期刊
JOURNAL OF IMMUNOLOGY
卷 168, 期 5, 页码 2091-2095出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.168.5.2091
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资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL036003] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R37 HL 36003] Funding Source: Medline
- NIAMS NIH HHS [R01 AR 45766] Funding Source: Medline
Persistent E-selectin expression on human dermal microvascular endothelial cells (HDMEC), believed to mediate skin-specific T cell homing, results from a slow rate of surface protein internalization after cytokine induction. Following transduction of unactivated HDMEC with E-selectin cDNA, the rate of internalization was largely independent of increasing levels of surface protein expression, leading to prolonged t(1/2) values of over 4 h, comparable to that observed following cytokine induction. In HUVEC, the rate of internalization increased with surface expression level, leading to an essentially constant t(1/2) of under 2 h. Thus, the internalization process rather than cytokine responsiveness or E-selectin structure underlies the difference in endothelial cell behavior. Mutational analysis of the cytoplasmic region demonstrated a role for a di-leucine-type motif involving I588 and L589 but not for a putative tyrosine-type motif. Control of E-selectin surface expression appears to be phosphoserine dependent, since alanine but not aspartic acid substitution for S581 slows E-selectin internalization.
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