Decay-accelerating factor is present on cultured human umbilical vein endothelial cells

doi:10.1084/jem.163.1.221

This Article

	Full Text (PDF)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JEM
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by Asch, A. S.
	Articles by Nussenzweig, V.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Asch, A. S.
	Articles by Nussenzweig, V.


Social Bookmarking

	What's this?

ARTICLES

Decay-accelerating factor is present on cultured human umbilical vein endothelial cells

AS Asch, T Kinoshita, EA Jaffe and V Nussenzweig

Decay-accelerating factor (DAF) has been previously described only in cells of bone marrow origin where it serves as a negative modulator of complement activation. Using mAb against human DAF, we demonstrated the presence of DAF in human umbilical vein endothelial cells by immunofluorescence microscopy and flow cytometry. By means of an immunoradiometric assay we detected an average of 3.3 X 10(5) molecules of DAF on each cell. When immunoisolates were analyzed in Western blots, endothelial cell DAF comigrated with DAF purified from normal erythrocytes. DAF was synthesized by the endothelial cells since 35S- labeled DAF could be immunoisolated from HUVEC cultured in medium containing [35S]methionine. This is the first evidence for the presence of DAF in cells of extra-marrow origin. DAF may protect endothelial cells from complement-mediated injury.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Add to Reddit Reddit Add to Technorati Technorati What's this?

This article has been cited by other articles:

Lin, F., Spencer, D., Hatala, D. A., Levine, A. D., Medof, M. E. (2004). Decay-Accelerating Factor Deficiency Increases Susceptibility to Dextran Sulfate Sodium-Induced Colitis: Role for Complement in Inflammatory Bowel Disease. J. Immunol. 172: 3836-3841 [Abstract] [Full Text]
Mason, J. C., Yarwood, H., Sugars, K., Morgan, B. P., Davies, K. A., Haskard, D. O. (1999). Induction of Decay-Accelerating Factor by Cytokines or the Membrane-Attack Complex Protects Vascular Endothelial Cells Against Complement Deposition. Blood 94: 1673-1682 [Abstract] [Full Text]
Cines, D. B., Pollak, E. S., Buck, C. A., Loscalzo, J., Zimmerman, G. A., McEver, R. P., Pober, J. S., Wick, T. M., Konkle, B. A., Schwartz, B. S., Barnathan, E. S., McCrae, K. R., Hug, B. A., Schmidt, A.-M., Stern, D. M. (1998). Endothelial Cells in Physiology and in the Pathophysiology of Vascular Disorders. Blood 91: 3527-3561 [Full Text]
Wang, G., Nonaka, M., He, C., Okada, N., Nakashima, I., Okada, H. (1998). Functional Differences Among Multiple Isoforms of Guinea Pig Decay-Accelerating Factor. J. Immunol. 160: 3014-3022 [Abstract] [Full Text]
Davitz, M., Hereld, D, Shak, S, Krakow, J, Englund, P., Nussenzweig, V (1987). A glycan-phosphatidylinositol-specific phospholipase D in human serum. Science 238: 81-84 [Abstract]
Mason, J. C., Lidington, E. A., Ahmad, S. R., Haskard, D. O. (2002). bFGF and VEGF synergistically enhance endothelial cytoprotection via decay-accelerating factor induction. Am. J. Physiol. Cell Physiol. 282: C578-C587 [Abstract] [Full Text]