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Low dose cadmium poisoning results in sustained ERK phosphorylation and caspase activation
Cadmium poisoning has been known to result in a wide variety of cellular responses, including oxidative stress and kinase activation. It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyz...
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Published in: | Biochemical and biophysical research communications 2006-11, Vol.350 (3), p.803-807 |
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creator | Martin, Patrick Poggi, Marie Christine Chambard, Jean Claude Boulukos, Kim E. Pognonec, Philippe |
description | Cadmium poisoning has been known to result in a wide variety of cellular responses, including oxidative stress and kinase activation. It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyzed different cell types for their responses to low concentrations of cadmium poisoning. We found that there is an association between cell susceptibility to cadmium toxicity and ERK activation. This activation is atypical, since it consists of a sustained ERK phosphorylation, that lasts up to 6 days post stimulation. This activation is associated with the appearance of cleaved caspases 8 and 3, processed PARP, and irreversible damage. Pharmacological inhibition of ERK phosphorylation results in the ability of cells to resist cadmium poisoning. Our data indicate that low cadmium concentrations result in an unconventional ERK sustained phosphorylation, which in turn leads to death signaling. |
doi_str_mv | 10.1016/j.bbrc.2006.09.126 |
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It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyzed different cell types for their responses to low concentrations of cadmium poisoning. We found that there is an association between cell susceptibility to cadmium toxicity and ERK activation. This activation is atypical, since it consists of a sustained ERK phosphorylation, that lasts up to 6 days post stimulation. This activation is associated with the appearance of cleaved caspases 8 and 3, processed PARP, and irreversible damage. Pharmacological inhibition of ERK phosphorylation results in the ability of cells to resist cadmium poisoning. 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It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyzed different cell types for their responses to low concentrations of cadmium poisoning. We found that there is an association between cell susceptibility to cadmium toxicity and ERK activation. This activation is atypical, since it consists of a sustained ERK phosphorylation, that lasts up to 6 days post stimulation. This activation is associated with the appearance of cleaved caspases 8 and 3, processed PARP, and irreversible damage. Pharmacological inhibition of ERK phosphorylation results in the ability of cells to resist cadmium poisoning. Our data indicate that low cadmium concentrations result in an unconventional ERK sustained phosphorylation, which in turn leads to death signaling.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Animals</subject><subject>APOPTOSIS</subject><subject>Apoptosis - drug effects</subject><subject>BIOLOGICAL STRESS</subject><subject>CADMIUM</subject><subject>Cadmium Poisoning - enzymology</subject><subject>Cadmium Poisoning - pathology</subject><subject>Caspase</subject><subject>Caspases - metabolism</subject><subject>Cell death</subject><subject>Cells, Cultured</subject><subject>DAMAGE</subject><subject>Dose-Response Relationship, Drug</subject><subject>DOSES</subject><subject>Enzyme Activation - drug effects</subject><subject>ERK</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>INHIBITION</subject><subject>LEAD</subject><subject>Osteoblasts - drug effects</subject><subject>Osteoblasts - enzymology</subject><subject>Osteoblasts - pathology</subject><subject>PHOSPHORYLATION</subject><subject>Phosphorylation - drug effects</subject><subject>POISONING</subject><subject>Rats</subject><subject>STIMULATION</subject><subject>Sustained activation</subject><subject>TOXICITY</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNp9kE1rFTEUhoMo9lr9Ay4kIHQ3Y04mmQ9wI6V-4IVCqSBuQr7G5jKTjEmmpf_eTO8Fdy4OgZPnvLw8CL0FUgOB9sOhVirqmhLS1mSogbbP0A7IQCoKhD1HO1J-KjrAzzP0KqUDIQCsHV6iM-gI7VrGd-jXPjxgE5LFWprZrTNegkvBO_8bR5vWKSfsPE5rytJ5a_DVzXe83IVUJj5OMrvgsfSmnKdFlhips7t_Wr9GL0Y5Jfvm9J6jH5-vbi-_VvvrL98uP-0rzaDJFW-M0q1WQ0d6ya020DBOOyBqtJ3UI-tpJ7uGD6NqKEDfc950RrW6AEzRtjlH74-5IWUnknbZ6jsdvLc6C0p6zvgAhbo4UksMf1absphd0naapLdhTQKGpgfGWQHpEdQxpBTtKJboZhkfBRCxeRcHsXkXm3dBBgFPHd6d0lc1W_Pv5CS6AB-PgC0m7p2NW1HrtTUubj1NcP_L_wuSU5Rh</recordid><startdate>20061124</startdate><enddate>20061124</enddate><creator>Martin, Patrick</creator><creator>Poggi, Marie Christine</creator><creator>Chambard, Jean Claude</creator><creator>Boulukos, Kim E.</creator><creator>Pognonec, Philippe</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope><scope>OTOTI</scope></search><sort><creationdate>20061124</creationdate><title>Low dose cadmium poisoning results in sustained ERK phosphorylation and caspase activation</title><author>Martin, Patrick ; Poggi, Marie Christine ; Chambard, Jean Claude ; Boulukos, Kim E. ; Pognonec, Philippe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-53dbc6cb9708a5ecd13452710bfe7acf4827a7359fb3211885537db6c0bf4b263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Animals</topic><topic>APOPTOSIS</topic><topic>Apoptosis - drug effects</topic><topic>BIOLOGICAL STRESS</topic><topic>CADMIUM</topic><topic>Cadmium Poisoning - enzymology</topic><topic>Cadmium Poisoning - pathology</topic><topic>Caspase</topic><topic>Caspases - metabolism</topic><topic>Cell death</topic><topic>Cells, Cultured</topic><topic>DAMAGE</topic><topic>Dose-Response Relationship, Drug</topic><topic>DOSES</topic><topic>Enzyme Activation - drug effects</topic><topic>ERK</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>INHIBITION</topic><topic>LEAD</topic><topic>Osteoblasts - drug effects</topic><topic>Osteoblasts - enzymology</topic><topic>Osteoblasts - pathology</topic><topic>PHOSPHORYLATION</topic><topic>Phosphorylation - drug effects</topic><topic>POISONING</topic><topic>Rats</topic><topic>STIMULATION</topic><topic>Sustained activation</topic><topic>TOXICITY</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martin, Patrick</creatorcontrib><creatorcontrib>Poggi, Marie Christine</creatorcontrib><creatorcontrib>Chambard, Jean Claude</creatorcontrib><creatorcontrib>Boulukos, Kim E.</creatorcontrib><creatorcontrib>Pognonec, Philippe</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martin, Patrick</au><au>Poggi, Marie Christine</au><au>Chambard, Jean Claude</au><au>Boulukos, Kim E.</au><au>Pognonec, Philippe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low dose cadmium poisoning results in sustained ERK phosphorylation and caspase activation</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2006-11-24</date><risdate>2006</risdate><volume>350</volume><issue>3</issue><spage>803</spage><epage>807</epage><pages>803-807</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Cadmium poisoning has been known to result in a wide variety of cellular responses, including oxidative stress and kinase activation. It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyzed different cell types for their responses to low concentrations of cadmium poisoning. We found that there is an association between cell susceptibility to cadmium toxicity and ERK activation. This activation is atypical, since it consists of a sustained ERK phosphorylation, that lasts up to 6 days post stimulation. This activation is associated with the appearance of cleaved caspases 8 and 3, processed PARP, and irreversible damage. Pharmacological inhibition of ERK phosphorylation results in the ability of cells to resist cadmium poisoning. Our data indicate that low cadmium concentrations result in an unconventional ERK sustained phosphorylation, which in turn leads to death signaling.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17027645</pmid><doi>10.1016/j.bbrc.2006.09.126</doi><tpages>5</tpages></addata></record> |
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subjects | 60 APPLIED LIFE SCIENCES Animals APOPTOSIS Apoptosis - drug effects BIOLOGICAL STRESS CADMIUM Cadmium Poisoning - enzymology Cadmium Poisoning - pathology Caspase Caspases - metabolism Cell death Cells, Cultured DAMAGE Dose-Response Relationship, Drug DOSES Enzyme Activation - drug effects ERK Extracellular Signal-Regulated MAP Kinases - metabolism INHIBITION LEAD Osteoblasts - drug effects Osteoblasts - enzymology Osteoblasts - pathology PHOSPHORYLATION Phosphorylation - drug effects POISONING Rats STIMULATION Sustained activation TOXICITY |
title | Low dose cadmium poisoning results in sustained ERK phosphorylation and caspase activation |
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