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F. C. Howarth - One of the best experts on this subject based on the ideXlab platform.
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The Pattern of mRNA Expression Is Changed in Sinoatrial Node from Goto-Kakizaki Type 2 Diabetic Rat Heart
Experimental Diabetes Research, 2018Co-Authors: F. C. Howarth, K. Parekh, Pychadathil Jayaprakash, M. A. Qureshi, Murat Oz, Halina Dobrzynski, T. E. AdrianAbstract:Background. In vivo experiments in Goto-Kakizaki (GK) type 2 diabetic rats have demonstrated reductions in heart rate from a young age. The expression of genes encoding more than 70 proteins that are associated with the generation and conduction of electrical activity in the GK sinoatrial node (SAN) have been evaluated to further clarify the molecular basis of the low heart rate. Materials and Methods. Heart rate and expression of genes were evaluated with an extracellular electrode and real-time RT-PCR, respectively. Rats aged 12-13 months were employed in these experiments. Results. Isolated spontaneous heart rate was reduced in GK heart (161 ± 12 bpm) compared to controls (229 ± 11 bpm). There were many differences in expression of mRNA, and some of these differences were of particular interest. Compared to control SAN, expression of some genes were downregulated in GK-SAN: gap junction, Gja1 (Cx43), GJA5 (Cx40), Gjc1 (Cx45), and Gjd3 (Cx31.9); cell membrane transport, Trpc1 (TRPC1) and Trpc6 (TRPC6); hyperpolarization-activated cyclic nucleotide-gated channels, Hcn1 (HCN1) and Hcn4 (HCN4); calcium channels, Cacna1d (Cav1.3), Cacna1g (Cav3.1), Cacna1h (Cav3.2), Cacna2d1 (Cavα2δ1), Cacna2d3 (Cavα2δ3), and Cacng4 (Cavγ4); and potassium channels, Kcna2 (Kv1.2), Kcna4 (Kv1.4), Kcna5 (Kv1.5), Kcnb1 (Kv2.1), Kcnd3 (Kv4.3), Kcnj2 (Kir2.1), Kcnk1 (TWIK1), Kcnk5 (K2P5.1), Kcnk6 (TWIK2), and Kcnn2 (SK2) whilst others were upregulated in GK-SAN: Ryr2 (RYR2) and Nppb (BNP). Conclusions. This study provides new insight into the changing expression of genes in the sinoatrial node of diabetic heart.
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P400Effects of a sucrose-enriched diet on the pattern of gene expression, contraction and Ca2+ transport in Goto-Kakizaki type 2 diabetic rat heart
Cardiovascular Research, 2014Co-Authors: F. C. Howarth, K. Parekh, M. A. Qureshi, E El Nebrisi, Petrilla Jayaprakash, Thomas E. AdrianAbstract:There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus and cardiovascular disease is the major cause of morbidity and mortality in diabetic patients. A variety of diastolic and systolic dysfunctions have been demonstrated in type 2 diabetic heart. The consumption of sugar-sweetened beverages has been linked to rising rates of obesity which in turn is a risk factor for development of type 2 diabetes mellitus. The effects of a sucrose-enriched diet on the pattern of gene expression, contraction and calcium transport in the Goto-Kakizaki (GK) type 2 diabetic rat heart have been investigated. Genes encoding cardiac muscle proteins (Myh7, Mybpc3, Myl1, Myl3, Mylpf), intercellular proteins (Gja4), cell membrane transport (Atp1b1), calcium channels (Cacna1c, Cacna1g, Cacnb1), potassium channels (Kcnj11) were upregulated and genes encoding potassium channels (Kcnb1) were downregulated in GK compared to Control rats. Genes encoding cardiac muscle proteins (Myh6, Mybpc3, Tnn2), intercellular proteins (Gja1, Gja4), intracellular calcium transport (Atp2a1, Ryr2), cell membrane transport (Atp1a2, Atp1b1), potassium channel (Kcnj2, Kcnj8) proteins were upregulated and genes encoding cardiac muscle proteins (Myh7) were downregulated in Control/Sucrose compared to Control rats. Genes encoding cardiac muscle proteins (Myh7), potassium channel (Kcnj11) proteins were downregulated in GK/Sucrose compared to Control rats. Amplitude of shortening was reduced in myocytes from Control/Sucrose compared to Control and in GK/Sucrose compared to GK rats. Amplitude of the calcium transient was increased in myocytes from Control/Sucrose compared to Control and decreased in GK/Sucrose compared to GK rats. Subtle alterations in the pattern of expression of genes encoding a variety of cardiac muscle proteins are associated with changes in shortening and intracellular calcium transport in ventricular myocytes from GK type 2 diabetic and Control rats fed a sucrose-enriched diet.
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Effects of exercise training on excitation–contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, Pychadathil Jayaprakash, M. Oz, M. A. Qureshi, T Iqbal, T. E. Adrian, J. Singh, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca^2+]_i and L-type Ca^2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca^2+ transients and L-type Ca^2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca^2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
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Effects of exercise training on excitation-contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats.
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, M. A. Qureshi, T Iqbal, J. Singh, Petrilla Jayaprakash, Thomas E. Adrian, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca2+]i and L-type Ca2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca2+ transients and L-type Ca2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
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Altered expression of gap junction connexin proteins may partly underlie heart rhythm disturbances in the streptozotocin-induced diabetic rat heart
Molecular and Cellular Biochemistry, 2007Co-Authors: F. C. Howarth, Norbert Nowotny, Erika Zilahi, M. A. El Haj, Ming LeiAbstract:Previous studies in isolated perfused heart and in atrial preparations have demonstrated significant reductions in beating rate in STZ-induced diabetic rats, which suggests that sinus arrhythmias in diabetes mellitus may be partly caused by intrinsic alteration of sino-atrial node (SAN) function. The effects of diabetes on electrical activity and expression levels of mRNA for gap junction proteins in the SAN have been investigated. Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg) administered to young male Wistar rats (200–250 g). Experiments were performed 8–10 weeks after treatment. Conduction time and pacemaker cycle length were measured in sino-atrial node preparations with extracellular electrodes. Expression levels of mRNA for GJA5 (C×40), Gja1 (C×43) and Gja7 (C×45) were measured in SAN and compared with right atrium and right ventricle with real-time quantitative reverse transcription-polymerase chain reaction. Diabetes was confirmed by a significant elevation of blood glucose (356 ± 21 mg/dl) compared to age-matched controls (66 ± 2 mg/dl). Pacemaker cycle length was significantly prolonged in diabetic heart (415 ± 43 ms, n = 6) compared to controls (255 ± 7 ms, n = 6). Sino-atrial conduction time was also significantly prolonged in diabetic hearts (12 ± 2 ms) compared to controls (7 ± 1 ms). Expression levels of mRNA for GJA5 (C×40) and Gja1 (C×43) were moderately increased and for Gja7 (C×45) was significantly increased in SAN from diabetic heart compared to controls. Expression levels for gap junction connexin proteins were not significantly altered in right atrium or right ventricle from diabetic heart compared to controls. Structural remodelling of gap junction connexin proteins may partly underlie electrophysiological defects in STZ-induced diabetic rat SAN.
M. A. Qureshi - One of the best experts on this subject based on the ideXlab platform.
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The Pattern of mRNA Expression Is Changed in Sinoatrial Node from Goto-Kakizaki Type 2 Diabetic Rat Heart
Experimental Diabetes Research, 2018Co-Authors: F. C. Howarth, K. Parekh, Pychadathil Jayaprakash, M. A. Qureshi, Murat Oz, Halina Dobrzynski, T. E. AdrianAbstract:Background. In vivo experiments in Goto-Kakizaki (GK) type 2 diabetic rats have demonstrated reductions in heart rate from a young age. The expression of genes encoding more than 70 proteins that are associated with the generation and conduction of electrical activity in the GK sinoatrial node (SAN) have been evaluated to further clarify the molecular basis of the low heart rate. Materials and Methods. Heart rate and expression of genes were evaluated with an extracellular electrode and real-time RT-PCR, respectively. Rats aged 12-13 months were employed in these experiments. Results. Isolated spontaneous heart rate was reduced in GK heart (161 ± 12 bpm) compared to controls (229 ± 11 bpm). There were many differences in expression of mRNA, and some of these differences were of particular interest. Compared to control SAN, expression of some genes were downregulated in GK-SAN: gap junction, Gja1 (Cx43), GJA5 (Cx40), Gjc1 (Cx45), and Gjd3 (Cx31.9); cell membrane transport, Trpc1 (TRPC1) and Trpc6 (TRPC6); hyperpolarization-activated cyclic nucleotide-gated channels, Hcn1 (HCN1) and Hcn4 (HCN4); calcium channels, Cacna1d (Cav1.3), Cacna1g (Cav3.1), Cacna1h (Cav3.2), Cacna2d1 (Cavα2δ1), Cacna2d3 (Cavα2δ3), and Cacng4 (Cavγ4); and potassium channels, Kcna2 (Kv1.2), Kcna4 (Kv1.4), Kcna5 (Kv1.5), Kcnb1 (Kv2.1), Kcnd3 (Kv4.3), Kcnj2 (Kir2.1), Kcnk1 (TWIK1), Kcnk5 (K2P5.1), Kcnk6 (TWIK2), and Kcnn2 (SK2) whilst others were upregulated in GK-SAN: Ryr2 (RYR2) and Nppb (BNP). Conclusions. This study provides new insight into the changing expression of genes in the sinoatrial node of diabetic heart.
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P400Effects of a sucrose-enriched diet on the pattern of gene expression, contraction and Ca2+ transport in Goto-Kakizaki type 2 diabetic rat heart
Cardiovascular Research, 2014Co-Authors: F. C. Howarth, K. Parekh, M. A. Qureshi, E El Nebrisi, Petrilla Jayaprakash, Thomas E. AdrianAbstract:There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus and cardiovascular disease is the major cause of morbidity and mortality in diabetic patients. A variety of diastolic and systolic dysfunctions have been demonstrated in type 2 diabetic heart. The consumption of sugar-sweetened beverages has been linked to rising rates of obesity which in turn is a risk factor for development of type 2 diabetes mellitus. The effects of a sucrose-enriched diet on the pattern of gene expression, contraction and calcium transport in the Goto-Kakizaki (GK) type 2 diabetic rat heart have been investigated. Genes encoding cardiac muscle proteins (Myh7, Mybpc3, Myl1, Myl3, Mylpf), intercellular proteins (Gja4), cell membrane transport (Atp1b1), calcium channels (Cacna1c, Cacna1g, Cacnb1), potassium channels (Kcnj11) were upregulated and genes encoding potassium channels (Kcnb1) were downregulated in GK compared to Control rats. Genes encoding cardiac muscle proteins (Myh6, Mybpc3, Tnn2), intercellular proteins (Gja1, Gja4), intracellular calcium transport (Atp2a1, Ryr2), cell membrane transport (Atp1a2, Atp1b1), potassium channel (Kcnj2, Kcnj8) proteins were upregulated and genes encoding cardiac muscle proteins (Myh7) were downregulated in Control/Sucrose compared to Control rats. Genes encoding cardiac muscle proteins (Myh7), potassium channel (Kcnj11) proteins were downregulated in GK/Sucrose compared to Control rats. Amplitude of shortening was reduced in myocytes from Control/Sucrose compared to Control and in GK/Sucrose compared to GK rats. Amplitude of the calcium transient was increased in myocytes from Control/Sucrose compared to Control and decreased in GK/Sucrose compared to GK rats. Subtle alterations in the pattern of expression of genes encoding a variety of cardiac muscle proteins are associated with changes in shortening and intracellular calcium transport in ventricular myocytes from GK type 2 diabetic and Control rats fed a sucrose-enriched diet.
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Effects of exercise training on excitation–contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, Pychadathil Jayaprakash, M. Oz, M. A. Qureshi, T Iqbal, T. E. Adrian, J. Singh, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca^2+]_i and L-type Ca^2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca^2+ transients and L-type Ca^2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca^2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
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Effects of exercise training on excitation-contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats.
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, M. A. Qureshi, T Iqbal, J. Singh, Petrilla Jayaprakash, Thomas E. Adrian, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca2+]i and L-type Ca2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca2+ transients and L-type Ca2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
K. Parekh - One of the best experts on this subject based on the ideXlab platform.
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The Pattern of mRNA Expression Is Changed in Sinoatrial Node from Goto-Kakizaki Type 2 Diabetic Rat Heart
Experimental Diabetes Research, 2018Co-Authors: F. C. Howarth, K. Parekh, Pychadathil Jayaprakash, M. A. Qureshi, Murat Oz, Halina Dobrzynski, T. E. AdrianAbstract:Background. In vivo experiments in Goto-Kakizaki (GK) type 2 diabetic rats have demonstrated reductions in heart rate from a young age. The expression of genes encoding more than 70 proteins that are associated with the generation and conduction of electrical activity in the GK sinoatrial node (SAN) have been evaluated to further clarify the molecular basis of the low heart rate. Materials and Methods. Heart rate and expression of genes were evaluated with an extracellular electrode and real-time RT-PCR, respectively. Rats aged 12-13 months were employed in these experiments. Results. Isolated spontaneous heart rate was reduced in GK heart (161 ± 12 bpm) compared to controls (229 ± 11 bpm). There were many differences in expression of mRNA, and some of these differences were of particular interest. Compared to control SAN, expression of some genes were downregulated in GK-SAN: gap junction, Gja1 (Cx43), GJA5 (Cx40), Gjc1 (Cx45), and Gjd3 (Cx31.9); cell membrane transport, Trpc1 (TRPC1) and Trpc6 (TRPC6); hyperpolarization-activated cyclic nucleotide-gated channels, Hcn1 (HCN1) and Hcn4 (HCN4); calcium channels, Cacna1d (Cav1.3), Cacna1g (Cav3.1), Cacna1h (Cav3.2), Cacna2d1 (Cavα2δ1), Cacna2d3 (Cavα2δ3), and Cacng4 (Cavγ4); and potassium channels, Kcna2 (Kv1.2), Kcna4 (Kv1.4), Kcna5 (Kv1.5), Kcnb1 (Kv2.1), Kcnd3 (Kv4.3), Kcnj2 (Kir2.1), Kcnk1 (TWIK1), Kcnk5 (K2P5.1), Kcnk6 (TWIK2), and Kcnn2 (SK2) whilst others were upregulated in GK-SAN: Ryr2 (RYR2) and Nppb (BNP). Conclusions. This study provides new insight into the changing expression of genes in the sinoatrial node of diabetic heart.
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P400Effects of a sucrose-enriched diet on the pattern of gene expression, contraction and Ca2+ transport in Goto-Kakizaki type 2 diabetic rat heart
Cardiovascular Research, 2014Co-Authors: F. C. Howarth, K. Parekh, M. A. Qureshi, E El Nebrisi, Petrilla Jayaprakash, Thomas E. AdrianAbstract:There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus and cardiovascular disease is the major cause of morbidity and mortality in diabetic patients. A variety of diastolic and systolic dysfunctions have been demonstrated in type 2 diabetic heart. The consumption of sugar-sweetened beverages has been linked to rising rates of obesity which in turn is a risk factor for development of type 2 diabetes mellitus. The effects of a sucrose-enriched diet on the pattern of gene expression, contraction and calcium transport in the Goto-Kakizaki (GK) type 2 diabetic rat heart have been investigated. Genes encoding cardiac muscle proteins (Myh7, Mybpc3, Myl1, Myl3, Mylpf), intercellular proteins (Gja4), cell membrane transport (Atp1b1), calcium channels (Cacna1c, Cacna1g, Cacnb1), potassium channels (Kcnj11) were upregulated and genes encoding potassium channels (Kcnb1) were downregulated in GK compared to Control rats. Genes encoding cardiac muscle proteins (Myh6, Mybpc3, Tnn2), intercellular proteins (Gja1, Gja4), intracellular calcium transport (Atp2a1, Ryr2), cell membrane transport (Atp1a2, Atp1b1), potassium channel (Kcnj2, Kcnj8) proteins were upregulated and genes encoding cardiac muscle proteins (Myh7) were downregulated in Control/Sucrose compared to Control rats. Genes encoding cardiac muscle proteins (Myh7), potassium channel (Kcnj11) proteins were downregulated in GK/Sucrose compared to Control rats. Amplitude of shortening was reduced in myocytes from Control/Sucrose compared to Control and in GK/Sucrose compared to GK rats. Amplitude of the calcium transient was increased in myocytes from Control/Sucrose compared to Control and decreased in GK/Sucrose compared to GK rats. Subtle alterations in the pattern of expression of genes encoding a variety of cardiac muscle proteins are associated with changes in shortening and intracellular calcium transport in ventricular myocytes from GK type 2 diabetic and Control rats fed a sucrose-enriched diet.
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Effects of exercise training on excitation–contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, Pychadathil Jayaprakash, M. Oz, M. A. Qureshi, T Iqbal, T. E. Adrian, J. Singh, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca^2+]_i and L-type Ca^2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca^2+ transients and L-type Ca^2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca^2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
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Effects of exercise training on excitation-contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats.
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, M. A. Qureshi, T Iqbal, J. Singh, Petrilla Jayaprakash, Thomas E. Adrian, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca2+]i and L-type Ca2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca2+ transients and L-type Ca2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
Thomas E. Adrian - One of the best experts on this subject based on the ideXlab platform.
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P400Effects of a sucrose-enriched diet on the pattern of gene expression, contraction and Ca2+ transport in Goto-Kakizaki type 2 diabetic rat heart
Cardiovascular Research, 2014Co-Authors: F. C. Howarth, K. Parekh, M. A. Qureshi, E El Nebrisi, Petrilla Jayaprakash, Thomas E. AdrianAbstract:There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus and cardiovascular disease is the major cause of morbidity and mortality in diabetic patients. A variety of diastolic and systolic dysfunctions have been demonstrated in type 2 diabetic heart. The consumption of sugar-sweetened beverages has been linked to rising rates of obesity which in turn is a risk factor for development of type 2 diabetes mellitus. The effects of a sucrose-enriched diet on the pattern of gene expression, contraction and calcium transport in the Goto-Kakizaki (GK) type 2 diabetic rat heart have been investigated. Genes encoding cardiac muscle proteins (Myh7, Mybpc3, Myl1, Myl3, Mylpf), intercellular proteins (Gja4), cell membrane transport (Atp1b1), calcium channels (Cacna1c, Cacna1g, Cacnb1), potassium channels (Kcnj11) were upregulated and genes encoding potassium channels (Kcnb1) were downregulated in GK compared to Control rats. Genes encoding cardiac muscle proteins (Myh6, Mybpc3, Tnn2), intercellular proteins (Gja1, Gja4), intracellular calcium transport (Atp2a1, Ryr2), cell membrane transport (Atp1a2, Atp1b1), potassium channel (Kcnj2, Kcnj8) proteins were upregulated and genes encoding cardiac muscle proteins (Myh7) were downregulated in Control/Sucrose compared to Control rats. Genes encoding cardiac muscle proteins (Myh7), potassium channel (Kcnj11) proteins were downregulated in GK/Sucrose compared to Control rats. Amplitude of shortening was reduced in myocytes from Control/Sucrose compared to Control and in GK/Sucrose compared to GK rats. Amplitude of the calcium transient was increased in myocytes from Control/Sucrose compared to Control and decreased in GK/Sucrose compared to GK rats. Subtle alterations in the pattern of expression of genes encoding a variety of cardiac muscle proteins are associated with changes in shortening and intracellular calcium transport in ventricular myocytes from GK type 2 diabetic and Control rats fed a sucrose-enriched diet.
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Effects of exercise training on excitation-contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats.
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, M. A. Qureshi, T Iqbal, J. Singh, Petrilla Jayaprakash, Thomas E. Adrian, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca2+]i and L-type Ca2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca2+ transients and L-type Ca2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.
T. E. Adrian - One of the best experts on this subject based on the ideXlab platform.
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The Pattern of mRNA Expression Is Changed in Sinoatrial Node from Goto-Kakizaki Type 2 Diabetic Rat Heart
Experimental Diabetes Research, 2018Co-Authors: F. C. Howarth, K. Parekh, Pychadathil Jayaprakash, M. A. Qureshi, Murat Oz, Halina Dobrzynski, T. E. AdrianAbstract:Background. In vivo experiments in Goto-Kakizaki (GK) type 2 diabetic rats have demonstrated reductions in heart rate from a young age. The expression of genes encoding more than 70 proteins that are associated with the generation and conduction of electrical activity in the GK sinoatrial node (SAN) have been evaluated to further clarify the molecular basis of the low heart rate. Materials and Methods. Heart rate and expression of genes were evaluated with an extracellular electrode and real-time RT-PCR, respectively. Rats aged 12-13 months were employed in these experiments. Results. Isolated spontaneous heart rate was reduced in GK heart (161 ± 12 bpm) compared to controls (229 ± 11 bpm). There were many differences in expression of mRNA, and some of these differences were of particular interest. Compared to control SAN, expression of some genes were downregulated in GK-SAN: gap junction, Gja1 (Cx43), GJA5 (Cx40), Gjc1 (Cx45), and Gjd3 (Cx31.9); cell membrane transport, Trpc1 (TRPC1) and Trpc6 (TRPC6); hyperpolarization-activated cyclic nucleotide-gated channels, Hcn1 (HCN1) and Hcn4 (HCN4); calcium channels, Cacna1d (Cav1.3), Cacna1g (Cav3.1), Cacna1h (Cav3.2), Cacna2d1 (Cavα2δ1), Cacna2d3 (Cavα2δ3), and Cacng4 (Cavγ4); and potassium channels, Kcna2 (Kv1.2), Kcna4 (Kv1.4), Kcna5 (Kv1.5), Kcnb1 (Kv2.1), Kcnd3 (Kv4.3), Kcnj2 (Kir2.1), Kcnk1 (TWIK1), Kcnk5 (K2P5.1), Kcnk6 (TWIK2), and Kcnn2 (SK2) whilst others were upregulated in GK-SAN: Ryr2 (RYR2) and Nppb (BNP). Conclusions. This study provides new insight into the changing expression of genes in the sinoatrial node of diabetic heart.
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Effects of exercise training on excitation–contraction coupling and related mRNA expression in hearts of Goto-Kakizaki type 2 diabetic rats
Molecular and Cellular Biochemistry, 2013Co-Authors: K. A. Salem, V. Sydorenko, K. Parekh, Pychadathil Jayaprakash, M. Oz, M. A. Qureshi, T Iqbal, T. E. Adrian, J. Singh, F. C. HowarthAbstract:Although, several novel forms of intervention aiming at newly identified therapeutic targets are currently being developed for diabetes mellitus (DM), it is well established that physical exercise continues to be one of the most valuable forms of non-pharmacological therapy. The aim of the study was to investigate the effects of exercise training on excitation–contraction coupling and related gene expression in the Goto-Kakizaki (GK) type 2 diabetic rat heart and whether exercise is able to reverse diabetes-induced changes in excitation–contraction coupling and gene expression. Experiments were performed in GK and control rats aged 10–11 months following 2–3 months of treadmill exercise training. Shortening, [Ca^2+]_i and L-type Ca^2+ current were measured in ventricular myocytes with video edge detection, fluorescence photometry and whole cell patch clamp techniques, respectively. Expression of mRNA was assessed in ventricular muscle with real-time RT-PCR. Amplitude of shortening, Ca^2+ transients and L-type Ca^2+ current were not significantly altered in ventricular myocytes from GK sedentary compared to control sedentary rats or by exercise training. Expression of mRNA encoding Tpm2, Gja4, Atp1b1, Cacna1g, Cacnb2, Hcn2, Kcna3 and Kcne1 were up-regulated and Gja1, Kcnj2 and Kcnk3 were down-regulated in hearts of sedentary GK rats compared to sedentary controls. Gja1, Cav3 and Kcnk3 were up-regulated and Hcn2 was down-regulated in hearts of exercise trained GK compared to sedentary GK controls. Ventricular myocyte shortening and Ca^2+ transport were generally well preserved despite alterations in the profile of expression of mRNA encoding a variety of cardiac muscle proteins in the adult exercise trained GK diabetic rat heart.