Large plasma-membrane depolarization precedes rapid blue-light-induced growth inhibition in cucumber

Planta ◽  
1989 ◽  
Vol 178 (3) ◽  
pp. 407-410 ◽  
Author(s):  
Edgar P. Spalding ◽  
Daniel J. Cosgrove
Keyword(s):  
Plasma Membrane ◽  
Growth Inhibition ◽  
Blue Light ◽  
Membrane Depolarization

Mechanism of blue-light-induced plasma-membrane depolarization in etiolated cucumber hypocotyls

Planta ◽  
1992 ◽  
Vol 188 (2) ◽  
pp. 199-205 ◽  
Author(s):  
EdgarP. Spalding ◽  
DanielJ. Cosgrove
Keyword(s):  
Plasma Membrane ◽  
Blue Light ◽  
Membrane Depolarization

scholarly journals Two Genetically Separable Phases of Growth Inhibition Induced by Blue Light in Arabidopsis Seedlings

1998 ◽  
Vol 118 (2) ◽  
pp. 609-615 ◽  
Author(s):  
Brian M. Parks ◽  
Myeon H. Cho ◽  
Edgar P. Spalding
Keyword(s):  
Growth Inhibition ◽  
Blue Light

scholarly journals Ethylene Is Not Involved in the Blue Light-Induced Growth Inhibition of Red Light-Grown Peas

1992 ◽  
Vol 100 (1) ◽  
pp. 95-99 ◽  
Author(s):  
Marta J. Laskowski ◽  
Espanta Seradge ◽  
James R. Shinkle ◽  
Winslow R. Briggs
Keyword(s):  
Growth Inhibition ◽  
Blue Light ◽  
Red Light

Oxidative burst and NO generation as initial response to ischemia in flow-adapted endothelial cells

2001 ◽  
Vol 280 (5) ◽  
pp. H2126-H2135 ◽  
Author(s):  
Yefim Manevich ◽  
Abu Al-Mehdi ◽  
Vladimir Muzykantov ◽  
Aron B. Fisher
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Oxidative Burst ◽  
Initial Response ◽  
Membrane Depolarization ◽  
No Synthase ◽  
Potential Production ◽  
Perfusion Chamber ◽  
Intracellular Ca ◽  
Static Conditions

Shear stress modulates endothelial physiology, yet the effect(s) of flow cessation is poorly understood. The initial metabolic responses of flow-adapted bovine pulmonary artery endothelial cells to the abrupt cessation of flow (simulated ischemia) was evaluated using a perfusion chamber designed for continuous spectroscopy. Plasma membrane potential, production of reactive O2 species (ROS), and intracellular Ca2+ and nitric oxide (NO) levels were measured with fluorescent probes. Within 15 s after flow cessation, flow-adapted cells, but not cells cultured under static conditions, showed plasma membrane depolarization and an oxidative burst with generation of ROS that was inhibited by diphenyleneiodonium. EGTA-inhibitable elevation of intracellular Ca2+ and NO were observed at ∼30 and 60 s after flow cessation, respectively. NO generation was decreased in the presence of inhibitors of NO synthase and calmodulin. Thus flow-adapted endothelial cells sense the altered hemodynamics associated with flow cessation and respond by plasma membrane depolarization, activation of NADPH oxidase, Ca2+ influx, and activation of Ca2+/calmodulin-dependent NO synthase. This signaling response is unrelated to cellular anoxia.

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