Overexpression of inducible 70-kDa heat shock protein in mouse attenuates skeletal muscle damage induced by cryolesioning

2006 ◽  
Vol 290 (4) ◽  
pp. C1128-C1138 ◽  
Author(s):  
Elen H. Miyabara ◽  
Jody L. Martin ◽  
Tina M. Griffin ◽  
Anselmo S. Moriscot ◽  
Ruben Mestril
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Muscle Damage ◽  
Neuronal Cell ◽  
Protective Agent ◽  
Wild Type ◽  
Cross Sectional ◽  
Skeletal Muscle Damage ◽  
Neuronal Cell Adhesion Molecule

Heat shock protein expression is elevated upon exposure to a variety of stresses and limits the extent of stress-induced damage. To investigate the putative role of inducible 70-kDa heat shock protein (HSP70) in skeletal muscle damage and regeneration, soleus and tibialis anterior (TA) muscles from HSP70-overexpressing transgenic mice were subjected to cryolesioning and analyzed after 1, 10, and 21 days. Histological analysis showed that the muscles from both HSP70 and wild-type mice treated with radicicol (a HSP inducer) had decreased necrosis after cryolesioning compared with controls. The decrease in muscle fiber cross-sectional area in both soleus and TA muscles in 10 days postlesioning was attenuated in HSP70 mice compared with wild-type mice. Glutathione peroxidase activity was increased 1 day after cryolesioning in both HSP70 and control mice and remained elevated for up to 21 days. Immunodetection of neuronal cell adhesion molecule (a satellite cell marker) and developmental/neonatal MHC were significantly lower in cryolesioned HSP70-overexpressing mice than in cryolesioned controls. These results suggest that HSP70 protects skeletal muscle against injury and radicicol might be useful as a skeletal muscle protective agent.

scholarly journals Effect of black chokeberry on skeletal muscle damage and neuronal cell death

2019 ◽  
Vol 23 (4) ◽  
pp. 26-31 ◽  
Author(s):  
Jisu Kim ◽  
Kang Pa Lee ◽  
Suji Beak ◽  
Hye Ra Kang ◽  
Yong Kyun Kim ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Death ◽  
Muscle Damage ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Skeletal Muscle Damage ◽  
Black Chokeberry

scholarly journals The effect of heat shock on acute hypertrophic signaling following skeletal muscle damage

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Chad D. Touchberry ◽  
Greg L Bomhoff ◽  
Anisha Gupte ◽  
Paige Geiger ◽  
Phil Gallagher
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Muscle Damage ◽  
Skeletal Muscle Damage ◽  
Hypertrophic Signaling

Cardiorespiratory and skeletal muscle damage due to COVID-19: making the urgent case for rehabilitation

2021 ◽  
pp. 1-14
Author(s):  
Rebeca Nunes Silva ◽  
Cássia Da Luz Goulart ◽  
Murilo Rezende Oliveira ◽  
Guilherme Yassuyuki Tacao ◽  
Guilherme Dionir Back ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Skeletal Muscle Damage ◽  
Urgent Case

Modifications in the Concentrations of Circulating Myoglobin after Treatment with Low Doses of Adriamycin

1985 ◽  
Vol 71 (5) ◽  
pp. 463-468 ◽  
Author(s):  
Giovanni Carulli ◽  
Aldo Clerico ◽  
Alessandra Marini ◽  
Maria Grazia Del Chicca ◽  
Renato Vanacore ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Cancer Patients ◽  
Muscle Damage ◽  
Low Doses ◽  
Skeletal Muscle Damage ◽  
Creatine Kinase Mb

The modifications in the concentration of circulating myoglobin have been studied by means of a radioimmunoassay in 15 cancer patients undergoing polychemotherapy including adriamycin. In 8 patients significant increases in myoglobin levels were found after injection of low doses of the drug (25-50 mg/m2). Moreover, a disturbance of the normal biorhythm of the protein was evident in 12 patients. Creatine kinase-MB was evaluated by means of a radioimmunoassay, but there was no relation between an increase in the isoenzyme and an increase in myoglobin. No ECG modifications were detected. These data indicate that the measurement of myoglobin may offer an indication of myocardial or skeletal muscle damage caused by adriamycin.

Isoform specific ALT measurement during liver and skeletal muscle damage

2012 ◽  
Vol 211 ◽  
pp. S48
Author(s):  
Björn Glinghammar ◽  
Ingalill Rafter ◽  
Ina Schuppe-Koistinen ◽  
Ian Cotgreave
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Skeletal Muscle Damage

scholarly journals Toll-Like Receptors in Ischaemia and Its Potential Role in the Pathophysiology of Muscle Damage in Critical Limb Ischaemia

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Hemanshu Patel ◽  
Sidney G. Shaw ◽  
Xu Shi-Wen ◽  
David Abraham ◽  
Daryll M. Baker ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Potential Role ◽  
Arterial Disease ◽  
Severe Form ◽  
Tissue Loss ◽  
Critical Limb Ischaemia ◽  
Limb Ischaemia ◽  
Toll Like Receptors ◽  
Skeletal Muscle Damage

Toll-like receptors (TLRs) are key receptors of the innate immune system which are expressed on immune and nonimmune cells. They are activated by both pathogen-associated molecular patterns and endogenous ligands. Activation of TLRs culminates in the release of proinflammatory cytokines, chemokines, and apoptosis. Ischaemia and ischaemia/reperfusion (I/R) injury are associated with significant inflammation and tissue damage. There is emerging evidence to suggest that TLRs are involved in mediating ischaemia-induced damage in several organs. Critical limb ischaemia (CLI) is the most severe form of peripheral arterial disease (PAD) and is associated with skeletal muscle damage and tissue loss; however its pathophysiology is poorly understood. This paper will underline the evidence implicating TLRs in the pathophysiology of cerebral, renal, hepatic, myocardial, and skeletal muscle ischaemia and I/R injury and discuss preliminary data that alludes to the potential role of TLRs in the pathophysiology of skeletal muscle damage in CLI.

scholarly journals Detrimental Role of Heat Shock Protein 60&70 and Toll-like Receptor 4 in Skeletal Muscle Ischaemia In Vitro

2013 ◽  
Vol 57 (5) ◽  
pp. 77S
Author(s):  
Ali Navi ◽  
Rebekah Yu ◽  
Xu Shi-Wen ◽  
Sidney Shaw ◽  
George Hamilton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Ischaemia
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