ArticleEnvironmental health perspectives2002
Expression of hsp 27, hsp 60, hsc 70, and hsp 70 stress response genes in cultured human urothelial cells (UROtsa) exposed to lethal and sublethal concentrations of sodium arsenite.
Article in Environmental health perspectives, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 59 citations in OpenAlex.
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- Disruption of canonical TGFβ-signaling in murine coronary progenitor cells by low level arsenic.Toxicology and applied pharmacology · 2013Article
- Protective effects of the nuclear factor kappa B inhibitor pyrrolidine dithiocarbamate in bladder ischemia-reperfusion injury in rats.Molecular biology reports · 2013Article
- Azacytidine induces necrosis of multiple myeloma cells through oxidative stress.Proteome science · 2013Article
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- Induction of DNA damage in human urothelial cells by the brominated flame retardant 2,2-bis(bromomethyl)-1,3-propanediol: role of oxidative stress.Toxicology · 2011Article
- Arsenic, cadmium and neuron specific enolase (ENO2, γ-enolase) expression in breast cancer.Cancer cell international · 2011Article
- Novel role of mitochondrial matrix metalloproteinase-2 in the development of diabetic retinopathy.Investigative ophthalmology & visual science · 2011Article
- A novel cell permeant peptide inhibitor of MAPKAP kinase II inhibits intimal hyperplasia in a human saphenous vein organ culture model.Journal of vascular surgery · 2010Article
- Absence of Metallothionein 3 Expression in Breast Cancer is a Rare, But Favorable Marker of Outcome that is Under Epigenetic Control.Toxicological and environmental chemistry · 2010Article
- Article
- Glutathione protects cells against arsenite-induced toxicity.Free radical biology & medicine · 2007Article
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6 authors at 1 institution in 1 country.
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Abstract
The stress response is one mechanism that the bladder urothelium could potentially employ to protect itself from cellular damage after exposure to arsenic and, in so doing, influence the shape of the dose-response curve at low concentrations of exposure to this environmental pollutant. In the present study, we used the cultured human urothelial cell line UROtsa, a model of human urothelium, to determine the expression of heat shock proteins hsp 27, hsp 60, hsc 70, and hsp 70 after acute and extended exposure of the cells to lethal and sublethal levels of sodium arsenite (NaAsO2). Acute exposure was modeled by exposing confluent cultures of UROtsa cells to 100 micro M NaAsO2 for 4 hr followed by a 48-hr recovery period. Extended exposure was modeled by exposing confluent UROtsa cells to 1, 4, and 8 micro M NaAsO2 for 16 days, with the highest concentration producing cell death by 4 days of exposure. The expression of hsp 27, hsp 60, hsc 70, and hsp 70 mRNA and protein was determined by reverse-transcription polymerase chain reaction and Western analysis. Cell viability was determined by the MTT [(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. The results demonstrated that the expression of hsp 27, hsp 60, and hsc 70 mRNA and protein were not consistently increased by either acute or extended exposure to NaAsO2. In contrast, hsp 70 expression was induced by NaAsO2 after both acute and extended exposure. The degree and duration of the induction of the hsp 70 protein in the extended time course of exposure to NaAsO2 correlated directly with UROtsa cell cytotoxicity. The substantial level of basal expression of hsp 27, hsp 60, and hsc 70 shown previously in human bladder urothelium, coupled with the inducible expression of hsp 70, could provide the human urothelium with a mechanism to withstand and recover from a low level of arsenite exposure.
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