Junctional adhesion molecule-A is abnormally expressed in diffuse cutaneous systemic sclerosis skin and mediates myeloid cell adhesion

Hou, Yong; Rabquer, Bradley J.; Gerber, Michele; Galdo, Francesco Del; Jimenez, Sergio A.; Haines, G. Kenneth; Barr, Walter G.; Massa, Mary C.; Seibold, James R.; Koch, Alisa E.

doi:10.1136/ard.2008.102624

Cited by 20 publications

(27 citation statements)

References 22 publications

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“…Having observed a similar inflammatory-induced alteration of cell-bound JAM-A expression as previously described in non-CNS EC types, we next investigated whether HBMEC show a basal or inducible release of sJAM-A as previously described in HUVEC and HDMEC [22], [23]. To measure sJAM-A, we developed a sandwich ELISA.…”

Section: Resultsmentioning

confidence: 70%

“…In HUVEC, sJAM-A was found to be shedded from the cell surface by the disintegrin and metalloproteinases (ADAM) 10 and 17 upon pro-inflammatory stimulation [23]. On a functional level, recombinant sJAM-A reduced adhesion of mononuclear cells to cultured HUVEC and HDMEC [22], [24]. Furthermore it reduced chemokine-triggered endothelial transmigration of CD4 + CD45RO + memory T cells across HUVEC under static and flow conditions [24].…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of Soluble Junctional Adhesion Molecule-A as a Biomarker of Human Brain Endothelial Barrier Breakdown

et al. 2010

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BackgroundAn inducible release of soluble junctional adhesion molecule-A (sJAM-A) under pro-inflammatory conditions was described in cultured non-CNS endothelial cells (EC) and increased sJAM-A serum levels were found to indicate inflammation in non-CNS vascular beds. Here we studied the regulation of JAM-A expression in cultured brain EC and evaluated sJAM-A as a serum biomarker of blood-brain barrier (BBB) function.Methodology/Principal FindingsAs previously reported in non-CNS EC types, pro-inflammatory stimulation of primary or immortalized (hCMEC/D3) human brain microvascular EC (HBMEC) induced a redistribution of cell-bound JAM-A on the cell surface away from tight junctions, along with a dissociation from the cytoskeleton. This was paralleled by reduced immunocytochemical staining of occludin and zonula occludens-1 as well as by increased paracellular permeability for dextran 3000. Both a self-developed ELISA test and Western blot analysis detected a constitutive sJAM-A release by HBMEC into culture supernatants, which importantly was unaffected by pro-inflammatory or hypoxia/reoxygenation challenge. Accordingly, serum levels of sJAM-A were unaltered in 14 patients with clinically active multiple sclerosis compared to 45 stable patients and remained unchanged in 13 patients with acute ischemic non-small vessel stroke over time.ConclusionSoluble JAM-A was not suited as a biomarker of BBB breakdown in our hands. The unexpected non-inducibility of sJAM-A release at the human BBB might contribute to a particular resistance of brain EC to inflammatory stimuli, protecting the CNS compartment.

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Section: Resultsmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Evaluation of Soluble Junctional Adhesion Molecule-A as a Biomarker of Human Brain Endothelial Barrier Breakdown

et al. 2010

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“…An immunohistochemical study in human arthritis has also demonstrated JAM-C expression on the synovial fibroblasts of both osteoarthritis and rheumatoid arthritis patients, in conjunction with JAM-C-dependent adhesion of myeloid cells to these fibroblasts (Rabquer et al, 2008). Enhanced expression of JAM-A has also been described on the skin of patients with the inflammatory disorder systemic sclerosis, in comparison to that on normal dermal fibroblasts (Hou et al, 2009). Aside from facilitating adhesion of leukocytic cells to stromal elements such as fibroblasts, another way in which JAM family members could influence the breast cancer microenvironment is by altering proliferation of fibroblasts or other accessory cells.…”

Section: Jam Proteins and The Regulation Of Stromal Cellsmentioning

confidence: 92%

Junctional Adhesion Molecules (JAMs) - New Players in Breast Cancer?

Offiah¹,

Brennan²,

Hopkins³

2011

Breast Cancer - Focusing Tumor Microenvironment, Stem Cells and Metastasis

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“…sJAM-A is elevated in the serum of patients with SSc compared with healthy volunteers [33]. However, membrane-bound JAM-A is decreased on ECs in SSc skin [33]. Therefore, SSc ECs may be unable to mount an angiogenic response to sJAM-A.…”

Section: Systemic Sclerosis Angiogenic Receptor Dysregulationmentioning

confidence: 97%

“…sJAM-A promotes angiogenesis by interacting with membrane-bound JAM-A on the surface of ECs. sJAM-A is elevated in the serum of patients with SSc compared with healthy volunteers [33]. However, membrane-bound JAM-A is decreased on ECs in SSc skin [33].…”

Section: Systemic Sclerosis Angiogenic Receptor Dysregulationmentioning

confidence: 99%

Angiogenesis and Vasculopathy in Systemic Sclerosis: Evolving Concepts

Rabquer

Koch

2011

Curr Rheumatol Rep

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Systemic sclerosis (scleroderma [SSc]) is a multifactorial disease characterized by inflammation, extensive and progressive fibrosis, and multiple vasculopathies. The vascular manifestations can be seen early in the pathogenesis of the disease and include malformed capillaries, Raynaud's phenomenon, and digital ulcers. As the disease progresses, the vasculopathy proceeds to significant clinical manifestations, including renal crisis and pulmonary arterial hypertension. Moreover, later stages of the disease are marked by increasingly avascular areas. Despite the obliteration of microvascular structures, compensatory vasculogenesis and angiogenesis do not occur normally. This is in spite of a general increase in many potent angiogenic factors. Recent studies are beginning to examine this paradox and subsequent paucity of an angiogenic response in SSc. In this review, we discuss these findings and examine the role that chemokine and growth factor receptors, proteases, adhesion molecules, and transcription factors play in the dysregulation of angiogenesis in SSc.

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Junctional adhesion molecule-A is abnormally expressed in diffuse cutaneous systemic sclerosis skin and mediates myeloid cell adhesion

Cited by 20 publications

References 22 publications

Evaluation of Soluble Junctional Adhesion Molecule-A as a Biomarker of Human Brain Endothelial Barrier Breakdown

Evaluation of Soluble Junctional Adhesion Molecule-A as a Biomarker of Human Brain Endothelial Barrier Breakdown

Junctional Adhesion Molecules (JAMs) - New Players in Breast Cancer?

Angiogenesis and Vasculopathy in Systemic Sclerosis: Evolving Concepts

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