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Involvement of heat shock proteins on Mn-induced toxicity in Caenorhabditis elegans
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Involvement of heat shock proteins on Mn-induced toxicity in Caenorhabditis elegans
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Journal Article
Involvement of heat shock proteins on Mn-induced toxicity in Caenorhabditis elegans
2016
Overview
Background
All living cells display a rapid molecular response to adverse environmental conditions, and the heat shock protein family reflects one such example. Hence, failing to activate heat shock proteins can impair the cellular response. In the present study, we evaluated whether the loss of different isoforms of heat shock protein (
hsp
) genes in
Caenorhabditis elegans
would affect their vulnerability to Manganese (Mn) toxicity.
Methods
We exposed wild type and selected
hsp
mutant worms to Mn (30 min) and next evaluated further the most susceptible strains. We analyzed survival, protein carbonylation (as a marker of oxidative stress) and Parkinson’s disease related gene expression immediately after Mn exposure. Lastly, we observed dopaminergic neurons in wild type worms and in
hsp-70
mutants following Mn treatment. Analysis of the data was performed by one-way or two way ANOVA, depending on the case, followed by post-hoc Bonferroni test if the overall
p
value was less than 0.05.
Results
We verified that the loss of
hsp-70, hsp-3 and chn-1
increased the vulnerability to Mn, as exposed mutant worms showed lower survival rate and increased protein oxidation. The importance of
hsp-70
against Mn toxicity was then corroborated in dopaminergic neurons, where Mn neurotoxicity was aggravated. The lack of
hsp-70
also blocked the transcriptional upregulation of
pink1
, a gene that has been linked to Parkinson’s disease.
Conclusions
Taken together, our data suggest that Mn exposure modulates heat shock protein expression, particularly HSP-70, in
C. elegans
. Furthermore, loss of
hsp-70
increases protein oxidation and dopaminergic neuronal degeneration following manganese exposure, which is associated with the inhibition of
pink1
increased expression, thus potentially exacerbating the vulnerability to this metal.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V
Subject
/ Animals, Genetically Modified
/ Biomedical and Life Sciences
/ Caenorhabditis elegans Proteins - antagonists & inhibitors
/ Caenorhabditis elegans Proteins - biosynthesis
/ Caenorhabditis elegans Proteins - genetics
/ Dopamine
/ Dose-Response Relationship, Drug
/ Exposure
/ Genes
/ Heat-Shock Proteins - antagonists & inhibitors
/ Heat-Shock Proteins - biosynthesis
/ Heat-Shock Proteins - genetics
/ Isoforms
/ Mammals
/ Mutants
/ Mutation
/ Neurons
/ Oxidative Stress - drug effects
/ Oxidative Stress - physiology
/ Proteins
/ PTEN-induced putative kinase
/ Survival
/ Toxicity
