BROWSE

Related Researcher

Author's Photo

Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

ITEM VIEW & DOWNLOAD

Hydrogen Peroxide-Induced VCAM-1 Expression in Pancreatic Islets and beta-Cells Through Extracellular Ca2+ Influx

Cited 4 times inthomson ciCited 4 times inthomson ci
Title
Hydrogen Peroxide-Induced VCAM-1 Expression in Pancreatic Islets and beta-Cells Through Extracellular Ca2+ Influx
Author
Lee, SukmookHa, In SuKim, Jae HyeonPark, Kyong SooHan, Kyu HyunKim, Sun-HeeChae, Young ChanKim, Sun HeeKim, Yun HeeSuh, Pann-GhillRyu, Sung HoKim, Jung-EunBang, KitaeHwang, Jong-IkYang, JaeseokPark, Kwang-WookChung, JunhoAhn, Curie
Issue Date
2008-11
Publisher
LIPPINCOTT WILLIAMS & WILKINS
Citation
TRANSPLANTATION, v.86, no.9, pp.1257 - 1266
Abstract
Background. The use of porcine islets as alternatives to transplantable human islets is hampered by xenotransplant rejection. To identify molecular mechanisms that would allow subversion of xenoislet rejection, we investigated the role of H2O2 in vascular cell adhesion molecule-1 (VCAM-1) expression by porcine and mouse islets and beta-cell lines. Methods. Porcine islets were treated with H2O2, tumor necrosis factor alpha, interferon-gamma, interleukin-1 beta, and lipopolysaccharide, to assess the effects of inflammatory stimulators on VCAM-1 expression using flow cytometry. The role of Ca2+ in H2O2-induced VCAM-1 expression was investigated in beta-cell lines using an extracellular Ca2+ chelator and Ca2+-depleted media. Furthermore, H2O2-induced VCAM-1 expression was measured in beta-cells, pretreated with inhibitors of protein kinase C, phospholipase D, and phosphatidylinositol-3 kinase/Akt. Finally, H2O2-induced VCAM-1 expression was evaluated in porcine islets and rodent beta-cell lines infected with an adenovirus encoding catalase, a H2O2-removing enzyme. Results. H2O2 was most potent inflammatory stimulator of VCAM-1 expression in porcine islets and had the greatest effect on VCAM-1 expression by beta-cells. Signaling pathway analysis demonstrated that extracellular Ca2+ influx was critical to H2O2-mediated VCAM-1 expression; however, protein kinase C, phospholipase D, and phosphatidylinositol-3 kinase/Akt activation were not required for VCAM-1 expression. Finally, catalase overexpression inhibited H2O2-induced VCAM-1 expression by islets and beta-cell lines. Conclusion. An extracellular calcium-dependent H2O2 pathway is the critical mediator of VCAM-1 expression by pancreatic islets and beta-cells. Inhibition of this pathway by catalase overexpression in donor islets can be exploited to protect against xenoislet immune responses.
URI
https://scholarworks.unist.ac.kr/handle/201301/10096
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=58149149955
DOI
10.1097/TP.0b013e318188ab04
ISSN
0041-1337
Appears in Collections:
BIO_Journal Papers
Files in This Item:
There are no files associated with this item.

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show full item record

qrcode

  • mendeley

    citeulike

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

MENU