ArticleCell stress & chaperones2009
Modulation of ASK1 expression during overexpression of Trx and HSP70 in stressed fish liver mitochondria.
Article in Cell stress & chaperones, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Does Predation Exacerbate the Risk of Endosymbiont Loss in Heat Stressed Hermatypic Corals? Molecular Cues Provide Insights Into Species-Specific Health Outcomes in a Multi-Stressor Ocean.Frontiers in physiology · 2022Article
- Differential regulation of pro- and antiapoptotic proteins in fish adipocytes during hypoxic conditions.Fish physiology and biochemistry · 2016Article
- Mitochondrial HSP70 cognate-mediated differential expression of JNK1/2 in the pollution stressed grey mullets, Mugil cephalus.Fish physiology and biochemistry · 2012Article
- Cynoglossus semilaevis thioredoxin: a reductase and an antioxidant with immunostimulatory property.Cell stress & chaperones · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial heat shock protein 70 (mtHSP70) is found to play a primary role in cellular defense against physiological stress like exposure to environmental contaminants and helpful in the maintenance of cellular homeostasis by promoting the cell survival. In the present investigation, the environmental-stress-induced increase in mtHSP70 levels along with the quantification of apoptosis signal regulating kinase 1 (ASK1) and thioredoxin (Trx) were measured in the liver mitochondria of grey mullets (Mugil cephalus) collected from the polluted Ennore estuary and the unpolluted Kovalam estuary for a period of 2 years. The results showed elevated lipid peroxide (LPO) and decreased total antioxidant capacity along with the decrease in mitochondrial viability percentage. Mitochondrial HSP70, ASK1, and Trx levels were increased under this stress condition. A 42% increase in LPO levels and 18% decrease in mitochondrial survivality were observed in the polluted-site fish liver mitochondria when compared to the results of unpolluted estuary. We also report that, under observed oxidative stress condition in Ennore fish samples, the ASK1 levels are only moderately elevated (13% increase). This may be due to mitochondrial-HSP70-induced adaptive tolerance signaling for the activation of Trx (22% increase) which suppresses the ASK1 expression thereby promoting the cell survival that leads to the maintenance of the cellular homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.