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Lyn- and ERK-mediated vs. Ca2+ -mediated neutrophil O responses with thermal injury.

Authors: Fazal, N  Al-Ghoul, WM  Schmidt, MJ  Choudhry, MA  Sayeed, MM 
Citation: Fazal N, etal., Am J Physiol Cell Physiol. 2002 Nov;283(5):C1469-79.
Pubmed: (View Article at PubMed) PMID:12372808
DOI: Full-text: DOI:10.1152/ajpcell.00114.2002

We evaluated the dependency of neutrophil O production on PTK-Lyn and MAPK-ERK1/2 in rats after thermal injury. Activation of PTK-Lyn was assessed by immunoprecipitation. Phosphorylation of ERK1/2 was assessed by Western blot analysis. O production was measured by isoluminol-enhanced luminometry. Imaging technique was employed to measure neutrophil [Ca2+](i) in individual cells. Thermal injury caused marked upregulation of Lyn and ERK1/2 accompanying enhanced neutrophil O production. Treatment of rats with PTK blocker (AG556) or MAPK blocker (AG1478) before burn injury caused complete inhibition of the respective kinase activation. Both AG556 and AG1478 produced an ~66% inhibition in O production. Treatment with diltiazem (DZ) produced an ~37% inhibition of O production without affecting Lyn or ERK1/2 activation with burn injury. Ca2+ mobilization was upregulated with burn injury but not affected by treatment of burn rats with AG556. Unlike the partial inhibition of burn-induced O production by AG556, AG1478, or DZ, platelet-activating factor antagonist (PAFa) treatment of burn rats produced near complete inhibition of O production. PAFa treatment also blocked activation of Lyn. The findings suggest that the near complete inhibition of O production by PAFa was a result of blockade of PTK as well as Ca2+ signaling. Overall, our studies show that enhanced neutrophil O production after thermal injury is a result of potentiation of Ca2+ -linked and -independent signaling triggered by inflammatory agents such as PAF.


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CRRD Object Information
CRRD ID: 2303719
Created: 2009-02-23
Species: All species
Last Modified: 2009-02-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.