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26 results on '"Bendall, Jennifer K"'

2. Cardiomyocyte Tetrahydrobiopterin Synthesis Regulates Fatty Acid Metabolism and Susceptibility to Ischemia Reperfusion Injury

Author

Chu, Sandy Minyin, primary, Heather, Lisa Claire, additional, Chuaiphichai, Surawee, additional, Nicol, Thomas, additional, Wright, Benjamin, additional, Miossec, Matthieu, additional, Lockstone, Helen, additional, Bendall, Jennifer K., additional, Douglas, Gillian, additional, Crabtree, Mark James, additional, and Channon, Keith, additional

Published
2022
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8. Endothelial Cell–Specific Reactive Oxygen Species Production Increases Susceptibility to Aortic Dissection

Author

Fan, Lampson M., primary, Douglas, Gillian, additional, Bendall, Jennifer K., additional, McNeill, Eileen, additional, Crabtree, Mark J., additional, Hale, Ashley B., additional, Mai, Anna, additional, Li, Jian-Mei, additional, McAteer, Martina A., additional, Schneider, Jurgen E., additional, Choudhury, Robin P., additional, and Channon, Keith M., additional

Published
2014
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11. Cardiomyocyte GTP Cyclohydrolase 1 and Tetrahydrobiopterin Increase NOS1 Activity and Accelerate Myocardial Relaxation

Author

Carnicer, Ricardo, primary, Hale, Ashley B., additional, Suffredini, Silvia, additional, Liu, Xing, additional, Reilly, Svetlana, additional, Zhang, Mei Hua, additional, Surdo, Nicoletta C., additional, Bendall, Jennifer K., additional, Crabtree, Mark J., additional, Lim, Gregory B.S., additional, Alp, Nicholas J., additional, Channon, Keith M., additional, and Casadei, Barbara, additional

Published
2012
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12. CCR2-Mediated Antiinflammatory Effects of Endothelial Tetrahydrobiopterin Inhibit Vascular Injury-Induced Accelerated Atherosclerosis

Author

Ali, Ziad A., primary, Bursill, Christina A., additional, Douglas, Gillian, additional, McNeill, Eileen, additional, Papaspyridonos, Marianna, additional, Tatham, Amy L., additional, Bendall, Jennifer K., additional, Akhtar, Asim M., additional, Alp, Nicholas J., additional, Greaves, David R., additional, and Channon, Keith M., additional

Published
2008
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17. Role of Myocardial Neuronal Nitric Oxide Synthase–Derived Nitric Oxide in β-Adrenergic Hyporesponsiveness After Myocardial Infarction–Induced Heart Failure in Rat

Author

Bendall, Jennifer K., primary, Damy, Thibaud, additional, Ratajczak, Philippe, additional, Loyer, Xavier, additional, Monceau, Virginie, additional, Marty, Isabelle, additional, Milliez, Paul, additional, Robidel, Estelle, additional, Marotte, Françoise, additional, Samuel, Jane-Lise, additional, and Heymes, Christophe, additional

Published
2004
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18. Cardiac Specific Increase in Aldosterone Production Induces Coronary Dysfunction in Aldosterone Synthase–Transgenic Mice

Author

Garnier, Anne, primary, Bendall, Jennifer K., additional, Fuchs, Sebastien, additional, Escoubet, Brigitte, additional, Rochais, Francesca, additional, Hoerter, Jacqueline, additional, Nehme, Johnny, additional, Ambroisine, Marie-Lory, additional, De Angelis, Noeleen, additional, Morineau, Gilles, additional, d’Estienne, Pauline, additional, Fischmeister, Rodolphe, additional, Heymes, Christophe, additional, Pinet, Florence, additional, and Delcayre, Claude, additional

Published
2004
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24. Targeting redox signaling in the vascular wall: from basic science to clinical practice.

Author

Antoniades C, Antonopoulos AS, Bendall JK, and Channon KM

Subjects
Animals, Atherosclerosis physiopathology, Atherosclerosis prevention & control, Clinical Trials as Topic, Homeostasis drug effects, Humans, Muscle, Smooth, Vascular metabolism, Oxidation-Reduction drug effects, Signal Transduction drug effects, Drug Delivery Systems, Oxidative Stress drug effects, Reactive Oxygen Species metabolism
Abstract

Oxidative stress is a key feature in vascular homeostasis. Reactive oxygen species (ROS) are produced by multiple enzymatic sources located in various anatomical structures of the vascular wall, such as the vascular endothelium, the smooth muscle cells and inflammatory cells infiltrating sub-endothelial space and the rest of the vascular wall. Although ROS behave as signaling molecules regulating important aspects of vascular physiology, their excess generation is harmful. Further to the cytotoxic effect of ROS in the vascular wall, they also activate various redox sensitive transcription pathways, regulating the expression of proinflammatory molecules with strong pro-atherogenic effects. The activation of redox-sensitive enzymatic systems in the vascular wall such as matrix metalloproteinases as well as the impairment of endothelial function have a significant impact on vascular elasticity and vascular mechanics in general. The impairment of vascular mechanics has a significant impact on vascular homeostasis, promoting atherogenesis. It is therefore crucial to regulate vascular redox signaling, by developing therapeutic strategies able to target the effectively intracellular ROS bioavailability. Statins, angiotensin converting enzyme inhibitors, thiazolidinediones, folates, tetrahydrobiopterin and other therapeutic strategies seem promising in targeting vascular redox signaling, although it is still unclear which of these treatments have the potential to effectively prevent atherogenesis. Future studies need to define the key redox sensitive pathways in the vascular wall in order to develop effective therapeutic strategies against atherosclerosis.

Published
2009
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25. Role of myocardial neuronal nitric oxide synthase-derived nitric oxide in beta-adrenergic hyporesponsiveness after myocardial infarction-induced heart failure in rat.

Author

Bendall JK, Damy T, Ratajczak P, Loyer X, Monceau V, Marty I, Milliez P, Robidel E, Marotte F, Samuel JL, and Heymes C

Subjects
Adrenergic beta-Agonists pharmacology, Animals, Autocrine Communication, Caveolin 3, Caveolins metabolism, Dobutamine pharmacology, Enzyme Induction, Heart Failure drug therapy, Heart Failure etiology, Isoproterenol pharmacology, Male, Myocardial Contraction drug effects, Nitric Oxide Synthase Type I, Rats, Rats, Wistar, Ryanodine Receptor Calcium Release Channel metabolism, Sarcolemma metabolism, Ventricular Dysfunction, Left enzymology, Ventricular Dysfunction, Left etiology, Heart Failure enzymology, Myocardial Contraction physiology, Myocardial Infarction complications, Myocardium enzymology, Nerve Tissue Proteins physiology, Nitric Oxide physiology, Nitric Oxide Synthase physiology, Receptors, Adrenergic, beta physiology
Abstract

Background: An emerging concept is that a neuronal isoform of nitric oxide synthase (NOS1) may regulate myocardial contractility. However, a role for NOS1-derived nitric oxide (NO) in heart failure (HF) has not been defined., Methods and Results: Using a model of myocardial infarction-induced HF, we demonstrated that cardiac NOS1 expression and activity increased in HF rats (P<0.05 and P<0.001 versus shams, respectively). This was associated with translocation of NOS1 from the ryanodine receptor to the sarcolemma through interactions with caveolin-3 in HF hearts. With ex vivo and in vivo pressure-volume analysis, cardiac NOS1-derived NO was found to be negatively inotropic in shams but not HF hearts. Ventricular elastance (E(es)) was significantly reduced in HF rats (P<0.05), and tau, the time constant of left ventricular relaxation, was prolonged (both P<0.05). Acute NOS1 inhibition significantly increased E(es) by 33+/-3% and tau by 17+/-2% (P<0.05) in shams, although these effects were significantly attenuated in HF hearts. beta-Adrenergic stimulation induced a marked increase in systolic performance in sham hearts, with the responses being significantly blunted in HF hearts. E(es) increased by 163+/-42% (P<0.01) in sham hearts and 56+/-9% in HF hearts, and LV +dP/dt increased by 97+/-9% (P<0.01) in shams and 37+/-7% (P<0.05) in the HF group. Interestingly, preferential NOS1 inhibition enhanced the blunted responses of LV +dP/dt and E(es) to beta-adrenergic stimulation in HF rats but had no effect in shams., Conclusions: These results provide the first evidence that increased NOS1-derived NO production may play a role in the autocrine regulation of myocardial contractility in HF.

Published
2004
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26. Pivotal role of a gp91(phox)-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy in mice.

Author

Bendall JK, Cave AC, Heymes C, Gall N, and Shah AM

Subjects
Angiotensin II, Animals, Atrial Natriuretic Factor biosynthesis, Atrial Natriuretic Factor genetics, Blood Pressure, Cardiomegaly chemically induced, Collagen metabolism, Membrane Glycoproteins genetics, Mice, Mice, Knockout, Myocardium metabolism, Myocardium pathology, Myosin Heavy Chains biosynthesis, Myosin Heavy Chains genetics, NADPH Oxidase 2, Organ Size, RNA, Messenger biosynthesis, Superoxides metabolism, Cardiomegaly enzymology, Cardiomegaly etiology, Membrane Glycoproteins physiology, NADPH Oxidases physiology
Abstract

Background: Angiotensin II induces both cardiac and vascular smooth muscle (VSM) hypertrophy. Recent studies suggest a central role for a phagocyte-type NADPH oxidase in angiotensin II-induced VSM hypertrophy. The possible involvement of an NADPH oxidase in the development of cardiac hypertrophy has not been studied. Methods and Results- Mice with targeted disruption of the NADPH oxidase subunit gp91(phox) (gp91(phox-/-)) and matched wild-type mice were subjected to subcutaneous angiotensin II infusion at a subpressor dose (0.3 mg/kg/day) for 2 weeks. Systolic blood pressure was unaltered by angiotensin II in either group. Angiotensin II significantly increased heart/body weight ratio, atrial natriuretic factor and beta-myosin heavy chain mRNA expression, myocyte area, and cardiac collagen content in wild-type but not gp91(phox-/-) mice. Angiotensin II treatment increased myocardial NADPH oxidase activity in wild-type but not gp91(phox-/-) mice., Conclusions: A gp91(phox)-containing NADPH oxidase plays an important role in the development of angiotensin II-induced cardiac hypertrophy, independent of changes in blood pressure.

Published
2002
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