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Role of Vascular Endothelial Growth Factor-D (VEGF-D) on IL-6 Expression in Cerulein-Stimulated Pancreatic Acinar Cells

Authors
 JANGWON LEE  ;  KYUNG HWAN KIM  ;  HYEYOUNG KIM 
Citation
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.1095 : 129-133, 2007 
Journal Title
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
ISSN
 0077-8923 
Issue Date
2007
Abstract
Cerulein pancreatitis is similar to human edematous pancreatitis with dysregulation of the digestive enzyme production and cytoplasmic vacuolization, the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. Our preliminary proteomic analysis showed increased expression of vascular endothelial growth factor-D (VEGF-D) in cerulein (10−8M)-treated pancreatic acinar cells. We hypothesized that VEGF-D may have a role in cerulein-induced cytokine expression in pancreatic acinar cells. This article was designed to elucidate whether cerulein induces VEGF-D expression in pancreatic AR42J cells, and whether VEGF-D expression is related to interleukin-6 (IL-6) expression by transfecting antisense oligonucleotide (AS ODN) for VEGF-D into pancreatic acinar AR42J cells. Cerulein-induced AP-1 activation was monitored in the cells transfected with AS ODN or sense ODN (S ODN) for VEGF-D. mRNA expression of IL-6 was determined by RT-PCR analysis. AP-1 activation was assessed by electrophoretic mobility shift assay (EMSA). VEGF-D expression was assessed by Western blotting. Cerulein induced IL-6 expression and VEGF-D expression in AR42J cells. Cerulein-induced AP-1 activation and IL-6 expression was inhibited in the cells transfected with AS ODN for VEGF-D as compared to S ODN. Cerulein-induced VEGF-D expression may have a role in AP-1 activation and IL-6 expression in pancreatic acinar cells.
Full Text
http://onlinelibrary.wiley.com/doi/10.1196/annals.1397.016/abstract
DOI
10.1196/annals.1397.016
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Hwan(김경환)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/95630
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