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| HUMAN DERMAL MICROVASCULAR ENDOTHELIAL BUT NOT HUMAN UMBILICAL VEIN ENDOTHELIAL-CELLS EXPRESS CD36 INVIVO AND INVITRO |
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| Author(s): SWERLICK RA, LEE KH, WICK TM, LAWLEY TJ |
| Source: JOURNAL OF IMMUNOLOGY Volume: 148 Issue: 1 Pages: 78-83 Published: JAN 1 1992 |
| Times Cited: 196 References: 20 |
| Abstract: CD36 is an 88-kDa glycoprotein that has been identified on platelets, monocytes, and some endothelial cells. Experimental evidence suggests that CD36 mediates the binding of Plasmodium falciparum-infected RBC to a variety of cells, and therefore may play a role in the vascular complications associated with malaria. Additionally, CD36 may also bind the extracellular matrix proteins thrombospondin and collagen. Human umbilical vein endothelial cells have been used in in vitro models examining the binding of P.falciparum RBC to endothelial cells, but they do not consistently express cell surface CD36. Inasmuch as human dermal microvascular endothelial cells (HDMEC) differ in a variety of ways from large vessel endothelial cells, we have examined HDMEC for cell surface expression of CD36 in vivo and in vitro. Direct immunofluorescence of skin showed bright staining of HDMEC with antibody recognizing CD36 and flow cytometric analysis of cultured HDMEC revealed cell surface expression. In contrast, large vessel endothelial cells were not stained with antibody recognizing CD36 in vivo and cultured cells derived from umbilical vein failed to express cell surface CD36 in vitro. Western immunoblots of lysates of HDMEC but not human umbilical vein endothelial cells demonstrated an 88-kDa protein that comigrated with CD36 from platelets. Functional studies demonstrated that adherence of PRBC to HDMEC was inhibited up to 66% by mAb recognizing CD36. Furthermore, the expression of CD36 on HDMEC was increased in a dose- and time-dependent manner by IFN-gamma, and was decreased by protein kinase C agonists. These data demonstrate that HDMEC express functionally active CD36 and this expression can be positively and negatively regulated by soluble factors. This study demonstrates that HDMEC are useful in the study of CD36-mediated binding of PRBC to endothelial cells in vitro and provides further evidence of distinct phenotypic differences between HDMEC and large vessel endothelial cells. |
| Document Type: Article |
| Language: English |
| Reprint Address: SWERLICK, RA (reprint author), EMORY UNIV, SCH MED, DEPT DERMATOL, DRAWER SS, WMB5014, ATLANTA, GA 30322 USA |
Addresses:
1. GEORGIA INST TECHNOL, SCH CHEM ENGN, ATLANTA, GA 30332 USA
2. GEORGIA INST TECHNOL, BIOMECH LAB, ATLANTA, GA 30332 USA |
| Publisher: AMER ASSOC IMMUNOLOGISTS, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 |
| Subject Category: Immunology |
| IDS Number: GX162 |
| ISSN: 0022-1767 |
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