Title page for etd-0127111-002704


[Back to Results | New Search]

URN etd-0127111-002704
Author Jeng-yu Tsai
Author's Email Address jengyutsai@yahoo.com
Statistics This thesis had been viewed 5091 times. Download 683 times.
Department Biological Sciences
Year 2010
Semester 1
Degree Ph.D.
Type of Document
Language zh-TW.Big5 Chinese
Title The Effect of Capsazepine and Nonylphenol on Calcium Signaling and Viability in MDCK Renal Tubular Cells
Date of Defense 2011-01-14
Page Count 163
Keyword
  • fura-2
  • MDCK
  • thapsigargin
  • nonylphenol
  • capsazepine
  • Ca2+
  • Abstract The effect of capsazepine and nonylphenol on cytosolic free Ca2+ concentrations ([Ca2+]i) in MDCK renal tubular cells is unclear. This study explored whether capsazepine and nonylphenol changed basal [Ca2+]i levels in suspended MDCK cells by using fura-2 as a Ca2+-selective fluorescent dye. Capsazepine at concentrations between 10 and 200 microM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partially by 40% after removing extracellular Ca2+. Capsazepine induced Mn2+ quench of fura-2 fluorescence, indirectly implicating Ca2+ entry. Capsazepine-induced Ca2+ influx was not changed by L-type Ca2+ entry inhibitors and protein kinase C modulators [phorbol 12-myristate 13-acetate (PMA) and GF109203X]. In Ca2+-free medium, 100microM capsazepine-induced Ca2+ release was substantially suppressed by pretreatment with thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Pretreatment with capsazepine nearly abolished thapsigargin-induced Ca2+ release.
    Nonylphenol also increased [Ca2+]i in a concentration- dependent manner like capsazepine does. Similar response in [Ca2+]i rise can be found by inhibition of phospholipase C and using thapsigargin. Different from capasazpine, the [Ca2+]i rise was inhibited by PMA. At concentrations between 5 and 100microM, nonylphenol killed cells in a concentration-dependent manner.
    Collectively, in MDCK cells, capsazepine induced [Ca2+]i rises by causing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via non-L-type Ca2+ channels. Nonylphenol induced [Ca2+]i increase in MDCK cells via evoking Ca2+ entry through protein kinase C-regulated Ca2+ channels, and releasing Ca2+ from endoplasmic reticulum and other cellular storage in a phospholipase C-independent manner.
    Advisory Committee
  • Ying-Huei Lee - chair
  • Tony Wu - co-chair
  • Chen-fu Shaw - co-chair
  • Chung-ren Jan - advisor
  • David Chao - advisor
  • Files
  • etd-0127111-002704.pdf
  • indicate access worldwide
    Date of Submission 2011-01-27

    [Back to Results | New Search]


    Browse | Search All Available ETDs

    If you have more questions or technical problems, please contact eThesys