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Selectin E (endothelial adhesion molecule 1)

PDB rendering based on 1esl.
Available structures
1esl, 1g1t
Identifiers
Symbols SELE; CD62E; ELAM; ELAM1; ESEL; LECAM2
External IDs OMIM131210 MGI98278 HomoloGene389 GeneCards: SELE Gene
RNA expression pattern
PBB GE SELE 206211 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 6401 20339
Ensembl ENSG00000007908 ENSMUSG00000026582
UniProt P16581 Q3U5F6
RefSeq (mRNA) NM_000450 NM_011345
RefSeq (protein) NP_000441 NP_035475
Location (UCSC) Chr 1:
167.96 - 167.97 Mb
Chr 1:
165.88 - 165.89 Mb
PubMed search [1] [2]

E-selectin, also known as CD62E, is a cell adhesion molecule expressed only on endothelial cells activated by cytokines. Like other selectins, it plays an important part in inflammation. In humans, E-selectin is encoded by the SELE gene.[1]

Contents

Ligands

E-selectin recognizes and binds to sialylated carbohydrates present on the surface proteins of certain leukocytes. These carbohydrates include members of the Lewis X and Lewis A families found on monocytes, granulocytes, and T-lymphocytes.[2]

Function

During inflammation, E-selectin plays an important part in recruiting leukocytes to the site of injury. The local release of cytokines IL-1 and TNF by damaged cells induces the over-expression of E-selectin on endothelial cells of nearby blood vessels.[2] Leukocytes in the blood expressing the correct ligand will bind with low affinity to E-selectin, causing the leukocytes to "roll" along the internal surface of the blood vessel as temporary interactions are made and broken.

As the inflammatory response progresses, chemokines released by injured tissue enter the blood vessels and activate the rolling leukocytes, which are now able to tightly bind to the endothelial surface and begin making their way into the tissue.[2]

P-selectin has a similar function, but is expressed on the endothelial cell surface within minutes as it is stored within the cell rather than produced on demand.[2]

Pathological relevance

In cases of elevated blood glucose levels, such as in sepsis, E-selectin expression is higher than normal, resulting in greater microvascular permeability. The greater permeability leads to edema of the skeletal endothelium, resulting in skeletal muscle ischemia and eventually necrosis. This underlying pathology is the cause of the symptomatic disease critical illness polyneuromyopathy (CIPNM).[3] Traditional Chinese herbal medicines, like berberine downregulate E-selectin.[4]

References

  1. ^ Collins T, Williams A, Johnston GI, Kim J, Eddy R, Shows T, Gimbrone MA, Bevilacqua MP (February 1991). "Structure and chromosomal location of the gene for endothelial-leukocyte adhesion molecule 1". J. Biol. Chem. 266 (4): 2466–73. PMID 1703529.  
  2. ^ a b c d Cotran; Kumar, Collins. Robbins Pathologic Basis of Disease. Philadelphia: W.B Saunders Company. ISBN 0-7216-7335-X.  
  3. ^ Visser LH (November 2006). "Critical illness polyneuropathy and myopathy: clinical features, risk factors and prognosis". Eur. J. Neurol. 13 (11): 1203–12. doi:10.1111/j.1468-1331.2006.01498.x. PMID 17038033.  
  4. ^ Hu Y, Chen X, Duan H, et al. (Oct 2009) "Chinese herbal medicinal ingredients inhibit secretion of IL-6, IL-8, E-selectin and TXB2 in LPS-induced rat intestinal microvascular endothelial cells." Immunopharmacol Immunotoxicol. 2009;31(4):550-5. Summary

Further reading

External links

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