- Email: [email protected]
PL07 Diallyl trisulfide (DATS) protects against heart failure via eNOS activation and nitric oxide mediated cardioprotection
S14
Abstracts / Nitric Oxide 31 (2013) S11–S65
more evidence emerged for a role of H2S in regulation and signalling. Sulfide stabilises the cysteine synthase complex, increasing so the synthesis of its acceptor O-acetylserine. H2S has been implicating in regulation of plant stress response, particularly draught stress. There are more and more examples of processes regulated by H2S in plants, and hydrogen sulfide is emerging as an important signalling molecule, similar to its role in the animal and human world. How far H2S function and homeostasis are similar in these diverse organisms, however, remains to be elucidated.
ABA crosstalk with NO and H2S. To understand the redox regulation of guard cells in different plant environmental scenarios is necessary to unveil how the physiology of guard cells makes use of NO and H2S as intermediates leading to selective PM ion channels activation/inhibition. Acknowledgements We thank CONICET, MINCyT, ANPCyT and UNMdP for financial support.
http://dx.doi.org/10.1016/j.niox.2013.06.015
References
PL06 Gasotransmitters in plant signalling: An exciting new field is emerging Lorenzo Lamattina, Denise Scuffi, Carlos García-Mata Instituto de Investigaciones Biológicas, Consejo Nacional de Investigaciones Científicas y Técnicas–Universidad Nacional de Mar del Plata (CONICET–UNMdP), Mar del Plata, Argentina Gaseous molecules are nowadays well established signalling components transmitting inter and intracellular information. Gasotransmitters are synthesized and metabolized by specific enzymatic activities, they possess specific cellular targets and regulate a number of physiological responses directed to keep cellular homeostasis in a changing environment. While typical messenger molecules amplify signal cascades, gasotransmitters can act through chemical modification of specific protein targets resulting in a rapid influence on cellular metabolism. In the last decade, findings describing the nitric oxide (NO) functions in plant cell signalling were a breakthrough in plant biology [1,2]. Recently, hydrogen sulfide (H2S) has emerged as a critical player in plant physiology acting as NO partner in some cases but within a yet unknown and unexplored scenario [3,4]. Plants control the gas exchange with the environment through the regulation of the stomatal pore formed by two specialized cells named guard cells. The size of the stomatal pore is finely regulated by volume changes of the guard cells, driven by the influx and efflux of osmotically active solutes through plasma membrane (PM) ion channels. Abscisic acid (ABA) is the master phytohormone controlling stomatal closure under water deficit conditions. We have demonstrated that ABA induces increases in NO concentration in guard cells [5]. NO, in turn, inactivates inward rectifying K+ Kþ channels by increasing cytosolic Ca2+ in concentrations [6] contributing to the net loss of solutes from guard cells required for stomatal closure. We have found that the gasotransmitter H2S induces the stomatal closure through a NO-mediated pathway [7]. The mutants of the plant model Arabidopsis are usually used as genetical tools for unravelling gene functions. Stomata of the Arabidopsis mutant atdes1 defective in L-cysteine desulfhydrase (DES), one of the enzymes responsible of H2S synthesis, do not respond to ABA treatment, indicating that H2S is required for ABA-mediated stomatal closure. The Arabidopsis mutant abi1 is impaired in ABA signalling and insensitive to H2S, suggesting that a functional ABA signalling is critical for H2S effect in guard cells. Thus, data support a connection between H2S and NO to operate a fine regulation of gas exchange resulting in a control of plant water status. Experiments are in progress to find experimentally H2S targets among the guard cell PM ion channels. The richness of the redox chemistry of the different NO forms (NO, NO and NO+) reacting with H2S (H+ and HS) in guard cells is an intriguing puzzle to decipher
[1] [2] [3] [4] [5] [6] [7]
Lamattina et al., Ann Rev Plant Biol (2003). Besson-Bard et al., Ann Rev Plant Biol (2008). García-Mata, LamattinaPlant Sci, 2013. Lisjak et al., Plant Cell Environ (2013). García-Mata, Lamattina, Plant Physiol (2002). García-Mata et al., PNAS (2003). Scuffi et al. submitted for publication.
http://dx.doi.org/10.1016/j.niox.2013.06.016
PL07 Diallyl trisulfide (DATS) protects against heart failure via eNOS activation and nitric oxide mediated cardioprotection David J. Lefer Department of Surgery-Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, GA 30308, USA Heart failure is the inability of the heart to meet hemodynamic demands and represents the end stage of various forms of cardiovascular disease. Current treatments for heart failure are inadequate and the availability of hearts for transplantation is extremely limited. Adjunctive therapies designed to coincide with the standard means of care are needed to slow the progression of adverse left ventricular remodeling during the development of heart failure. As the heart progresses rapidly from a compensated state to a state of decompensated failure, vascular growth cannot keep pace with myocyte growth. As such, therapies designed to induce angiogenesis or maintain coronary vascularity remain an attractive therapeutic option for the treatment of heart failure. Recent studies have shown that hydrogen sulfide (H2S) induces angiogenesis and promotes vessel growth in the setting of hindlimb ischemia. Here, we provide evidence that the administration of the stable, long-acting H2S donor, diallyl trisulfide (DATS), improves left ventricular remodeling and preserves left ventricular (LV) function in the setting of pressure-overload-induced heart failure. H2S therapy increased the expression of a number of pro-angiogenic factors, such as vascular endothelial cell growth factor, and Akt, the angiogenesis inhibitor, angiostatin. Importantly, these changes were associated with an increase in vascular density within the H2S-treated hearts. Additional studies demonstrated that H2S therapy resulted in activation of eNOS via phosphorylation of serine1177 with significant increases in (nitric oxide) NO bioavailability in the myocardium and circulation. These results suggest that H2S attenuates LV remodeling and dysfunction in the setting of heart failure by augmenting nitric oxide production via eNOS and creating a pro-angiogenic environment for the growth of new vessels. http://dx.doi.org/10.1016/j.niox.2013.06.017
Abstracts / Nitric Oxide 31 (2013) S11–S65
more evidence emerged for a role of H2S in regulation and signalling. Sulfide stabilises the cysteine synthase complex, increasing so the synthesis of its acceptor O-acetylserine. H2S has been implicating in regulation of plant stress response, particularly draught stress. There are more and more examples of processes regulated by H2S in plants, and hydrogen sulfide is emerging as an important signalling molecule, similar to its role in the animal and human world. How far H2S function and homeostasis are similar in these diverse organisms, however, remains to be elucidated.
ABA crosstalk with NO and H2S. To understand the redox regulation of guard cells in different plant environmental scenarios is necessary to unveil how the physiology of guard cells makes use of NO and H2S as intermediates leading to selective PM ion channels activation/inhibition. Acknowledgements We thank CONICET, MINCyT, ANPCyT and UNMdP for financial support.
http://dx.doi.org/10.1016/j.niox.2013.06.015
References
PL06 Gasotransmitters in plant signalling: An exciting new field is emerging Lorenzo Lamattina, Denise Scuffi, Carlos García-Mata Instituto de Investigaciones Biológicas, Consejo Nacional de Investigaciones Científicas y Técnicas–Universidad Nacional de Mar del Plata (CONICET–UNMdP), Mar del Plata, Argentina Gaseous molecules are nowadays well established signalling components transmitting inter and intracellular information. Gasotransmitters are synthesized and metabolized by specific enzymatic activities, they possess specific cellular targets and regulate a number of physiological responses directed to keep cellular homeostasis in a changing environment. While typical messenger molecules amplify signal cascades, gasotransmitters can act through chemical modification of specific protein targets resulting in a rapid influence on cellular metabolism. In the last decade, findings describing the nitric oxide (NO) functions in plant cell signalling were a breakthrough in plant biology [1,2]. Recently, hydrogen sulfide (H2S) has emerged as a critical player in plant physiology acting as NO partner in some cases but within a yet unknown and unexplored scenario [3,4]. Plants control the gas exchange with the environment through the regulation of the stomatal pore formed by two specialized cells named guard cells. The size of the stomatal pore is finely regulated by volume changes of the guard cells, driven by the influx and efflux of osmotically active solutes through plasma membrane (PM) ion channels. Abscisic acid (ABA) is the master phytohormone controlling stomatal closure under water deficit conditions. We have demonstrated that ABA induces increases in NO concentration in guard cells [5]. NO, in turn, inactivates inward rectifying K+ Kþ channels by increasing cytosolic Ca2+ in concentrations [6] contributing to the net loss of solutes from guard cells required for stomatal closure. We have found that the gasotransmitter H2S induces the stomatal closure through a NO-mediated pathway [7]. The mutants of the plant model Arabidopsis are usually used as genetical tools for unravelling gene functions. Stomata of the Arabidopsis mutant atdes1 defective in L-cysteine desulfhydrase (DES), one of the enzymes responsible of H2S synthesis, do not respond to ABA treatment, indicating that H2S is required for ABA-mediated stomatal closure. The Arabidopsis mutant abi1 is impaired in ABA signalling and insensitive to H2S, suggesting that a functional ABA signalling is critical for H2S effect in guard cells. Thus, data support a connection between H2S and NO to operate a fine regulation of gas exchange resulting in a control of plant water status. Experiments are in progress to find experimentally H2S targets among the guard cell PM ion channels. The richness of the redox chemistry of the different NO forms (NO, NO and NO+) reacting with H2S (H+ and HS) in guard cells is an intriguing puzzle to decipher
[1] [2] [3] [4] [5] [6] [7]
Lamattina et al., Ann Rev Plant Biol (2003). Besson-Bard et al., Ann Rev Plant Biol (2008). García-Mata, LamattinaPlant Sci, 2013. Lisjak et al., Plant Cell Environ (2013). García-Mata, Lamattina, Plant Physiol (2002). García-Mata et al., PNAS (2003). Scuffi et al. submitted for publication.
http://dx.doi.org/10.1016/j.niox.2013.06.016
PL07 Diallyl trisulfide (DATS) protects against heart failure via eNOS activation and nitric oxide mediated cardioprotection David J. Lefer Department of Surgery-Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, GA 30308, USA Heart failure is the inability of the heart to meet hemodynamic demands and represents the end stage of various forms of cardiovascular disease. Current treatments for heart failure are inadequate and the availability of hearts for transplantation is extremely limited. Adjunctive therapies designed to coincide with the standard means of care are needed to slow the progression of adverse left ventricular remodeling during the development of heart failure. As the heart progresses rapidly from a compensated state to a state of decompensated failure, vascular growth cannot keep pace with myocyte growth. As such, therapies designed to induce angiogenesis or maintain coronary vascularity remain an attractive therapeutic option for the treatment of heart failure. Recent studies have shown that hydrogen sulfide (H2S) induces angiogenesis and promotes vessel growth in the setting of hindlimb ischemia. Here, we provide evidence that the administration of the stable, long-acting H2S donor, diallyl trisulfide (DATS), improves left ventricular remodeling and preserves left ventricular (LV) function in the setting of pressure-overload-induced heart failure. H2S therapy increased the expression of a number of pro-angiogenic factors, such as vascular endothelial cell growth factor, and Akt, the angiogenesis inhibitor, angiostatin. Importantly, these changes were associated with an increase in vascular density within the H2S-treated hearts. Additional studies demonstrated that H2S therapy resulted in activation of eNOS via phosphorylation of serine1177 with significant increases in (nitric oxide) NO bioavailability in the myocardium and circulation. These results suggest that H2S attenuates LV remodeling and dysfunction in the setting of heart failure by augmenting nitric oxide production via eNOS and creating a pro-angiogenic environment for the growth of new vessels. http://dx.doi.org/10.1016/j.niox.2013.06.017