PMID- 15880446
OWN - NLM
STAT- MEDLINE
DCOM- 20051104
LR  - 20131121
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 205
IP  - 1
DP  - 2005 Oct
TI  - Effect of selenium-supplement on the calcium signaling in human endothelial 
      cells.
PG  - 97-106
AB  - Intracellular Ca2+ signaling controls many cellular functions. Understanding its 
      regulation by selenoproteins is essential for understanding the role of 
      selenoproteins in regulating cell functions. The activity of thioredoxin 
      reductase (TrxR), thioredoxin (Trx) content, and the activity of glutathione 
      peroxidase (GPx) in the human endothelial cells cultured in selenium-supplemented 
      medium (refer as Se+ cells) was found 70%, 40%, and 20% higher, respectively than 
      those in the cells cultured in normal medium (refer as Se0 cells). The 
      intracellular Ca2+ signaling initiated by inositol 1,4,5-trisphosphate (IP3), 
      histamine, thapsigargin (TG), carbonyl cyanide p-(tri-fluoromethoxy) 
      phenyl-hydrazone (FCCP), and cyclosporin A (CsA) was investigated in both Se+ and 
      Se0 cells. It was interestingly found that the higher activity of selenoproteins 
      reduced the sensitivity of IP3 receptor to the IP3-triggered Ca2+ release from 
      intracellular stores, but enhanced activation of the receptor-coupled 
      phospholipase C in histamine-stimulated Se+ cells by showing much more generation 
      of IP3 and higher elevation of cytosolic Ca2+. The higher selenoprotein activity 
      also reduced susceptibility of the uniporter to the mitochondrial uncoupler, 
      susceptibility of the permeability transition pore (PTP) to its inhibitor, and 
      the vulnerability of endoplasmic reticulum (ER) Ca2+-ATPase to its inhibitor in 
      selenium-supplementing cells. The results suggest that cell calcium signaling is 
      subjected to thiol-redox regulation by selenoproteins.
FAU - Zheng, Yi
AU  - Zheng Y
AD  - Institute of Biophysics, Chinese Academy of Science, Beijing, China.
FAU - Zhong, Liangwei
AU  - Zhong L
FAU - Shen, Xun
AU  - Shen X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Calcium Channels)
RN  - 0 (ITPR1 protein, human)
RN  - 0 (Inositol 1,4,5-Trisphosphate Receptors)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Triglycerides)
RN  - 370-86-5 (Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone)
RN  - 52500-60-4 (Thioredoxins)
RN  - 820484N8I3 (Histamine)
RN  - 83HN0GTJ6D (Cyclosporine)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.8.1.9 (Thioredoxin-Disulfide Reductase)
RN  - H6241UJ22B (Selenium)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/metabolism
MH  - Calcium Channels/metabolism
MH  - Calcium Signaling/*drug effects
MH  - Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone/pharmacology
MH  - Cell Line
MH  - Cell Proliferation/drug effects
MH  - Cyclosporine/pharmacology
MH  - Endothelial Cells/*drug effects/*metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Histamine/pharmacology
MH  - Humans
MH  - Inositol 1,4,5-Trisphosphate/metabolism
MH  - Inositol 1,4,5-Trisphosphate Receptors
MH  - Mitochondria/drug effects/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/metabolism
MH  - Selenium/*pharmacology
MH  - Thioredoxin-Disulfide Reductase/metabolism
MH  - Thioredoxins/metabolism
MH  - Triglycerides/metabolism
EDAT- 2005/05/10 09:00
MHDA- 2005/11/05 09:00
CRDT- 2005/05/10 09:00
PHST- 2005/05/10 09:00 [pubmed]
PHST- 2005/11/05 09:00 [medline]
PHST- 2005/05/10 09:00 [entrez]
AID - 10.1002/jcp.20378 [doi]
PST - ppublish
SO  - J Cell Physiol. 2005 Oct;205(1):97-106. doi: 10.1002/jcp.20378.