Stress Protein Gene Expression in Amphibians

Author(s):  
John J. Heikkila ◽  
Adnan Ali ◽  
Nick Ohan ◽  
Ying Tam
1999 ◽  
Vol 276 (4) ◽  
pp. R990-R996 ◽  
Author(s):  
Suzanne Currie ◽  
Bruce L. Tufts ◽  
Christopher D. Moyes

The physiological and biochemical signals that induce stress protein (HSP) synthesis remain conjectural. In this study, we used the nucleated red blood cells from rainbow trout, Oncorhynchus mykiss, to address the interaction between energy status and HSP gene expression. Heat shock (25°C) did not significantly affect ATP levels but resulted in an increase in HSP70 mRNA. Hypoxia alone did not induce HSPtranscription in these cells despite a significant depression in ATP. Inhibition of oxidative phosphorylation with azide, in the absence of thermal stress, decreased ATP by 56% and increased lactate production by 62% but did not induce HSP gene transcription. Inhibition of oxidative phosphorylation and glycolysis with azide and iodoacetic acid respectively, decreased ATP by 79% and prevented lactate production, but did not induce either HSP70 or HSP30 gene transcription in these cells. This study demonstrates that a reduction in the cellular energy status will not induce stress protein gene transcription in rainbow trout red blood cells and may, in fact, limit induction during extreme metabolic inhibition.


1990 ◽  
Vol 68 (12) ◽  
pp. 1428-1432 ◽  
Author(s):  
Craig L. J. Parfett ◽  
Katarzyna Brudzynski ◽  
Calvin Stiller

Using 78-kilodalton glucose-regulated protein cDNA as a probe of Northern blots, we have examined the distribution and inducibility of mRNA encoding the 78-kilodalton glucose-regulated protein in three tissues of nonobese diabetic mice. The gene was constitutively expressed in normal, unstressed cells of liver, brain, and spleen. Developing diabetes correlated with elevated expression in only liver and brain of diabetic mice. This induction of gene expression was associated with the transition from the prediabetic stage to the onset of hyperglycemia and coincided with falling levels of plasma insulin and rising hyperglycemia. The activation of 78-kilodalton glucose-regulated protein gene expression appeared to be transient. We suggest that the temporally differential, tissue-specific expression of this gene in adult nonobese diabetic mice offers an opportunity to study a physiologically relevant regulation of this stress-induced gene.Key words: stress protein, gene expression, diabetes, liver, brain.


2000 ◽  
Vol 245 (2) ◽  
pp. 265-276 ◽  
Author(s):  
Matthias Wiens ◽  
Mohammed S.A Ammar ◽  
Ahmed H Nawar ◽  
Claudia Koziol ◽  
Hamdy M.A Hassanein ◽  
...  

2004 ◽  
Vol 78 (10) ◽  
pp. 1479-1487 ◽  
Author(s):  
Anisha Patel ◽  
Marcel C. G. van de Poll ◽  
Jan W. M. Greve ◽  
Wim A. Buurman ◽  
Kenneth C. H. Fearon ◽  
...  

1990 ◽  
Vol 14 ◽  
pp. 185
Author(s):  
L SCHIAFFONATI ◽  
L TACCHINI ◽  
E RAPPOCCIOLO ◽  
G CAIRO ◽  
A BERNELLIZAZZERA

2010 ◽  
Vol 34 (8) ◽  
pp. S27-S27
Author(s):  
Jianqi Cui ◽  
Xiuying Pei ◽  
Qian Zhang ◽  
Bassel E. Sawaya ◽  
Xiaohong Lu ◽  
...  

1990 ◽  
Vol 265 (34) ◽  
pp. 21375-21380
Author(s):  
L Wood ◽  
M Mills ◽  
N Hatzenbuhler ◽  
G Vogeli

2021 ◽  
Vol 22 (3) ◽  
pp. 1068
Author(s):  
Katarzyna Dominika Kania ◽  
Waldemar Wagner ◽  
Łukasz Pułaski

Two immortalized brain microvascular endothelial cell lines (hCMEC/D3 and RBE4, of human and rat origin, respectively) were applied as an in vitro model of cellular elements of the blood–brain barrier in a nanotoxicological study. We evaluated the impact of CdSe/ZnS core-shell-type quantum dot nanoparticles on cellular homeostasis, using gold nanoparticles as a largely bioorthogonal control. While the investigated nanoparticles had surprisingly negligible acute cytotoxicity in the evaluated models, a multi-faceted study of barrier-related phenotypes and cell condition revealed a complex pattern of homeostasis disruption. Interestingly, some features of the paracellular barrier phenotype (transendothelial electrical resistance, tight junction protein gene expression) were improved by exposure to nanoparticles in a potential hormetic mechanism. However, mitochondrial potential and antioxidant defences largely collapsed under these conditions, paralleled by a strong pro-apoptotic shift in a significant proportion of cells (evidenced by apoptotic protein gene expression, chromosomal DNA fragmentation, and membrane phosphatidylserine exposure). Taken together, our results suggest a reactive oxygen species-mediated cellular mechanism of blood–brain barrier damage by quantum dots, which may be toxicologically significant in the face of increasing human exposure to this type of nanoparticles, both intended (in medical applications) and more often unintended (from consumer goods-derived environmental pollution).


2005 ◽  
Vol 567 (2) ◽  
pp. 401-413 ◽  
Author(s):  
Maria Toledo-Rodriguez ◽  
Philip Goodman ◽  
Milena Illic ◽  
Caizhi Wu ◽  
Henry Markram

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