CD31 expressed on distinctive T cell subsets is a preferential amplifier of beta 1 integrin-mediated adhesion.

Tanaka, Yoshiya; Albelda, Steven Μ.; Horgan, Kevin J.; Seventer, Gijs A. van; Shimizu, Yoji; Newman, Walter; Hallam, John A.; Newman, Peter J.; Buck, Clayton A.; Shaw, Stephen

doi:10.1084/jem.176.1.245

Cited by 344 publications

(205 citation statements)

References 53 publications

(66 reference statements)

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“…CD31 has been shown to amplify β1-mediated adhesion to endothelial cells (Tanaka et al, 1992). We found no inhibitory effects on PC3 binding to endothelial cells using a CD31-blocking antibody.…”

Section: Discussioncontrasting

confidence: 52%

Interactions of human prostatic epithelial cells with bone marrow endothelium: binding and invasion

Scott

Clarke²,

George

et al. 2001

Br J Cancer

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The second commonest cause of cancer death in the Western world is attributed to prostate cancer (Jensen et al, 1990). It is well documented that prostatic carcinoma shows a predilection to metastasize to the bone marrow (Jacobs, 1983). Metastatic prostate cancer remains an incurable disease and as such, is a massive clinical problem. There is clearly a need to elucidate the factors underlying the spread of prostate cancer, particularly to the skeleton.It has been suggested that the bone marrow microenvironment is conducive to the growth of prostate cancer cells, which nonselectively enter the bone marrow from the circulation (Galasko, 1981;Jacobs, 1983;Paget, 1989;Body, 1992). However, the strikingly consistent pattern of prostate metastasis within the red marrow suggests that this process may in fact be regulated (Fidler et al, 1978). The mechanism of metastasis is a complex multi-step process that is not fully understood. One critical step in this mechanism may be the attachment to and extravasation through endothelial barriers by malignant cells possibly leading to selective metastatic sites. Tumour cell binding to endothelium involves two distinct steps, an initial docking step mediated via lectin-carbohydrate interactions followed by an integrin-mediated locking step (Honn and Tang, 1992). Several endothelial and tumour adhesion molecules have been associated with metastasis. In particular the integrins β1, α2 and α5 have been shown to be expressed by prostate epithelial cells and bone marrow cells (Soligo et al, 1990;Nagle et al, 1994;Rokhlin and Cohen, 1995). The carbohydrate sialyl Lewis X has also been associated with breast and lung cancer metastasis and its ligand P selectin is found on endothelial cells (Soligo et al, 1990). Some lung, brain, liver and ovary metastatic tumour cells have been demonstrated to bind selectively to endothelial cells isolated from lung, brain, liver and ovary respectively (Nicolson and Winkelhake, 1975;Auerbach et al, 1987). These studies suggest an active regulatory role for the endothelium in metastasis (Zetter, 1990).We have shown previously that primary prostatic epithelia from both benign and malignant tissue show an accelerated growth rate within bone marrow stroma compared to control stroma (Lang et al, 1998) and also that integrin α2β1 is a major contributor to the binding of primary prostatic epithelial cells to bone marrow stroma (Lang et al, 1997). This pattern of primary prostatic epithelial cell adhesion (α2β1) is mimicked by the prostate cell line, PC3 (Kostenuik et al, 1996) and our experiments were therefore conducted with this cell line. These studies have now been extended to develop a model to investigate the interactions of prostatic epithelial cells (primary and cell lines) with the bone marrow endothelium. MATERIALS AND METHODS MaterialsGeneral chemicals were purchased from Sigma (Poole, UK). Tissue culture media and supplements were obtained from Gibco Summary Prostate cancer shows a propensity to form secondary tumours within the bone marrow. Such ...

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Section: Discussioncontrasting

confidence: 52%

Interactions of human prostatic epithelial cells with bone marrow endothelium: binding and invasion

Scott

Clarke²,

George

et al. 2001

Br J Cancer

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“…Although there was variation in the expression of CD31 between different CD8 TIL preparations, all of them contained a substantial subset of cells that were CD31 positive (Table 1), and it is possible that CD31 expression might have facilitated the original entry of this TILs into tumour. This is supported by the proposal that CD31 on T cells can act as an amplifier of T-cell integrin function when it engages an, as yet unknown, endothelial receptor Tanaka et al, 1992) and by recent studies proposing a role for CD31 in the entry of TILs into murine tumours (Schmitt-Verhulst, 1994) (B Imhof, personal communication). However, CD31 expression cannot be an absolute requirement for TIL recruitment as the CD31-dull CD4+ TILs that we studied (TIL6) migrated to tumour deposits in vivo.…”

Section: Tils Display Strong Activation-independent Binding To Endothmentioning

confidence: 81%

Adhesion of tumour-infiltrating lymphocytes to endothelium: a phenotypic and functional analysis

Adams

Yannelli²,

Newman³

et al. 1997

Br J Cancer

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Summary Efficacy of cancer immunotherapy with cultured tumour-infiltrating lymphocytes (TlLs) depends upon infused TILs migrating into tumour-bearing tissue, in which they mediate an anti-tumour response. For TILs to enter a tumour, they must first bind to tumour endothelium, and this process depends on TILs expressing and regulating the function of relevant cell-surface receptors. We analysed the cell-surface phenotype and endothelial binding of TILs cultured from human melanoma and compared them with peripheral blood T cells and with allostimulated T cells cultured under similar conditions. Compared with peripheral blood T cells, TILs expressed high levels of five integrins, two other adhesion molecules, including the skin homing molecule CLA, and several activation markers and showed markedly enhanced integrin-mediated adhesion to a dermal microvascular endothelial cell line in vitro. Compared with the allostimulated T cells, TILs expressed higher levels of the cutaneous lymphocyte antigen (CLA), the adhesion molecule CD31 and the activation markers CD30 and CD69, but lower levels of several other adhesion and activation molecules. These phenotypic and functional properties of TILs should have complex effects on their migration in vivo. Expression of CLA, the skin homing receptor, may increase migration to melanoma (a skin cancer), whereas integrin activation may cause non-specific binding of TILs to other endothelium. Manipulation of the culture conditions in which TILs are expanded might result in a phenotype that is more conducive to selective tumour homing in vivo.

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“…26 PECAM-1 is also associated with cadherin and several cytoplasmic proteins to modulate intercellular transport, 27 and with extracellular matrix-binding protein to control adhesive and migratory cellular activities. [28][29][30] Our present study has demonstrated effects of CHH on expression levels of junctional proteins and their function in vascular endothelial EA.hy926 cells. Because most important function of these junctional proteins is serving as a fence for soluble permeability, we monitored TER as an index of their function.…”

Section: Resultsmentioning

confidence: 97%

Hypobaric hypoxia down-regulated junctional protein complex: Implications to vascular leakage

Souvannakitti

Peerapen

Thongboonkerd

2016

Cell Adhesion & Migration

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Acute mountain sickness (AMS) can cause capillary hyper-permeability and vasogenic edema. However, its underlying mechanisms remained unclear and there is no previous in vitro study on AMS. We therefore conducted an in vitro study and examined whether continuous hypobaric hypoxia (CHH) could alter expression of junctional protein complex of vascular endothelial cells, causing hyper-permeabilization. EA.hy926 human endothelial cells were exposed to either CHH or normoxia for up to 24 h. Flow cytometry using annexin V/propidium iodide co-staining demonstrated that cell death had no significant difference at 12-h, but was increased by CHH at 24-h. Transendothelial resistance (TER) of endothelial cell monolayer was progressively decreased by CHH from 1-h to 24-h. Western blot analysis and immunofluorescence study demonstrated decreased expression levels of VE-cadherin, PECAM-1 and ZO-1 junctional proteins at both 12-h and 24-h exposure time-points. Interestingly, while the main form of ZO-1 (220 kDa) was decreased, its degraded form (100 kDa) was increased by 24-h CHH that might be linked to the increased cell death. Our data have demonstrated that CHH caused vascular endothelial hyper-permeability and defective junctional protein complex by reducing expression levels of VE-cadherin, PECAM-1, and ZO-1. Taken together, these data may explain pathophysiology underlying vascular hyperpermeability in AMS.

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CD31 expressed on distinctive T cell subsets is a preferential amplifier of beta 1 integrin-mediated adhesion.

Cited by 344 publications

References 53 publications

Interactions of human prostatic epithelial cells with bone marrow endothelium: binding and invasion

Interactions of human prostatic epithelial cells with bone marrow endothelium: binding and invasion

Adhesion of tumour-infiltrating lymphocytes to endothelium: a phenotypic and functional analysis

Hypobaric hypoxia down-regulated junctional protein complex: Implications to vascular leakage

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