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Altered de novo sphingolipid biosynthesis is involved in the serum deprivation-induced cell death in LLC-PK1 cells

Title
Altered de novo sphingolipid biosynthesis is involved in the serum deprivation-induced cell death in LLC-PK1 cells
Authors
Yu M.U.Jae M.Y.Youn S.L.Yong M.L.Jin T.H.Ki W.O.Song S.Yeo P.Y.Hwan S.Y.Oh S.
Ewha Authors
오세관
SCOPUS Author ID
오세관scopus
Issue Date
2004
Journal Title
Journal of Toxicology and Environmental Health - Part A
ISSN
1528-7394JCR Link
Citation
Journal of Toxicology and Environmental Health - Part A vol. 67, no. 23-24, pp. 2085 - 2094
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Conference Paper
Abstract
Fumonisin B 1, a specific inhibitor of ceramide synthase, and ISP1 (Myriocin), a serine palmitoyl-transferase inhibitor, modulate the de novo sphingolipid biosynthesis pathway. This study was conducted to determine whether serum deprivation-induced cell death is regulated by de novo sphingolipid biosynthesis in pig kidney LLC-PK1 cells. Serum withdrawal from the culture medium produced cell death in LLC-PK1 cells. Fumonisin B 1 at concentrations ranging from 5 M to 30 M delayed until 48 h this cell death resulting from the absence of fetal bovine serum (FBS) in cell culture. Pretreatment of cultured cells with fumonisin B 1 in the presence of serum for 24 h increased by approximately 70% this cytoprotective activity of fumonisin B 1 against serum deprivation-induced cell death. Serum deprivation increased sphingolipid biosynthesis threefold compared to 5% serum-enriched culture. Fumonisin B 1 at 5-30 M lowered the content of total complex sphingolipids to levels of 50% and 77% of the content in serum-enriched culture, although the concentration of intracellular free sphinganine was elevated. ISP1 alone at greater than 1 nM concentration reduced total complex sphingolipid content to values in LLC-PK1 cells grown in the presence of 5% FBS. The results suggest that the de novo complex sphingolipid biosynthesis modulated by either fumonisin B 1 or ISP1 may regulate serum deprivation-induced cell death in LLC-PK1 cells.
DOI
10.1080/15287390490515065
Appears in Collections:
의과대학 > 의학과 > Journal papers
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