scholarly journals Morphing mitochondria: understanding the development of the mitochondrial reticulum in skeletal muscle

2019 ◽  
Vol 597 (10) ◽  
pp. 2619-2620
Author(s):  
Terence E. Ryan
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Reticulum

Mitochondrial reticulum in limb skeletal muscle

1986 ◽  
Vol 251 (3) ◽  
pp. C395-C402 ◽  
Author(s):  
S. P. Kirkwood ◽  
E. A. Munn ◽  
G. A. Brooks
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Vastus Lateralis ◽  
Skeletal Muscle Fiber ◽  
Muscle Fiber Types ◽  
Mitochondrial Morphology ◽  
Fiber Types ◽  
Fast Twitch ◽  
Mitochondrial Reticulum ◽  
Superficial Portion

High-voltage electron microscopy at 1,500 kV was used to examine mitochondrial morphology in three skeletal muscles of the rat. The soleus, deep portion of the vastus lateralis, and superficial portion of the vastus lateralis muscles were examined to represent slow-twitch oxidative, fast-twitch oxidative, glycolytic, and fast-twitch glycolytic skeletal muscle fiber types, respectively. Muscle samples were removed from six female Wistar rats. The tissues were fixed using standard electron microscopic techniques and were sectioned transversely with respect to muscle fiber orientation to approximately 0.5-micron thickness. The sections were stained on grids with uranyl acetate and Reynolds' lead citrate. Results revealed a mitochondrial reticulum in all three skeletal muscle fiber types. Stereological analyses of the electron micrographs were performed to measure volume densities and surface-to-volume ratios of mitochondria in the muscle samples. Cross-sectional volume densities of mitochondria in the soleus (15.5 +/- 1%) and deep portion of the vastus lateralis (16.1 +/- 2%) were significantly greater (P less than 0.05) than in the superficial portion of the vastus lateralis (8.7 +/- 1%). Surface-to-volume ratios of mitochondria were not significantly different between fiber types. It was concluded that the mitochondria in mammalian limb skeletal muscle are a reticulum, or network.

EFFECTS OF ENDURANCE TRAINING ON A MITOCHONDRIAL RETICULUM IN SKELETAL MUSCLE

1985 ◽  
Vol 17 (2) ◽  
pp. 244-245
Author(s):  
S. P. Kirkwood ◽  
E. A. Munn ◽  
L. Packer ◽  
G. A. Brooks
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Mitochondrial Reticulum

MITOCHONDRIAL RETICULUM IN RAT SKELETAL MUSCLE

1984 ◽  
Vol 16 (2) ◽  
pp. 120
Author(s):  
S. P. Kirkwood ◽  
E. A. Munn ◽  
L. Packer ◽  
G. A. Brooks
Keyword(s):  
Skeletal Muscle ◽  
Rat Skeletal Muscle ◽  
Mitochondrial Reticulum

scholarly journals PO-033 Mitochondria-associated Ampk mediates mitochondrial quality control in skeletal muscle

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Joshua Drake ◽  
Rebecca Wilson ◽  
Rhianna Laker ◽  
Yuntian Guan ◽  
Tatiana Coverdell ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Acute Exercise ◽  
Ischemia Reperfusion ◽  
Treadmill Running ◽  
Future Research ◽  
Dependent Manner ◽  
Mitochondrial Fractions ◽  
Mitochondrial Remodeling ◽  
Mitochondrial Reticulum

Objective Mitochondria exist as a complex, interconnected reticulum with the degree of complexity at homeostasis varying by cell type. Declines in mitochondrial quality is a hallmark of numerous diseases and is partly maintained through the targeted removal and degradation of damaged/dysfunctional regions of the reticulum known as mitophagy. We have demonstrated that acute exercise causes targeted degradation of a subset (<1%) of the mitochondrial reticulum through mitophagy in an AMPK-dependent manner. However, how such spatial regulation is achieved is unclear.  Given that AMPK is a well-known bioenergetics sensor critical for maintenance of energetic homoeostasis, and numerous studies have linked AMPK-signaling to mitochondrial remodeling and functional adaptations under physiological and pathological conditions, we hypothesized that AMPK regulates mitophagy by being physically associated with the mitochondria.  Methods C57BL/6 mice (3 or 20 months of age) were kept in standard conditions (12:12 light, dark cycle) on normal chow.  Enriched mitochondrial fractions from skeletal muscle were obtained via differential centrifugation and percoll gradient isolation. Skeletal muscle energetic stress was induced via acute treadmill running, direct electrical stimulation, or hindlimb ischemia-reperfusion. Somatic gene transfer into skeletal muscle was done via electraporation. Confocal microscopy of whole mount skeletal muscle was performed at least 10 days post-electraporation to assess MitoTimer fluorescence Red:Green Ratio and Mitophagy (i.e. presence of pure red puncta). Results We have discovered that AMPK is enriched in isolated mitochondria from both mouse and human skeletal muscle (mitoAMPK) and that, in mice, mitoAMPK consists exclusively of ⍺1/β2/γ1 isoforms. Furthermore, skeletal muscle mitoAMPK Thr172 phosphorylation, indicative of activation, is increased following electrical stimulation, ischemia-reperfusion, and acute treadmill running. By co-transfecting mouse FDB muscle with pMitoTimer and a mitochondrially-targeted AMPK inhibitor peptide (mitoAIP), we show that mitoAMPK activity is required to maintain mitochondrial quality (as evidenced by increased MitoTimer Red:Green ratio) and exercise-induced mitophagy (MitoTimer pure red puncta).  Interestingly, association of mitoAMPK with mitochondria declines by ~50% in skeletal muscle in old mice and coincides with poor mitochondrial quality (increased MitoTimer Red:Green ratio), which may explain the loss of mitochondrial quality and metabolic flexibility with aging. Conclusions Our current working hypothesis is that activation of mitoAMPK by exercise plays an instrumental role in promoting mitochondrial remodeling, hence contractile and metabolic adaptations, by spatially recognizing damaged regions of the mitochondrial reticulum. Future research on mitoAMPK will significantly improve the mechanistic understanding of exercise training-induced adaptation in skeletal muscle and AMPK biology.

scholarly journals Grx2 Regulates Skeletal Muscle Mitochondrial Structure and Autophagy

2021 ◽  
Vol 12 ◽  
Author(s):  
Ava Liaghati ◽  
Chantal A. Pileggi ◽  
Gaganvir Parmar ◽  
David A. Patten ◽  
Nina Hadzimustafic ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dynamics ◽  
Immunoblot Analysis ◽  
Redox Status ◽  
Autophagic Flux ◽  
Complex Iv ◽  
Mitochondrial Structure ◽  
Disease States ◽  
First Results ◽  
Mitochondrial Reticulum

Glutathione is an important antioxidant that regulates cellular redox status and is disordered in many disease states. Glutaredoxin 2 (Grx2) is a glutathione-dependent oxidoreductase that plays a pivotal role in redox control by catalyzing reversible protein deglutathionylation. As oxidized glutathione (GSSG) can stimulate mitochondrial fusion, we hypothesized that Grx2 may contribute to the maintenance of mitochondrial dynamics and ultrastructure. Here, we demonstrate that Grx2 deletion results in decreased GSH:GSSG, with a marked increase of GSSG in primary muscle cells isolated from C57BL/6 Grx2−/− mice. The altered glutathione redox was accompanied by increased mitochondrial length, consistent with a more fused mitochondrial reticulum. Electron microscopy of Grx2−/− skeletal muscle fibers revealed decreased mitochondrial surface area, profoundly disordered ultrastructure, and the appearance of multi-lamellar structures. Immunoblot analysis revealed that autophagic flux was augmented in Grx2−/− muscle as demonstrated by an increase in the ratio of LC3II/I expression. These molecular changes resulted in impaired complex I respiration and complex IV activity, a smaller diameter of tibialis anterior muscle, and decreased body weight in Grx2 deficient mice. Together, these are the first results to show that Grx2 regulates skeletal muscle mitochondrial structure, and autophagy.

Coordinated development of the mitochondrial reticulum in skeletal muscle

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Yuho Kim ◽  
Eric Lindberg ◽  
Christopher K.E. Bleck ◽  
Brian Glancy
Keyword(s):  
Skeletal Muscle ◽  
Coordinated Development ◽  
Mitochondrial Reticulum

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

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