Tumor necrosis factor alpha stimulates p62 accumulation and enhances proteasome activity independently of ROS

Cell Biology and Toxicology
Caleigh M Opperman, Balindiwe J N Sishi

Abstract

Circulating TNF-α levels are elevated in a wide variety of cardiovascular pathologies including congestive heart failure (CHF). This cytokine is one of the leading mediators of the immune inflammatory response with widespread biological functions regulated by membrane receptors. The pathophysiological implication of the downstream effects of activating the TNF-α system in CHF appears to depend on its direct effects on the heart and endothelium. Evidence supporting the notion that circulating TNF-α promotes protein breakdown was initially obtained from studies utilizing transgenic animals overexpressing TNF-α, animals with experimental diseases that augment TNF-α and in animals treated with exogenous TNF-α. It was then demonstrated that TNF-α acts directly on cultured myotubes to stimulate catabolism; however, whether the effects are the same in the heart remains poorly understood. The present study shows that TNF-α treatment induces autophagy, but clearance through this pathway appears obstructed and, consequently, results in increased protein ubiquitination. Furthermore, prolonged TNF-α treatment enhanced E3 ubiquitin ligase expression but reduced activity of the proteasome. These results suggest that TNF-α induces sarcomeric ...Continue Reading

References

Jul 26, 1990·The New England Journal of Medicine·B LevineM Packer
Jul 1, 1996·Journal of the American College of Cardiology·J GurevitchV Yakirevich
Sep 1, 1996·Journal of Cardiac Failure·Y SetaD L Mann
Jul 10, 1998·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Y P LiM B Reid
Aug 26, 1998·Progress in Cardiovascular Diseases·C CeconiR Ferrari
Oct 15, 1998·Proceedings of the National Academy of Sciences of the United States of America·A K NussbaumH Schild
Sep 27, 2000·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Y P Li, M B Reid
Feb 13, 2001·Biochemical and Biophysical Research Communications·E KuusistoA Salminen
Mar 13, 2001·Annual Review of Immunology·M Feldmann, R N Maini
Aug 22, 2001·Chemistry & Biology·A F Kisselev, A L Goldberg
Apr 2, 2002·Cardiovascular Research·William S BradhamFrancis G Spinale
Mar 30, 2002·Journal of the American College of Cardiology·Naoya MaekawaMitsuru Seishima
Apr 25, 2003·American Journal of Physiology. Cell Physiology·Yi-Ping Li
Oct 1, 1995·Trends in Cell Biology·P VandenabeeleW Fiers
Aug 10, 2005·The International Journal of Biochemistry & Cell Biology·David J Glass
Oct 4, 2005·The Journal of Clinical Investigation·Beth Levine, Junying Yuan
Feb 18, 2006·Biochemical and Biophysical Research Communications·Peter RazeghiHeinrich Taegtmeyer
Oct 19, 2006·Journal of Molecular and Cellular Cardiology·Kuljeet KaurPawan K Singal
Mar 7, 2007·Current Topics in Developmental Biology·Devrim Gozuacik, Adi Kimchi
Jul 6, 2007·Autophagy·Noboru Mizushima, Tamotsu Yoshimori
Nov 22, 2007·Trends in Molecular Medicine·Wim MartinetGuido R Y De Meyer
Jun 12, 2008·International Review of Cell and Molecular Biology·Eeva-Liisa Eskelinen
Oct 10, 2008·Circulation·Meijing WangDaniel R Meldrum
Jan 31, 2009·Circulation Research·Asa B Gustafsson, Roberta A Gottlieb
Mar 7, 2009·Chemical Reviews·António J MarquesR Jürgen Dohmen
Aug 4, 2010·Basic Research in Cardiology·Lydia LacerdaSandrine Lecour
Dec 18, 2010·Cancer Research·Pippa F Cosper, Leslie A Leinwand
Jan 25, 2011·The Journal of Biological Chemistry·Andrea L PortburyCam Patterson
May 6, 2011·Molecular & Cellular Proteomics : MCP·Charity T AikenLan Huang
Dec 15, 2012·Circulation·Alan S GoUNKNOWN American Heart Association Statistics Committee and Stroke Statistics Subcommittee

❮ Previous
Next ❯

Citations

Apr 17, 2016·Journal of Cellular and Molecular Medicine·Diane C WangChengshui Chen
Jul 7, 2016·Journal of Crohn's & Colitis·Kirsty M HooperPaul Henderson
May 26, 2017·Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire·Haifeng ShaoQiang Li
Jun 22, 2018·Oncotarget·Suryakant NitureDeepak Kumar
Mar 19, 2021·Medicine and Science in Sports and Exercise·Camila S PadilhaRafael Deminice

❮ Previous
Next ❯

Related Concepts

Related Feeds

Parkinson's Disease & Autophagy

Autophagy leads to degradation of damaged proteins and organelles by the lysosome. Impaired autophagy has been implicated in several diseases. Here is the role of autophagy in Parkinson’s disease.

Autophagy & Model Organisms

Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms

Autophagy & Disease

Autophagy is an important cellular process for normal physiology and both elevated and decreased levels of autophagy are associated with disease. Here is the latest research.