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There was a significant increase in 4-HNE positive proteins observed in Nrf2- null relative to WT mice under basal conditions. Under resting state, ubiquitin-protein conjugates were significantly higher in Nrf2- null compared to WT skeletal muscle. Upon AEES, both WT and Nrf2- null mice had increased levels of ubiquitinated skeletal muscle proteins and the magnitude of ubiquitination was much greater in Nrf2- null compared to WT skeletal muscle Fig. These results suggest that abrogation of Nrf2, coupled with induction of oxidative stress, could accelerate the age-associated augmentation of protein degradation pathways that contribute to skeletal muscle loss.

Regenerative capacity of skeletal muscle in response to oxidative stress or aging might require activation of quiescent muscle precursor cells 65 - Therefore, we analyzed the protein expression for PAX7 stem cell marker and MyoD muscle differentiation factor by immunoblotting. Next, we assessed the PAX7 population of skeletal muscle cells using immunofluorescence followed by microscopic examination Fig. Under basal conditions, the number of Pax7 cells was higher in Nrf2- null than WT mice. Moreover, regenerative capacity was significantly decreased in Nrf2- null compared to WT mice.

These results indicate that AEES abrogation of Nrf2 might be a confounding factor contributing to age-associated degeneration of myocytes. These results suggest that WT and Nrf2- null mice respond differently to AEES, and this could be related to the differences in the degree of oxidative stress and compensatory defense mechanisms Biswal KF-3802 these genotypes. Histograms of regeneration ability for WT and Nrf2- null mice were determined by calculating the percent of myocytes with active nuclei.

  • Thieme E-Journals - Synthesis / Abstract
  • Nrf2 Deficiency Promotes Apoptosis and Impairs Pax7/MyoD Expression in Aging Skeletal Muscle Cells
  • Introduction

Notably, down regulation of these proteins were sustained in Nrf2-null mice versus WT compare lane 3 vs lane 4; Biswal KF-3802. Overall, these data suggest that abrogation of Nrf2 results in a delayed regeneration of the skeletal muscle.

Effect of recovery from AEES on skeletal muscle regeneration. Oxidative stress associated pathological processes in Biswal KF-3802 skeletal muscles of aged humans has been an important research focus for decades. While Nrf2-Keap1 pathway is one of the critical regulators of intracellular redox homeostasis in skeletal muscle 96869the age-dependent effect of Nrf2 signaling in skeletal muscle is poorly understood. We recently demonstrated that either ablation or age-dependent decline of Nrf2 is coupled with increased oxidative stress and accelerated skeletal muscle degeneration through induction of apoptotic and ubiquitin Biswal KF-3802 protein degradation pathways 9.

We also demonstrate that abrogation of Nrf2 in combination with oxidative stress aggravates age-associated muscle degeneration and impairs stem cell-based regenerative mechanisms.

Nrf2 Deficiency Promotes Apoptosis and Impairs Pax7/MyoD Expression in Aging Skeletal Muscle Cells

Biswal KF-3802 The role of NF-kB-mediated transcription of antioxidant genes in the context of aging muscle regeneration under forced stress or Nrf2 ablation is not known. Recently, we demonstrated that loss of Biswal KF-3802 with aging is associated with increased ubiquitination, lipid peroxidation and activation of apoptotic cascades in the heart 8.

Several reports have indicated that oxidative stress and other pathological conditions are strongly correlated with protein degradation and increased cell death 1516343563Biswal KF-3802 However, there is limited information on Nrf2 signaling in skeletal muscle regeneration with aging. We Biswal KF-3802 that activation of antioxidant and pro-survival pathways in response to stress might be associated with diminished apoptotic signals. Therefore, we further analyzed apoptotic pathways under basal and stressed conditions in WT and Nrf2- null mice.

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This Biswal KF-3802 account for the significant structure alterations we observed in Nrf2- null skeletal muscle and perhaps functional changes. Effective regeneration of skeletal muscle could occur through activation and proliferation of satellite cells 767 Defects in activation or a decrease in number of satellite cells results in reduced muscle regeneration.

It has been reported that redox-dependent regulation is involved in self-renewal of stem cells and myogenic differentiation 72 - Biswal KF-3802 Upon skeletal muscle injury, activated satellite cells rapidly enter the cell cycle and proliferate, augmenting skeletal muscle in the presence of Pax7 78 - Biswal KF-3802 Further, activated satellite cells possess the ability to induce the downstream genes such as Myf5 and MyoD, which promote differentiation into myoblasts 83 Pax7 expressing satellite cells are necessary for muscle regeneration We postulated that chronic oxidative stress plays a role in stem cell renewal.

Our results indicate that loss of Nrf2 signaling is associated with increased oxidative stress over time that facilitates a compensatory activation of stem cells as indicated by increased Pax7 positive cells. This suggests that moderate pro-oxidative states are able to promote expression of stem cell lineage cells even in the absence of Nrf2 signaling, indicating Pax7 can be regulated by an Nrf2-independent pathway. Interestingly, the observed increase in Pax7 and MyoD in WT skeletal muscle in response to AEES suggests that induction of moderate oxidative stress might have a key role in activation of satellite cells and muscle regeneration.

Further, Nrf2- null mice displayed a delayed rescue of regeneration after withdrawal of AEES due to overwhelming oxidative stress that is a consequence of loss of Nrf2 and aging. Therefore, we suggest that Nrf2 signaling is necessary to protect stem cells by diminishing harmful oxidative stress conditions. Clearly, while mild oxidative stress favors stem cell and MyoD lineage, severe oxidative stress Nrf2 abrogation is detrimental to these mechanisms. Taken together, these findings implicate a role for Nrf2 in the regulation of stem cell lineage and muscle differentiation during aging.


In summary, we Biswal KF-3802 Nrf2 as Biswal KF-3802 critical component in the transcriptional signaling of antioxidants to maintain skeletal muscle during AEES. In summary, suppression of survival and activation of apoptotic signals along with ubiquitination and oxidation of proteins impair skeletal muscle regeneration through decreasing Pax7 and MyoD lineage. This study supports Nrf2 as a key player in skeletal muscle protection and opens up new avenues for potential therapeutic treatment of aging skeletal muscle disorders. National Center for Biotechnology InformationU.


Free Radic Biol Med. Author manuscript; available in PMC Jul 7. Muthusamy1 Christopher J.

Download the latest Biswal KM device drivers (Official and Certified). About The Author: Jay Geater is the President and CEO of Solvusoft Corporation. Download the latest Biswal Mouse device drivers Biswal KF-3802 and Certified).


About The Author: Jay Geater is the President and CEO of Solvusoft Corporation.

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