Susceptibility to ATP depletion of primary proximal tubular cell cultures derived from mice lacking either the α1 or the α2 ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-12

AUTHORS

Wilfred Lieberthal, Meiyi Tang, Leiqing Zhang, Benoit Viollet, Vimal Patel, Jerrold S Levine

ABSTRACT

BACKGROUND: The purpose of this study was to determine whether AMPK influences the survival of primary cultures of mouse proximal tubular (MPT) cells subjected to metabolic stress. Previous studies, using an immortalized MPT cell line, suggest that AMPK is activated during metabolic stress, and ameliorates stress-induced apoptosis of these cells. METHODS: Primary MPT cells were cultured from AMPK knockout (KO) mice lacking either the α1 or the α2 isoform of the catalytic domain of AMPK. MPT cells were subjected to ATP depletion using antimycin A. RESULTS: Surprisingly, there was no difference in the amount of death induced by metabolic stress of MPT cells from either type of AMPK KO mice compared to its WT control. Moreover, inhibition of the activity of the α1 isoform in primary MPT cells from α2-/- mice (pharmacologically, via compound C) or inhibition of the α2 isoform in primary MPT cells from α1-/- mice (molecularly, via knockdown) both decreased cell viability equivalently in response to metabolic stress. The explanation for this unexpected result appears to be an adaptive increase in expression of the non-deleted α-isoform. As a consequence, total α-domain expression (i.e. α1 + α2), is comparable in kidney cortex and in cultured MPT cells derived from either type of KO mouse versus its WT control. Importantly, each α-isoform appears able to compensate fully for the absence of the other, with respect to both the phosphorylation of downstream targets of AMPK and the amelioration of stress-induced cell death. CONCLUSIONS: These findings not only confirm the importance of AMPK as a pro-survival kinase in MPT cells during metabolic stress, but also show, for the first time, that each of the two α-isoforms can substitute for the other in MPT cells from AMPK KO mice with regard to amelioration of stress-induced loss of cell viability. More... »

PAGES

251

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2369-14-251

DOI

http://dx.doi.org/10.1186/1471-2369-14-251

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022703055

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24228806


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    "description": "BACKGROUND: The purpose of this study was to determine whether AMPK influences the survival of primary cultures of mouse proximal tubular (MPT) cells subjected to metabolic stress. Previous studies, using an immortalized MPT cell line, suggest that AMPK is activated during metabolic stress, and ameliorates stress-induced apoptosis of these cells.\nMETHODS: Primary MPT cells were cultured from AMPK knockout (KO) mice lacking either the \u03b11 or the \u03b12 isoform of the catalytic domain of AMPK. MPT cells were subjected to ATP depletion using antimycin A.\nRESULTS: Surprisingly, there was no difference in the amount of death induced by metabolic stress of MPT cells from either type of AMPK KO mice compared to its WT control. Moreover, inhibition of the activity of the \u03b11 isoform in primary MPT cells from \u03b12-/- mice (pharmacologically, via compound C) or inhibition of the \u03b12 isoform in primary MPT cells from \u03b11-/- mice (molecularly, via knockdown) both decreased cell viability equivalently in response to metabolic stress. The explanation for this unexpected result appears to be an adaptive increase in expression of the non-deleted \u03b1-isoform. As a consequence, total \u03b1-domain expression (i.e. \u03b11 + \u03b12), is comparable in kidney cortex and in cultured MPT cells derived from either type of KO mouse versus its WT control. Importantly, each \u03b1-isoform appears able to compensate fully for the absence of the other, with respect to both the phosphorylation of downstream targets of AMPK and the amelioration of stress-induced cell death.\nCONCLUSIONS: These findings not only confirm the importance of AMPK as a pro-survival kinase in MPT cells during metabolic stress, but also show, for the first time, that each of the two \u03b1-isoforms can substitute for the other in MPT cells from AMPK KO mice with regard to amelioration of stress-induced loss of cell viability.", 
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Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1186/1471-2369-14-251'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1186/1471-2369-14-251'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1186/1471-2369-14-251'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1186/1471-2369-14-251'


 

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295 Université Paris Descartes, Sorbonne Paris Cité, Paris, France
296 rdf:type schema:Organization
297 https://www.grid.ac/institutes/grid.280892.9 schema:alternateName Jesse Brown VA Medical Center
298 schema:name Department of Medicine, University of Illinois at Chicago, IL 60612, Chicago, USA
299 Jesse Brown Veterans Affairs Medical Center, IL 60612, Chicago, USA
300 rdf:type schema:Organization
301 https://www.grid.ac/institutes/grid.413840.a schema:alternateName Northport VA Medical Center
302 schema:name Department of Medicine, Stony Brook University Medical Center, NY 11794, Stony Brook, USA
303 Northport Veterans Affairs Medical Center, NY 11768, Northport, USA
304 rdf:type schema:Organization
 




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