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We are analyzing https://link.springer.com/article/10.1007/s00395-017-0604-7.

Title:
RETRACTED ARTICLE: Compensatory role of the NBCn1 sodium/bicarbonate cotransporter on Ca2+-induced mitochondrial swelling in hypertrophic hearts | Basic Research in Cardiology
Description:
NBC Na+/HCO3 − cotransporter (NBCn1) and NHE1 Na+/H+ exchanger have been associated with cardiac disorders and recently located in coronary endothelial cells (CEC) and cardiomyocytes mitochondria, respectively. Mitochondrial NHE1 blockade delays permeability transition pore (MPTP) opening and reduces superoxide levels, two critical events exacerbated in cells of diseased hearts. Conversely, activation of NBCn1 prevented apoptosis in CEC subjected to ischemic stress. We characterized the role of the NHE1 and NBCn1 transporters in heart mitochondria from hypertrophic (SHR) and control (Wistar) rats. Expression of NHE1 was analyzed in left ventricular mitochondrial lysates (LVML), by immunoblots. NHE1 expression increased by ~40% in SHR compared to control (P < 0.05, n = 4). To examine NHE1-mediated Na+/H+ exchange activity in cardiac hypertrophy, mitochondria were loaded with BCECF-AM dye and the maximal rate of pHm change measured after the addition of 50 mM NaCl. SHR mitochondria had greater changes in pHm compared to Wistar, 0.10 Â± 0.01 vs. 0.06 Â± 0.01, respectively (P < 0.05, n = 5). In addition, mitochondrial suspensions from SHR and control myocardium were exposed to 200 ÎŒM CaCl2 to induce MPTP opening (light-scattering decrease, LSD) and swelling. Surprisingly, SHR rats showed smaller LSD and a reduction in mitochondrial swelling, 67 Â± 10% (n = 15), compared to control, 100 Â± 8% (n = 13). NBC inhibition with S0859 (1 ÎŒM) significantly increased swelling in both control 139 Â± 10% (n = 8) and SHR 115 Â± 10% (n = 4). Finally, NBCn1 Na+/HCO3 − cotransporter increased by twofold its expression in SHR LVML, compared to normal (P < 0.05, n = 5). We conclude that increased NBCn1 activity may play a compensatory role in hypertrophic hearts, protecting mitochondria from Ca2+-induced MPTP opening and swelling.
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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

article, pubmed, google, scholar, cas, mitochondrial, cardiac, physiol, central, res, role, heart, mitochondria, cotransporter, alvarez, permeability, rats, cell, nhe, nah, transition, cingolani, nbcn, pore, control, inhibition, cardiovasc, myocardial, cardiol, exchanger, basic, swelling, hearts, nahco, shr, hypertrophy, hypertrophic, ventricular, injury, karmazyn, disease, circ, privacy, cookies, function, content, research, retracted, sodiumbicarbonate, vargas,

Topics {✒}

month download article/chapter pacing-induced heart failure permeability transition pore nbcn1 sodium/bicarbonate cotransporter de giusti vc cardiac sodium/bicarbonate cotransporter mitochondrial fusion-fission proteins dl-3-n-butylphthalide protects ca2+-induced mptp opening guinea-pig ventricular myocyte article basic research myocardial beta-adrenoceptor system sodium–hydrogen antiporter protein ca2+-induced mitochondrial swelling examine nhe1-mediated na+/ mitochondrial permeability transition sensitive mitochondrial pore na+–hco3 − cotransporter nhe-1 inhibition-induced cardioprotection ischemia/reperfusion-induced damage full article pdf fernanda carrizo velasquez & bernardo pathological cardiac hypertrophy phm change measured reverts cardiomyocyte hypertrophy reactive oxygen species pressure overload hypertrophy lesnefsky ej villa-abrille mc privacy choices/manage cookies mitochondrial death pathway normotensive wistar–kyoto rats na+–hco3 − symport reduces superoxide levels transport influences renin-angiotensin system delays atp depletion transient complex de cingolani ge heart failure cardiac sodium/bicarbonate cardiac myocyte apoptosis chiappe de cingolani nbcn1 prevented apoptosis van de sand sodium/proton antiporters mitochondrial ph gradient mitochondrial calcium handling permeability transition increased nbcn1 activity

Questions {❓}

  • Alterations of sodium-hydrogen exchanger 1 function in response to SGLT2 inhibitors: what is the evidence?
  • Jullig M, Hickey AJ, Chai CC, Skea GL, Middleditch MJ, Costa S, Choong SY, Philips AR, Cooper GJ (2008) Is the failing heart out of fuel or a worn engine running rich?

Schema {đŸ—ș}

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         description:NBC Na+/HCO3 − cotransporter (NBCn1) and NHE1 Na+/H+ exchanger have been associated with cardiac disorders and recently located in coronary endothelial cells (CEC) and cardiomyocytes mitochondria, respectively. Mitochondrial NHE1 blockade delays permeability transition pore (MPTP) opening and reduces superoxide levels, two critical events exacerbated in cells of diseased hearts. Conversely, activation of NBCn1 prevented apoptosis in CEC subjected to ischemic stress. We characterized the role of the NHE1 and NBCn1 transporters in heart mitochondria from hypertrophic (SHR) and control (Wistar) rats. Expression of NHE1 was analyzed in left ventricular mitochondrial lysates (LVML), by immunoblots. NHE1 expression increased by ~40% in SHR compared to control (P < 0.05, n = 4). To examine NHE1-mediated Na+/H+ exchange activity in cardiac hypertrophy, mitochondria were loaded with BCECF-AM dye and the maximal rate of pHm change measured after the addition of 50 mM NaCl. SHR mitochondria had greater changes in pHm compared to Wistar, 0.10 ± 0.01 vs. 0.06 ± 0.01, respectively (P < 0.05, n = 5). In addition, mitochondrial suspensions from SHR and control myocardium were exposed to 200 ΌM CaCl2 to induce MPTP opening (light-scattering decrease, LSD) and swelling. Surprisingly, SHR rats showed smaller LSD and a reduction in mitochondrial swelling, 67 ± 10% (n = 15), compared to control, 100 ± 8% (n = 13). NBC inhibition with S0859 (1 ΌM) significantly increased swelling in both control 139 ± 10% (n = 8) and SHR 115 ± 10% (n = 4). Finally, NBCn1 Na+/HCO3 − cotransporter increased by twofold its expression in SHR LVML, compared to normal (P < 0.05, n = 5). We conclude that increased NBCn1 activity may play a compensatory role in hypertrophic hearts, protecting mitochondria from Ca2+-induced MPTP opening and swelling.
         datePublished:2017-01-24T00:00:00Z
         dateModified:2018-04-18T00:00:00Z
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            Myocardium
            Mitochondrial permeability transition pore
            NBCn1 Na+/HCO3 − cotransporter
            Cardiology
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      headline:RETRACTED ARTICLE: Compensatory role of the NBCn1 sodium/bicarbonate cotransporter on Ca2+-induced mitochondrial swelling in hypertrophic hearts
      description:NBC Na+/HCO3 − cotransporter (NBCn1) and NHE1 Na+/H+ exchanger have been associated with cardiac disorders and recently located in coronary endothelial cells (CEC) and cardiomyocytes mitochondria, respectively. Mitochondrial NHE1 blockade delays permeability transition pore (MPTP) opening and reduces superoxide levels, two critical events exacerbated in cells of diseased hearts. Conversely, activation of NBCn1 prevented apoptosis in CEC subjected to ischemic stress. We characterized the role of the NHE1 and NBCn1 transporters in heart mitochondria from hypertrophic (SHR) and control (Wistar) rats. Expression of NHE1 was analyzed in left ventricular mitochondrial lysates (LVML), by immunoblots. NHE1 expression increased by ~40% in SHR compared to control (P < 0.05, n = 4). To examine NHE1-mediated Na+/H+ exchange activity in cardiac hypertrophy, mitochondria were loaded with BCECF-AM dye and the maximal rate of pHm change measured after the addition of 50 mM NaCl. SHR mitochondria had greater changes in pHm compared to Wistar, 0.10 ± 0.01 vs. 0.06 ± 0.01, respectively (P < 0.05, n = 5). In addition, mitochondrial suspensions from SHR and control myocardium were exposed to 200 ΌM CaCl2 to induce MPTP opening (light-scattering decrease, LSD) and swelling. Surprisingly, SHR rats showed smaller LSD and a reduction in mitochondrial swelling, 67 ± 10% (n = 15), compared to control, 100 ± 8% (n = 13). NBC inhibition with S0859 (1 ΌM) significantly increased swelling in both control 139 ± 10% (n = 8) and SHR 115 ± 10% (n = 4). Finally, NBCn1 Na+/HCO3 − cotransporter increased by twofold its expression in SHR LVML, compared to normal (P < 0.05, n = 5). We conclude that increased NBCn1 activity may play a compensatory role in hypertrophic hearts, protecting mitochondria from Ca2+-induced MPTP opening and swelling.
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         Myocardium
         Mitochondrial permeability transition pore
         NBCn1 Na+/HCO3 − cotransporter
         Cardiology
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