Effects of ACE inhibitor and AT blocker on dystrophin-related proteins and calpain in failing heart

Takahashi, Masaya; Tanonaka, Kouichi; Yoshida, Hiroyuki; Oikawa, Ryo; Koshimizu, Miki; Daicho, Takuya; Toyo’oka, Toshimasa; Takeo, Satoshi

doi:10.1016/j.cardiores.2004.09.022

Cited by 26 publications

(22 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sample preparation for western blotting was performed according to the method of Takahashi et al (19). The heart was isolated and divided into LV wall, septum (Sep), and RV wall; and then these tissues were weighed.…”

Section: Western Blotting and Detection Of Proteinsmentioning

confidence: 99%

“…Then, the fluid was filtered and centrifuged at 1,000 × g for 10 min. Western blotting analysis was performed according to the method described previously with some modifications (19,20). Anti-HSP72/73 mouse monoclonal (Merck Billerica, MA, USA), anti-HSF1 rabbit polyclonal (Enzo Life Science, Inc., Farmingdale, NY, USA), anti-HSF1 rat monoclonal (Thermo Fisher Scientific Inc., Waltham, MA, USA), anti-HSP90 mouse monoclonal (StressMarq, Victoria, Canada), anti-HSP40 rabbit polyclonal (Enzo Life Science, Inc.), anti-HSC70 mouse monoclonal (Thermo Fisher Scientific Inc.), anti-CHIP rabbit polyclonal (Sigma-Aldrich Co., St. Louis, MO, USA), anti-histone H1 rabbit polyclonal (Sigma-Aldrich Co.), anti-GAPDH mouse monoclonal (Merck), and anti-actin mouse monoclonal (SigmaAldrich Co.) antibodies were used.…”

Section: Western Blotting and Detection Of Proteinsmentioning

confidence: 99%

“…Anti-HSP72/73 mouse monoclonal (Merck Billerica, MA, USA), anti-HSF1 rabbit polyclonal (Enzo Life Science, Inc., Farmingdale, NY, USA), anti-HSF1 rat monoclonal (Thermo Fisher Scientific Inc., Waltham, MA, USA), anti-HSP90 mouse monoclonal (StressMarq, Victoria, Canada), anti-HSP40 rabbit polyclonal (Enzo Life Science, Inc.), anti-HSC70 mouse monoclonal (Thermo Fisher Scientific Inc.), anti-CHIP rabbit polyclonal (Sigma-Aldrich Co., St. Louis, MO, USA), anti-histone H1 rabbit polyclonal (Sigma-Aldrich Co.), anti-GAPDH mouse monoclonal (Merck), and anti-actin mouse monoclonal (SigmaAldrich Co.) antibodies were used. Detection and quantification of these proteins on PVDF membranes were performed by the method described previously (19,20).…”

Section: Western Blotting and Detection Of Proteinsmentioning

confidence: 99%

See 2 more Smart Citations

Possible Involvement of HSP90-HSF1 Multichaperone Complex in Impairment of HSP72 Induction in the Failing Heart Following Myocardial Infarction in Rats

et al. 2013

View full text Add to dashboard Cite

Abstract. It is generally accepted that an increase in the myocardial level of heat-shock protein 72 (HSP72) protects viable cardiac tissue against myocardial infarction (MI)-induced stress. However, the induction of HSP72 after exposure to heat shock (HS) is blunted in the failing rat heart following MI. The mechanisms underlying this impairment in the HSP72 induction ability of the failing heart are not yet clearly defined. In the present study, we examined the involvement in heat-shock factor 1 (HSF1), a transcription factor of HSPs, in decreased ability for HSP72 induction in the failing rat heart following MI. In the failing heart, nuclear translocation of the HSF1 after exposure to hyperthermia was markedly reduced, whereas HSF1 in the cytosolic fraction and the HSP90 chaperone complex containing HSF1, a repressor of HSF1, were increased. Treatment with an HSP90 inhibitor, 17-allylamino-17-demethoxygel-danamycin, appeared to dissociate the interaction of HSF1 with HSP90, and then induced HSP72 in the failing heart after exposure to hyperthermia. These results suggest that an increase in the multichaperone complex, especially the HSF1-HSP90 interaction, associated with attenuation of HSF1 translocation into the nucleus, was involved in the impairment of HS-induced HSP72 induction in the failing heart following MI.

show abstract

Section: Western Blotting and Detection Of Proteinsmentioning

confidence: 99%

Section: Western Blotting and Detection Of Proteinsmentioning

confidence: 99%

Section: Western Blotting and Detection Of Proteinsmentioning

confidence: 99%

See 1 more Smart Citation

Possible Involvement of HSP90-HSF1 Multichaperone Complex in Impairment of HSP72 Induction in the Failing Heart Following Myocardial Infarction in Rats

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Central venous pressure was measured via a catheter that was placed in the right jugular vein and advanced to the level of the right atrium. The mean arterial blood pressure and heart rate were measured by means of a pressure transducer attached to a cannula placed into the left femoral artery and a heart rate counter, respectively (16).…”

Section: Hemodynamic Parametersmentioning

confidence: 99%

“…-dependent neutral cysteine protease present in all mammalian cells, in the failing heart following coronary artery ligation (10,16,34). Yoshida et al (10) reported that incubation of a sarcolemmal membrane fraction in the presence of m-calpain under in vitro experimental conditions resulted in decreases in α-sarcoglycan, β-sarcoglycan, and dystrophin contents.…”

Section: +mentioning

confidence: 99%

Alterations in Dystrophin-Related Glycoproteins in Development of Right Ventricular Failure in Rats

et al. 2009

View full text Add to dashboard Cite

Abstract. Genetic depletion of the dystrophin-related glycoprotein (DRGP) complex causes cardiomyopathy in animals and humans. The present study was undertaken to explore the possible involvement of alterations in DRGP in the development of the right ventricular failure in monocrotaline-administered rats (MCT rats). At the 6th and 8th weeks after subcutaneous administration of 60 mg/kg monocrotaline, echocardiographic examination showed that cardiac output indices were decreased and that the right ventricular Tei indices were increased, suggesting that right ventricular failure occurs, at the latest, by 6 weeks after monocrotaline-administration. The levels of α-and β-sarcoglycan and β-dystroglycan in the right ventricle of the MCT rats at the 6th and 8th weeks were markedly decreased, and these decreases were inversely related to the increase in the right ventricular Tei index of the MCT-administered animals. The content and activity of the Ca 2+-activated neutral protease m-calpain in the right ventricle of the MCT rats were increased at the 4th to 8th weeks and those of matrix metalloproteinase-2, at the 6th and 8th weeks. These results suggest that m-calpain-and/or matrix metalloproteinase-2-mediated alterations in the contents of α-sarcoglycan, β-sarcoglycan, and β-dystroglycan may be involved in the development of right ventricular failure in MCT rats.

show abstract

Adding the acetylcholinesterase inhibitor, donepezil, to losartan treatment markedly improves long‐term survival in rats with chronic heart failure

Zheng

Kawada

et al. 2014

European J of Heart Fail

View full text Add to dashboard Cite

AimsModulation of vagal tone using electrical vagal nerve stimulation or pharmacological acetylcholinesterase inhibition by donepezil exerts beneficial effects in an animal model of chronic heart failure (CHF). Considering different treatment mechanisms underlying renin-angiotensin system (RAS) suppression and parasympathetic activation, we hypothesized that parasympathetic activation together with RAS inhibition could attenuate CHF progression. To test this hypothesis, we investigated the therapeutic effects of a combination of donepezil and losartan in CHF rats with extensive myocardial infarction (MI Methods and resultsRats (n = 85) that had survived extensive MI were implanted with a blood pressure transmitter and were randomly assigned to receive either a combination of donepezil and losartan (DLT group) or losartan alone (LT group). Compared with the LT group, the DLT group showed a significantly lower heart rate without hypotension. DLT therapy further improved 280-day overall survival relative to the LT group (31% vs. 8%, P = 0.022) by preventing cardiac dysfunction (LV dP/dt max , 4064 ± 170 vs. 3430 ± 117 mmHg/s, P < 0.01; LV end-diastolic pressure, 17 ± 2 vs. 22 ± 2 mmHg, P < 0.05). DLT therapy was also associated with lower plasma BNP and catecholamine levels, lower cardiac angiotensin II concentrations, and higher capillary density in the peri-infarct region.

show abstract

Effects of ACE inhibitor and AT blocker on dystrophin-related proteins and calpain in failing heart

Abstract: These results suggest that attenuation in calpain-induced degradation of DRP complex is a possible mechanism for the Tra- or Can-mediated improvement of the pathogenesis of CHF following myocardial infarction.

Cited by 26 publications

References 25 publications

Possible Involvement of HSP90-HSF1 Multichaperone Complex in Impairment of HSP72 Induction in the Failing Heart Following Myocardial Infarction in Rats

Possible Involvement of HSP90-HSF1 Multichaperone Complex in Impairment of HSP72 Induction in the Failing Heart Following Myocardial Infarction in Rats

Alterations in Dystrophin-Related Glycoproteins in Development of Right Ventricular Failure in Rats

Adding the acetylcholinesterase inhibitor, donepezil, to losartan treatment markedly improves long‐term survival in rats with chronic heart failure

Contact Info

Product

Resources

About