MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo. / Mattox, Taylor A; Young, Martin E; Rubel, Carrie E; Spaniel, Carolyn; Rodríguez, Jessica E; Grevengoed, Trisha J; Gautel, Mathias; Xu, Zhelong; Anderson, Ethan J; Willis, Monte S.

In: Journal of Bioenergetics and Biomembranes, Vol. 46, No. 3, 06.2014, p. 173-87.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Mattox, TA, Young, ME, Rubel, CE, Spaniel, C, Rodríguez, JE, Grevengoed, TJ, Gautel, M, Xu, Z, Anderson, EJ & Willis, MS 2014, 'MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo', Journal of Bioenergetics and Biomembranes, vol. 46, no. 3, pp. 173-87. https://doi.org/10.1007/s10863-014-9549-9

APA

Mattox, T. A., Young, M. E., Rubel, C. E., Spaniel, C., Rodríguez, J. E., Grevengoed, T. J., Gautel, M., Xu, Z., Anderson, E. J., & Willis, M. S. (2014). MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo. Journal of Bioenergetics and Biomembranes, 46(3), 173-87. https://doi.org/10.1007/s10863-014-9549-9

Vancouver

Mattox TA, Young ME, Rubel CE, Spaniel C, Rodríguez JE, Grevengoed TJ et al. MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo. Journal of Bioenergetics and Biomembranes. 2014 Jun;46(3):173-87. https://doi.org/10.1007/s10863-014-9549-9

Author

Mattox, Taylor A ; Young, Martin E ; Rubel, Carrie E ; Spaniel, Carolyn ; Rodríguez, Jessica E ; Grevengoed, Trisha J ; Gautel, Mathias ; Xu, Zhelong ; Anderson, Ethan J ; Willis, Monte S. / MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo. In: Journal of Bioenergetics and Biomembranes. 2014 ; Vol. 46, No. 3. pp. 173-87.

Bibtex

@article{c5eb6ee791144736a9b8fe7b7d52c030,
title = "MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo",
abstract = "MuRF1 is a previously reported ubiquitin-ligase found in striated muscle that targets troponin I and myosin heavy chain for degradation. While MuRF1 has been reported to interact with mitochondrial substrates in yeast two-hybrid studies, no studies have identified MuRF1's role in regulating mitochondrial function to date. In the present study, we measured cardiac mitochondrial function from isolated permeabilized muscle fibers in previously phenotyped MuRF1 transgenic and MuRF1-/- mouse models to determine the role of MuRF1 in intermediate energy metabolism and ROS production. We identified a significant decrease in reactive oxygen species production in cardiac muscle fibers from MuRF1 transgenic mice with increased α-MHC driven MuRF1 expression. Increased MuRF1 expression in ex vivo and in vitro experiments revealed no alterations in the respiratory chain complex I and II function. Working perfusion experiments on MuRF1 transgenic hearts demonstrated significant changes in glucose oxidation. However, total oxygen consumption was decreased [corrected]. This data provides evidence for MuRF1 as a novel regulator of cardiac ROS, offering another mechanism by which increased MuRF1 expression may be cardioprotective in ischemia reperfusion injury, in addition to its inhibition of apoptosis via proteasome-mediate degradation of c-Jun. The lack of mitochondrial function phenotype identified in MuRF1-/- hearts may be due to the overlapping interactions of MuRF1 and MuRF2 with energy regulating proteins found by yeast two-hybrid studies reported here, implying a duplicity in MuRF1 and MuRF2's regulation of mitochondrial function.",
keywords = "Animals, Cells, Cultured, Citric Acid Cycle, Energy Metabolism, Enzyme Activation, Mice, Mice, Knockout, Mitochondria, Heart, Muscle Proteins, Oxygen, Oxygen Consumption, Reactive Oxygen Species, Ubiquitin-Protein Ligases",
author = "Mattox, {Taylor A} and Young, {Martin E} and Rubel, {Carrie E} and Carolyn Spaniel and Rodr{\'i}guez, {Jessica E} and Grevengoed, {Trisha J} and Mathias Gautel and Zhelong Xu and Anderson, {Ethan J} and Willis, {Monte S}",
year = "2014",
month = jun,
doi = "10.1007/s10863-014-9549-9",
language = "English",
volume = "46",
pages = "173--87",
journal = "Journal of Bioenergetics and Biomembranes",
issn = "0145-479X",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo

AU - Mattox, Taylor A

AU - Young, Martin E

AU - Rubel, Carrie E

AU - Spaniel, Carolyn

AU - Rodríguez, Jessica E

AU - Grevengoed, Trisha J

AU - Gautel, Mathias

AU - Xu, Zhelong

AU - Anderson, Ethan J

AU - Willis, Monte S

PY - 2014/6

Y1 - 2014/6

N2 - MuRF1 is a previously reported ubiquitin-ligase found in striated muscle that targets troponin I and myosin heavy chain for degradation. While MuRF1 has been reported to interact with mitochondrial substrates in yeast two-hybrid studies, no studies have identified MuRF1's role in regulating mitochondrial function to date. In the present study, we measured cardiac mitochondrial function from isolated permeabilized muscle fibers in previously phenotyped MuRF1 transgenic and MuRF1-/- mouse models to determine the role of MuRF1 in intermediate energy metabolism and ROS production. We identified a significant decrease in reactive oxygen species production in cardiac muscle fibers from MuRF1 transgenic mice with increased α-MHC driven MuRF1 expression. Increased MuRF1 expression in ex vivo and in vitro experiments revealed no alterations in the respiratory chain complex I and II function. Working perfusion experiments on MuRF1 transgenic hearts demonstrated significant changes in glucose oxidation. However, total oxygen consumption was decreased [corrected]. This data provides evidence for MuRF1 as a novel regulator of cardiac ROS, offering another mechanism by which increased MuRF1 expression may be cardioprotective in ischemia reperfusion injury, in addition to its inhibition of apoptosis via proteasome-mediate degradation of c-Jun. The lack of mitochondrial function phenotype identified in MuRF1-/- hearts may be due to the overlapping interactions of MuRF1 and MuRF2 with energy regulating proteins found by yeast two-hybrid studies reported here, implying a duplicity in MuRF1 and MuRF2's regulation of mitochondrial function.

AB - MuRF1 is a previously reported ubiquitin-ligase found in striated muscle that targets troponin I and myosin heavy chain for degradation. While MuRF1 has been reported to interact with mitochondrial substrates in yeast two-hybrid studies, no studies have identified MuRF1's role in regulating mitochondrial function to date. In the present study, we measured cardiac mitochondrial function from isolated permeabilized muscle fibers in previously phenotyped MuRF1 transgenic and MuRF1-/- mouse models to determine the role of MuRF1 in intermediate energy metabolism and ROS production. We identified a significant decrease in reactive oxygen species production in cardiac muscle fibers from MuRF1 transgenic mice with increased α-MHC driven MuRF1 expression. Increased MuRF1 expression in ex vivo and in vitro experiments revealed no alterations in the respiratory chain complex I and II function. Working perfusion experiments on MuRF1 transgenic hearts demonstrated significant changes in glucose oxidation. However, total oxygen consumption was decreased [corrected]. This data provides evidence for MuRF1 as a novel regulator of cardiac ROS, offering another mechanism by which increased MuRF1 expression may be cardioprotective in ischemia reperfusion injury, in addition to its inhibition of apoptosis via proteasome-mediate degradation of c-Jun. The lack of mitochondrial function phenotype identified in MuRF1-/- hearts may be due to the overlapping interactions of MuRF1 and MuRF2 with energy regulating proteins found by yeast two-hybrid studies reported here, implying a duplicity in MuRF1 and MuRF2's regulation of mitochondrial function.

KW - Animals

KW - Cells, Cultured

KW - Citric Acid Cycle

KW - Energy Metabolism

KW - Enzyme Activation

KW - Mice

KW - Mice, Knockout

KW - Mitochondria, Heart

KW - Muscle Proteins

KW - Oxygen

KW - Oxygen Consumption

KW - Reactive Oxygen Species

KW - Ubiquitin-Protein Ligases

U2 - 10.1007/s10863-014-9549-9

DO - 10.1007/s10863-014-9549-9

M3 - Journal article

C2 - 24733503

VL - 46

SP - 173

EP - 187

JO - Journal of Bioenergetics and Biomembranes

JF - Journal of Bioenergetics and Biomembranes

SN - 0145-479X

IS - 3

ER -

ID: 146698812