSC homing, may finally turn the tor-1 (SDF-1) may also play roles in the recruitment of MSCs (17,20,25), and inhibition of the SDF-1/CXCR4 sword into a plowshare.…”

Section: Discussionmentioning

confidence: 99%

Platelet-Mediated Mesenchymal Stem Cells Homing to the Lung Reduces Monocrotaline-Induced Rat Pulmonary Hypertension

et al. 2012

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Bone marrow mesenchymal stem cell (BM-MSC) transplantation has been suggested to be a promising method for the treatment of pulmonary arterial hypertension (PAH), a fatal disease currently without effective preventive/therapeutic strategies. However, the detailed mechanisms underlying BM-MSC therapy are largely unknown. We designed the present study to test the hypothesis that circulating platelets facilitate BM-MSC homing to the lung vasculature in a rat model of PAH induced by monocrotalin (MCT). A single subcutaneous administration of MCT induced a marked rise in right ventricular systolic pressure (RVSP) and the weight ratio of right to left ventricle plus septum (RV/LV+S) 3 weeks after injection. The injection of MSCs via tail vein 3 days after MCT significantly reduced the increase of RVSP and RV/LV+S. The fluorescence-labeled MSCs injected into the PAH rat circulation were found mostly distributed in the lungs, particularly on the pulmonary vascular wall, whereas cell homing was abolished by an anti-P-selectin antibody and the GPIIb/IIIa inhibitor tirofiban. Furthermore, using an in vitro flow chamber, we demonstrated that MSC adhesion to the major extracellular matrix collagen was facilitated by platelets and their P-selectin and GPIIb/IIIa. Therefore, the current study suggested that platelet-mediated MSC homing prevented the aggravation of MCT-induced rat PAH, via P-selectin and GPIIb/IIIa-mediated mechanisms.

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“…Preferential release of MPs containing active ␣ M ␤ 2 may be one mechanism for down-regulating the proinflammatory status of activated leukocytes, together with shedding 56 and internalization of the integrin as well as apoptosis of the cells. By virtue of its capacity to bind numerous ligands, including ICAM-1, 57 GPIb␣, 20,21 JAM-3, 22 fibronectin, 58 and Fg, 59 active ␣ M ␤ 2 on MPs may mediate their interaction with endothelial cells, platelets, and extracellular matrix. MPs also were shown to interact with plasminogen and to form plasmin on their surface, 60 and activated ␣ M ␤ 2 can bind plasminogen and urokinase.…”

Section: Discussionmentioning

confidence: 99%

Expression, activation, and function of integrin αMβ2 (Mac-1) on neutrophil-derived microparticles

Pluskota

Woody

Szpak

et al. 2008

Blood

178

148

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IntroductionLeukocyte-platelet cross-talk plays multiple and important roles in inflammatory and thrombotic responses. 1 Activated platelets and platelet-released mediators, such as PDGF and PAF, activate leukocytes enhancing their responses such as adhesion, chemotaxis, phagocytosis, and superoxide generation. [2][3][4][5] Conversely, activated leukocytes induce platelet activation as evidenced by increased platelet P-selectin expression. 6 In vivo studies show that leukocytes and platelets colocalize within atherosclerotic and restenotic lesions, at sites of hemorrhage and ischemia-reperfusion injury. [7][8][9][10] Indeed, increased levels of leukocyte-platelet aggregates are found in patients with diabetes, acute coronary syndromes, trauma, and sepsis. [11][12][13] Numerous studies have analyzed the receptors involved in leukocyte-platelet interactions. P-selectin on activated platelets binds PSGL-1 on leukocytes 14,15 to support their rolling on adherent platelets and to activate leukocyte integrin ␣ M ␤ 2 , which mediates firm leukocyte adhesion. [16][17][18] Several ␣ M ␤ 2 counterreceptors on platelets have been proposed, including Fg-bound ␣ IIb ␤ 3 , 19 GPIb␣,20,21 and JAM-3. 22 Recognition of these counterreceptors requires that ␣ M ␤ 2 be in an activated conformation. ␣ M ␤ 2 can be activated by stimulation of leukocytes by agonists and can be monitored with monoclonal antibodies (mAbs), CBRM1/5 and mAb24, which react selectively with the activated conformation.Microparticles (MPs) are released by membrane blebbing from cells undergoing activation or apoptosis. MPs are usually defined by 2 criteria: size (Ͻ 1 m) and surface expression of negatively charged phosphatidylserine (reviewed in Boulanger et al, 23 Morel et al, 24 Martinez et al, 25 and Distler et al 26 ). MPs are not simply the markers of cell activation or damage but may exert pleiotropic effects on blood and vascular cells. MPs of platelet and endothelial origin have procoagulant and proinflammatory activities (reviewed in Boulanger et al, 23 Morel et al, 24 Martinez et al, 25 and Distler et al 26 ) and are markers of acute coronary syndromes. 27,28 The functions of leukocyte-derived MPs are less clear. MPs shed by PMNs behave as inflammatory mediators and activate endothelial cells 29,30 but also exert antiinflammatory effects on macrophages. 31 One of the most important features of leukocyte-derived MPs is the expression of tissue factor 32 and negatively charged phospholipids, suggesting that they may contribute to blood coagulation. Indeed, in vivo studies have shown that leukocyte MPs are captured by activated platelets within thrombi by a P-selectin/PSGL-1-dependent mechanism that leads to accumulation of tissue factor and ultimately enhanced fibrin deposition. 33,34 Although the interactions of leukocyte-derived MPs with activated platelets have been well documented, additional mechanisms in which leukocyte MPs may activate resting platelets, when platelet P-selectin expression is low, have not been examined. In this study, we show...

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β1 integrin activation on human neutrophils promotes β2 integrin-mediated adhesion to fibronectin

Cited by 56 publications

References 36 publications

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Platelet-Mediated Mesenchymal Stem Cells Homing to the Lung Reduces Monocrotaline-Induced Rat Pulmonary Hypertension

Expression, activation, and function of integrin αMβ2 (Mac-1) on neutrophil-derived microparticles

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