Subcellular Distribution of Calpain and Calpastatin Immunoreactivity and Fodrin Proteolysis in Rabbit Hippocampus After Hypoxia and Glucocorticoid Treatment

Ostwald, Klas; Hayashi, Masami; Nakamura, Megumi; Kawashima, Seiichi

doi:10.1046/j.1471-4159.1994.63031069.x

Cited by 27 publications

(15 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ND6 can be a substrate of the matrix m-calpain, assuming that it is exposed to the matrix. Although mcalpain is abundant in the cytosolic fraction [28], the lack of the cytosolic marker GAPDH in this fraction excluded contamination of the mitochondrial preparation with cytosolic proteins in our studies. The mitochondrial m-calpains are not likely to be derived from the SR, Golgi [29] or plasma membrane [30], according to Percoll/OptiPrep gradient analysis of isolated mitochondria.…”

Section: Discussionmentioning

confidence: 80%

Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia–reperfusion

Shintani-Ishida

Yoshida

2015

International Journal of Cardiology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 80%

Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia–reperfusion

Shintani-Ishida

Yoshida

2015

International Journal of Cardiology

View full text Add to dashboard Cite

“…In another study, treatment of mdx myotubes with methylprednisolone reduced calpain substrate hydrolysis to nearly normal levels (44). Glucocorticoid pretreatment of rabbits subjected to hypoxia prevented the increase in aII-spectrin breakdown that occurred in untreated animals during hypoxia, indicating impairment of calpain activation (47).…”

Section: Discussionmentioning

confidence: 93%

Effects of Acute Administration of Corticosteroids during Mechanical Ventilation on Rat Diaphragm

Maes¹,

Testelmans²,

Cadot³

et al. 2008

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Rationale: Mechanical ventilation is known to induce ventilatorinduced diaphragm dysfunction. Patients submitted to mechanical ventilation often receive massive doses of corticosteroids that may cause further deterioration of diaphragm function. Objectives: To examine whether the combination of 24 hours of controlled mechanical ventilation with corticosteroid administration would exacerbate ventilator-induced diaphragm dysfunction. Methods: Rats were randomly assigned to a group submitted to 24 hours of controlled mechanical ventilation receiving an intramuscular injection of saline or 80 mg/kg methylprednisolone, a group submitted to 24 hours of spontaneous breathing receiving saline, or methylprednisolone and a control group. Measurements and Main Results: The diaphragm force-frequency curve was shifted downward in the mechanical ventilation group, but this deleterious effect was prevented when corticosteroids were administered. Diaphragm cross-sectional area of type I fibers was similarly decreased in both mechanical ventilation groups while atrophy of type IIx/b fibers was attenuated after corticosteroid administration. The mechanical ventilation-induced reduction in diaphragm MyoD and myogenin protein expression was attenuated after corticosteroids. Plasma cytokine levels were unchanged while diaphragm lipid hydroperoxides were similarly increased in both mechanical ventilation groups. Diaphragmatic calpain activity was significantly increased in the mechanical ventilation group, but calpain activation was abated with corticosteroid administration. Inverse correlations were found between calpain activity and diaphragm force. Conclusions: A single high dose of methylprednisolone combined with controlled mechanical ventilation protected diaphragm function from the deleterious effects of controlled mechanical ventilation. Inhibition of the calpain system is most likely the mechanism by which corticosteroids induce this protective effect.

show abstract

“…In patients with Duchenne muscular dystrophy, treatment with prednisolone significantly improved muscle strength and this beneficial effect appeared to be associated with an increase in muscle mass probably mediated by inhibition of muscle proteolysis rather than by stimulation of muscle protein synthesis [27]. Inhibition of muscle proteolysis, in particular the calpain system, by corticosteroids has been suggested in several in vitro [7,19,28,29] and in vivo [14,30,31] studies. In addition, treatment with methylprednisolone has been shown to reduce caspase-3 mRNA and protein expression in several animal models [11-13].…”

Section: Discussionmentioning

confidence: 99%

“…This was also confirmed in several in vivo studies where different doses of corticosteroids were administered to animals. In rabbits, calpain activation caused by hypoxia was prevented by betametasone pretreatment, indicating inhibition of calpain activation [30]. In a rat model of ischemia-induced liver injury pretreatment of animals with 10 mg/kg of prednisolone (corresponding ~1.6 mg/kg in humans [19]) significantly inhibited calpain activation in the liver while lower doses (1 mg/kg, corresponding ~0.2 mg/kg in humans [19]and 3 mg/kg, corresponding ~0.5 mg/kg in humans [19]) did not [8].…”

Section: Discussionmentioning

confidence: 99%

Corticosteroid effects on ventilator-induced diaphragm dysfunction in anesthetized rats depend on the dose administered

et al. 2010

View full text Add to dashboard Cite

BackgroundHigh dose of corticosteroids has been previously shown to protect against controlled mechanical ventilation (CMV)-induced diaphragmatic dysfunction while inhibiting calpain activation. Because literature suggests that the calpain inhibiting effect of corticosteroid depends on the dose administered, we determined whether lower doses of corticosteroids would also provide protection of the diaphragm during CMV. This may be important for patients undergoing mechanical ventilation and receiving corticosteroids.MethodsRats were assigned to controls or to 24 hours of CMV while being treated at the start of mechanical ventilation with a single intramuscular administration of either saline, or 5 mg/kg (low MP) or 30 mg/kg (high MP) of methylprednisolone.ResultsDiaphragmatic force was decreased after CMV and this was exacerbated in the low MP group while high MP rescued this diaphragmatic dysfunction. Atrophy was more severe in the low MP group than after CMV while no atrophy was observed in the high MP group. A significant and similar increase in calpain activity was observed in both the low MP and CMV groups whereas the high dose prevented calpain activation. Expression of calpastatin, the endogenous inhibitor of calpain, was decreased in the CMV and low MP groups but its level was preserved to controls in the high MP group. Caspase-3 activity increased in all CMV groups but to a lesser extent in the low and high MP groups. The 20S proteasome activity was increased in CMV only.ConclusionsAdministration of 30 mg/kg methylprednisolone during CMV protected against CMV-induced diaphragm dysfunction while 5 mg/kg was more deleterious. The protective effect is due mainly to an inhibition of the calpain system through preservation of calpastatin levels and to a lesser extent to a caspase-3 inhibition.

show abstract

Subcellular Distribution of Calpain and Calpastatin Immunoreactivity and Fodrin Proteolysis in Rabbit Hippocampus After Hypoxia and Glucocorticoid Treatment

Cited by 27 publications

References 31 publications

Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia–reperfusion

Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia–reperfusion

Effects of Acute Administration of Corticosteroids during Mechanical Ventilation on Rat Diaphragm

Corticosteroid effects on ventilator-induced diaphragm dysfunction in anesthetized rats depend on the dose administered

Contact Info

Product

Resources

About