Research article summary (published 30 Dec 1995):

Necessary but not sufficient: the role of glucocorticoids in the acidosis-induced increase in levels of mRNAs encoding proteins of the ATP-dependent proteolytic pathway in rat muscle.

Full Abstract

Muscle protein degradation is accelerated by the acidosis associated with chronic renal failure. In isolated muscles from acidotic rats, a cytosolic, ATP-dependent proteolytic pathway is stimulated with a concurrent increase in the abundance of mRNAs encoding ubiquitin and subunits of the 26S proteasome complex associated with this degradative pathway. Adrenalectomy (ADX) prevents the acidosis-induced increase in muscle protein degradation unless high physiologic doses of glucocorticoids are administered to acidotic, adrenalectomized rats. We have examined the roles that acidosis and glucocorticoids have in the increase in mRNAs encoding proteins of the ATP-dependent-ubiquitin-proteasome proteolytic pathway in ADX rats. We found that ubiquitin and proteasome C2 and C9 subunit mRNA levels are increased in the white fiber, extensor digitorus longus (EDL) and mixed fiber, gastrocnemius muscles from acidotic ADX rats that received dexamethasone whereas acidosis alone or dexamethasone alone failed to increase these mRNAs. In contrast, acidosis plus dexamethasone decreased the total RNA content in both muscles. These data suggest that in muscle, the response to acidosis involves the specific activation of the ATP-ubiquitin-proteasome proteolytic pathway. Moreover, glucocorticoids are required but not directly responsible for the acidosis-induced increase in the mRNAs encoding proteins of this degradative pathway.

Author information

Author/s: Price, S R (SR); Bailey, J L (JL); England, B K (BK);

Affiliation: Renal Division, Emory University School of Medicine, Atlanta, Ga. 30322, USA.

Grants: DK 37175 (Agency:NIDDK NIH HHS) ; DK 45215 (Agency:NIDDK NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, U.S. Gov't, P.H.S.; Review

Journal: Mineral and electrolyte metabolism (Miner Electrolyte Metab), published in SWITZERLAND. (Language: eng)

Reference: 1996-; vol 22 (issue 1-3) : pp 72-5

Dates: Created 1996/08/12; Completed 1996/08/12; Revised 2007/11/14;

PMID: 8676830, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acidosis - metabolism Adenosine Triphosphate - metabolism Adrenalectomy Animals Cysteine Endopeptidases - biosynthesis Endopeptidases - metabolism Gene Expression Regulation, Enzymologic - drug effects Glucocorticoids - pharmacology; physiology

Glucocorticoids - pharmacology; physiology Multienzyme Complexes - biosynthesis Muscle, Skeletal - drug effects; metabolism Proteasome Endopeptidase Complex RNA, Messenger - metabolism Rats Transcription, Genetic Ubiquitins - blood

Associated Chemicals: Glucocorticoids (0) ; Multienzyme Complexes (0) ; RNA, Messenger (0) ; Ubiquitins (0) ; Adenosine Triphosphate (56-65-5) ; Endopeptidases (EC 3.4.-) ; Cysteine Endopeptidases (EC 3.4.22.-) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)

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