Selected Publication:
SHR
Neuro
Cancer
Cardio
Lipid
Metab
Microb
Paltauf-Doburzynska, J; Malli, R; Graier, WF. 
Hyperglycemic conditions affect shape and Ca2+ homeostasis of mitochondria in endothelial cells.
J CARDIOVASC PHARMACOL. 2004; 44(4): 423-436. 
 Doi: 10.1097%2F01.fjc.0000139449.64337.1b
 [OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
Google Scholar
 
- Leading authors Med Uni Graz
 
- 
Graier Wolfgang
 
- Co-authors Med Uni Graz
 
- 
Malli Roland
 
-  Altmetrics: 
 
-  Dimensions Citations: 
 
-  Plum Analytics: 
 
-  Scite (citation analytics): 
 
- Abstract:
 
- In this study the contribution of alternating architecture and Ca2+ handling of mitochondria to cytosolic Ca2+ homeostasis was elucidated under normoglycemic and hyperglycemic (HGC) conditions in the human endothelial cell line EA.hy926. Exposure of endothelial cells to hyperglycemic medium elevated basal cytosolic free Ca2+ concentration ([Ca2+]cyto), the histamine-initiated cytosolic Ca2+ signaling, and the mitochondrial Ca2+ content after cell stimulation. The latter was possibly due to the prolonged mitochondrial Ca2+ elevation in response to agonists found in HGC-pretreated cells. Moreover, under HGC mitochondrial free radical production was increased and mitochondrial shape changed from a mainly tubular, highly interconnected network toward multiple, isolated singular structures. Such changes could not be correlated with HGC-induced alterations of cytosolic Ca2+ signaling that became normalized with antimycin A, an inhibitor of the respiratory chain. These data suggest that although mitochondrial structure changes considerably during HGC, alterations in cytosolic Ca2+ signaling are more likely due to the enhanced energy status/metabolism of the mitochondria. On the other hand, in normoglycemic cells of unforced fragmentation of mitochondria yielded elevated basal [Ca2+]cyto, while the global Ca2+ signaling in response to histamine remained unchanged. Thus, mitochondrial architecture (ie, tubular versus fragmented structure) per se does not have a detectable impact on agonist-initiated global cytosolic Ca2+ signaling, while this organelle represents an early target in hyperglycemia leading to alterations in cytosolic Ca2+ signaling.
 
- Find related publications in this database (using NLM MeSH Indexing)
 
- 
Calcium - metabolism 
 
- 
Calcium Signaling - metabolism 
 
- 
Cell Line - metabolism 
 
- 
Cytosol - metabolism 
 
- 
Endothelial Cells - ultrastructure 
 
- 
Endothelium, Vascular - ultrastructure 
 
- 
Free Radicals - metabolism 
 
- 
Homeostasis - metabolism 
 
- 
Humans - metabolism 
 
- 
Hyperglycemia - pathology 
 
- 
Mitochondria - metabolism 
 
- 
Signal Transduction - metabolism 
 
- 
Time Factors - metabolism
 
- Find related publications in this database (Keywords)
 
- 
endothelial Ca2+
 
- 
mitochondrial Ca2+ homeostasis
 
- 
diabetes
 
- 
histamine
 
- 
ratiometric pericam-mt