Platelet-endothelial cell adhesion molecule-1 (PECAM-1)–deficient mice demonstrate a transient and cytokine-specific role for PECAM-1 in leukocyte migration through the perivascular basement membrane

Thompson, Richard; Noble, Karen E.; Larbi, Karen Y.; Dewar, A.; Duncan, Gordon S.; Mak, Tak W.; Nourshargh, Sussan

doi:10.1182/blood.v97.6.1854

Cited by 165 publications

(194 citation statements)

References 49 publications

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“…26 CD31 has widespread distribution and in addition to cell adhesion, may have a role in regulating cell signaling and angiogenesis. 27,28 The gene expression profile associated with t(14;18)-negative cases was dominated by genes involved in cell cycle progression and regulation. These included genes involved in regulating mitotic spindle functions, activation of anaphase promoting complex (APC) and events essential for cytokinesis (eg, PLK, mitotic kinesin-like protein-1, or KNSL5, P55CDC, and CKS1).…”

Section: Discussionmentioning

confidence: 99%

BCL2 Translocation Defines a Unique Tumor Subset within the Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma

Iqbal

Sanger

Horsman

et al. 2004

The American Journal of Pathology

267

173

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Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) has revealed prognostically important subgroups: germinal center B-cell-like (GCB) DL-BCL, activated B cell-like (ABC) DLBCL, and primary mediastinal large B-cell lymphoma. The t(14;18)(q32; q21) has been reported previously to define a unique subset within the GCB-DLBCL. We evaluated for the translocation in 141 cases of DLBCL that were successfully gene expression profiled. Using a dual-probe fluorescence in situ hybridization assay, we detected the t(14;18) in 17% of DLBCLs and in 34% of the GCB subgroup which contained the vast majority of positive cases. In addition, 12 t(14;18)-positive cases detected by polymerase chain reaction assays on additional samples were added to the fluorescence in situ hybridization-positive cases for subsequent analysis. Immunohistochemical data indicated that BCL2, BCL6, and CD10 protein were preferentially expressed in the t(14;18)-positive cases as compared to t(14;18)-negative cases. Within the GCB subgroup, the expression of BCL2 and CD10, but not BCL6, differed significantly between cases with or without the t(14; 18): 88% versus 24% for BCL2 and 72% versus 32% for CD10, respectively. In the GCB-DLBCL subgroup, a heterogeneous group of genes is overexpressed in the t(14;18)-positive subset, among which BCL2 is a significant discriminator. Interestingly, the t(14;18)-negative subset is dominated by overexpression of cell cycle-associated genes, indicating that these tumors are significantly more proliferative, suggesting distinctive pathogenetic mechanisms. However, despite this higher proliferative activity, there was no significant difference in overall or failure-free survival between the t(14;18)-positive and -negative subsets within the GCB subgroup. Diffuse large B-cell lymphoma (DLBCL) is an aggressive malignancy of mature B cells with an annual incidence of ϳ25,000 cases in the United States. DLBCL is a heterogeneous entity both clinically and morphologically. We have recently shown by gene expression profiling that DLBCL can be classified into two major subgroups. 1 The germinal center B-cell-like (GCB) subgroup expresses genes characteristic of normal GC B cells and is associated with a good outcome after multiagent chemotherapy, whereas the activated B-cell-like (ABC) subgroup expresses genes characteristic of activated blood B cells and is associated with a poor clinical outcome. Nonetheless, considerable molecular heterogeneity exists within each subgroup. A small number of DLBCL cases are unclassifiable and do not express the GCB or ABC sig-

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Section: Discussionmentioning

confidence: 99%

BCL2 Translocation Defines a Unique Tumor Subset within the Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma

Iqbal

Sanger

Horsman

et al. 2004

The American Journal of Pathology

267

173

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“…injection of IL-1β as observed using an upright fi xed-stage microscope (Zeiss Axioskop FS; Carl Zeiss MicroImaging). Leukocyte responses of rolling, fi rm adhesion, and extravasation in postcapillary venules of 20-40 μm diameter were quantifi ed as described previously (45). Leukocyte transmigration was defi ned as the number of leukocytes in the extravascular tissue across a 100-μm vessel segment and within 50 μm of the vessel of interest.…”

Section: Induction Of Infl Ammation and Intravital Microscopy Of Cremmentioning

confidence: 99%

Venular basement membranes contain specific matrix protein low expression regions that act as exit points for emigrating neutrophils

Wang¹,

Voisin²,

Larbi³

et al. 2006

The Journal of Cell Biology

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“…This process is predominantly mediated by a group of cellular adhesion molecules (CAMs) expressed on the cell surface, such as selectins, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1, CD 31). PECAM-1 is one of the endothelial junction proteins playing a distinct role in leukocyte trans-endothelial migration (TEM) as it has been demonstrated in both in vivo [10][11][12] and in vitro [13,14] studies.…”

Section: Introductionmentioning

confidence: 99%

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

Wei¹,

Lü²,

Song³

et al. 2005

FEBS Letters

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The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are known to inhibit leukocyte recruitment to endothelium but the mechanism is less understood. Platelet endothelial cell adhesion molecule-1 (PECAM-1) is an endothelial junction protein involved in leukocyte diapedesis. We hypothesize that in endothelial cells, statins may well recruit PECAM-1 to exert their inhibitory effect on leukocyte transendothelial migration (TEM). In lovastatin-treated resting human umbilical vein endothelial cells (HUVECs), increased levels of mRNA and protein of PECAM-1 as well as its bio-synthesis (all 2-fold) were observed by real-time PCR, Western blotting and 35 S-labeled methionine incorporation assay, respectively. Moreover, in lovastatin treated resting cells as well as TNF-a activated endothelial cells, unanimously decreased Triton X-100 insoluble and soluble PECAM-1 ratio was observed. Such changes were accompanied by decreased TEM of U-937 cells (a promonocyte cell line). All lovastatinÕs effects were abrogated by mevalonic acid. In resting HUVECs, geranylgeranyl pyrophosphate (GGPP), but not farnesyl pyrophosphate (FPP) (both are isoprenoid intermediates in the cholesterol biosynthesis pathway) compromised the effect of lovastatin on PECAM-1 expression, whereas C3 toxin, an inhibitor of small G proteins, exerted statin-like effect.Conclusion: Statin-reduced endothelial permeability could be attributed to altered intracellular distribution of PECAM-1 in endothelial cells. We speculate that lovastatin regulates PE-CAM-1 expression in HUVECs through the mevalonate-GGPP pathway by inhibiting of Rho small GTPase.

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Platelet-endothelial cell adhesion molecule-1 (PECAM-1)–deficient mice demonstrate a transient and cytokine-specific role for PECAM-1 in leukocyte migration through the perivascular basement membrane

Cited by 165 publications

References 49 publications

BCL2 Translocation Defines a Unique Tumor Subset within the Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma

BCL2 Translocation Defines a Unique Tumor Subset within the Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma

Venular basement membranes contain specific matrix protein low expression regions that act as exit points for emigrating neutrophils

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

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