Low intensity shear stress increases endothelial ELR+ CXC chemokine production via a focal adhesion kinase-p38β MAPK-NF-κB pathway

Sadiq S. Shaik, Thomas D. Soltau, Gaurav Chaturvedi, Balagangadhar Totapally, James S. Hagood, William W. Andrews, Mohammad Athar, Nikolai N. Voitenok, Cheryl R. Killingsworth, Rakesh P. Patel, Michael B. Fallon, Akhil Maheshwari

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


CXC chemokines with a glutamate-leucine-arginine (ELR) tripeptide motif (ELR+ CXC chemokines) play an important role in leukocyte trafficking into the tissues. For reasons that are not well elucidated, circulating leukocytes are recruited into the tissues mainly in small vessels such as capillaries and venules. Because ELR+ CXC chemokines are important mediators of endothelial-leukocyte interaction, we compared chemokine expression by microvascular and aortic endothelium to investigate whether differences in chemokine expression by various endothelial types could, at least partially, explain the microvascular localization of endothelial-leukocyte interaction. Both in vitro and in vivo models indicate that ELR+ CXC chemokine expression is higher in microvascular endothelium than in aortic endothelial cells. These differences can be explained on the basis of the preferential activation of endothelial chemokine production by low intensity shear stress. Low shear activated endothelial ELR+ CXC chemokine production via cell surface heparan sulfates, β 3-integrins, focal adhesion kinase, the mitogen-activated protein kinase p38β, mitogen- and stress-associated protein kinase-1, and the transcription factor.

Original languageEnglish (US)
Pages (from-to)5945-5955
Number of pages11
JournalJournal of Biological Chemistry
Issue number9
StatePublished - Feb 27 2009
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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