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Regulated release a...
Regulated release and functional modulation of junctional adhesion molecule A by disintegrin metalloproteinases
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Koenen, RR (författare)
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Pruessmeyer, J (författare)
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- Soehnlein, O (författare)
- Karolinska Institutet
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Fraemohs, L (författare)
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Zernecke, A (författare)
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Schwarz, N (författare)
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Reiss, K (författare)
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Sarabi, A (författare)
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- Lindbom, L (författare)
- Karolinska Institutet
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Hackeng, TM (författare)
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Weber, C (författare)
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Ludwig, A (författare)
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(creator_code:org_t)
- American Society of Hematology, 2009
- 2009
- Engelska.
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Ingår i: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 113:19, s. 4799-4809
- Relaterad länk:
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http://kipublication...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Junctional adhesion molecule A (JAM-A) is a transmembrane adhesive glycoprotein that participates in the organization of endothelial tight junctions and contributes to leukocyte transendothelial migration. We demonstrate here that cultured endothelial cells not only express a cellular 43-kDa variant of JAM-A but also release considerable amounts of a 33-kDa soluble JAM-A variant. This release is enhanced by treatment with proinflammatory cytokines and is associated with the down-regulation of surface JAM-A. Inhibition experiments, loss/gain-of-function experiments, and cleavage experiments with recombinant proteases indicated that cleavage of JAM-A is mediated predominantly by the disintegrin and metalloproteinase (ADAM) 17 and, to a lesser extent, by ADAM10. Cytokine treatment of mice increased JAM-A serum level and in excised murine aortas increased ADAM10/17 activity correlated with enhanced JAM-A release. Functionally, soluble JAM-A blocked migration of cultured endothelial cells, reduced transendothelial migration of isolated neutrophils in vitro, and decreased neutrophil infiltration in a murine air pouch model by LFA-1– and JAM-A–dependent mechanisms. Therefore, shedding of JAM-A by inflamed vascular endothelium via ADAM17 and ADAM10 may not only generate a biomarker for vascular inflammation but could also be instrumental in controlling JAM-A functions in the molecular zipper guiding transendothelial diapedesis of leukocytes.
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Blood
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- Av författaren/redakt...
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Koenen, RR
-
Pruessmeyer, J
-
Soehnlein, O
-
Fraemohs, L
-
Zernecke, A
-
Schwarz, N
-
visa fler...
-
Reiss, K
-
Sarabi, A
-
Lindbom, L
-
Hackeng, TM
-
Weber, C
-
Ludwig, A
-
visa färre...
- Artiklar i publikationen
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Blood
- Av lärosätet
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Karolinska Institutet