scholarly journals Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension

2019 ◽  
Vol 31 (12) ◽  
pp. 898-915 ◽  
Author(s):  
Laura Weise-Cross ◽  
Thomas C. Resta ◽  
Nikki L. Jernigan
Keyword(s):  
Pulmonary Hypertension ◽  
Ion Channels ◽  
Redox Regulation

Pathogenic Roles of Ca2+ and Ion Channels in Hypoxia-Mediated Pulmonary Hypertension

2010 ◽  
pp. 683-694 ◽  
Author(s):  
Jian Wang ◽  
Dandan Zhang ◽  
Carmelle V. Remillard ◽  
Jason X.-J. Yuan
Keyword(s):  
Pulmonary Hypertension ◽  
Ion Channels

Regulation of ion transport by oxidants

2013 ◽  
Vol 305 (9) ◽  
pp. L595-L603 ◽  
Author(s):  
Charles A. Downs ◽  
My N. Helms
Keyword(s):  
Oxidative Stress ◽  
Ion Channels ◽  
Ion Channel ◽  
Redox Regulation ◽  
Experimental Biology ◽  
Cellular Functions ◽  
Ion Channel Regulation ◽  
Channel Regulation ◽  
Made In

Ion channels perform a variety of cellular functions in lung epithelia. Oxidant- and antioxidant-mediated mechanisms (that is, redox regulation) of ion channels are areas of intense research. Significant progress has been made in our understanding of redox regulation of ion channels since the last Experimental Biology report in 2003. Advancements include: 1) identification of nonphagocytic NADPH oxidases as sources of regulated reactive species (RS) production in epithelia, 2) an understanding that excessive treatment with antioxidants can result in greater oxidative stress, and 3) characterization of novel RS signaling pathways that converge upon ion channel regulation. These advancements, as discussed at the 2013 Experimental Biology Meeting in Boston, MA, impact our understanding of oxidative stress in the lung, and, in particular, illustrate that the redox state has profound effects on ion channel and cellular function.

scholarly journals Redox Regulation of Ion Channels

2014 ◽  
Vol 21 (6) ◽  
pp. 859-862 ◽  
Author(s):  
Ivan Bogeski ◽  
Barbara A. Niemeyer
Keyword(s):  
Ion Channels ◽  
Redox Regulation

Redox regulation of Ito remodeling in diabetic rat heart

2005 ◽  
Vol 288 (3) ◽  
pp. H1417-H1424 ◽  
Author(s):  
Xun Li ◽  
Zhi Xu ◽  
Shumin Li ◽  
George J. Rozanski
Keyword(s):  
Ion Channels ◽  
Rat Heart ◽  
Redox Regulation ◽  
Control Level ◽  
Diabetic Rat ◽  
Cell Functions ◽  
Control Heart ◽  
Rat Hearts ◽  
Glucose 6 Phosphate Dehydrogenase

Oxidative stress and the resulting change in cell redox state are proposed to contribute to pathogenic alterations in ion channels that underlie electrical remodeling of the diseased heart. The present study examined whether K+ channel remodeling is controlled by endogenous oxidoreductase systems that regulate redox-sensitive cell functions. Diabetes was induced in rats by streptozotocin, and experiments were conducted after 3–5 wk of hyperglycemia. Spectrophotometric assays of ventricular tissue extracts from diabetic rat hearts revealed divergent changes in two major oxidoreductase systems. The thioredoxin (TRX) system in diabetic rat heart was characterized by a 52% decrease in TRX reductase (TRXR) activity from control heart ( P < 0.05), whereas TRX activity was 1.7-fold greater than control heart ( P < 0.05). Diabetes elicited similar changes in the glutaredoxin (GRX) system: glutathione reductase was decreased 35% from control level ( P < 0.05), and GRX activity was 2.5-fold greater than in control heart ( P < 0.05). The basal activity of glucose-6-phosphate dehydrogenase, which generates NADPH required by the TRX and GRX systems, was not altered by diabetes. Voltage-clamp studies showed that the characteristically decreased density of the transient outward K+ current ( Ito) in isolated diabetic rat myocytes was normalized by in vitro treatment with insulin (0.1 μM) or the metabolic activator dichloroacetate (1.5 mM). The effect of these agonists on Ito was blocked by inhibitors of glucose-6-phosphate dehydrogenase. Moreover, inhibitors of TRXR, which controls the reducing activity of TRX, also blocked upregulation of Ito by insulin and dichloroacetate. These data suggest that K+ channels underlying Ito are regulated in a redox-sensitive manner by the TRX system and the remodeling of Ito that occurs in diabetes may be due to decreased TRXR activity. We propose that oxidoreductase systems are an important repair mechanism that protects ion channels and associated regulatory proteins from irreversible oxidative damage.

scholarly journals Redox Regulation of Ion Channels in the Pulmonary Circulation

2015 ◽  
Vol 22 (6) ◽  
pp. 465-485 ◽  
Author(s):  
Andrea Olschewski ◽  
Edward Kenneth Weir
Keyword(s):  
Ion Channels ◽  
Pulmonary Circulation ◽  
Redox Regulation

scholarly journals Redox and trace metal regulation of ion channels in the pain pathway

2015 ◽  
Vol 470 (3) ◽  
pp. 275-280 ◽  
Author(s):  
J. Grayson Evans ◽  
Slobodan M. Todorovic
Keyword(s):  
Ion Channels ◽  
Trace Metal ◽  
Redox Regulation ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Pain Pathway ◽  
Alternative Means ◽  
Potential Channels ◽  
Transient Receptor

Given the clinical significance of pain disorders and the relative ineffectiveness of current therapeutics, it is important to identify alternative means of modulating nociception. The most obvious pharmacological targets are the ion channels that facilitate nervous transmission from pain sensors in the periphery to the processing regions within the brain and spinal cord. In order to design effective pharmacological tools for this purpose, however, it is first necessary to understand how these channels are regulated. A growing area of research involves the investigation of the role that trace metals and endogenous redox agents play in modulating the activity of a diverse group of ion channels within the pain pathway. In the present review, the most recent literature concerning trace metal and redox regulation of T-type calcium channels, NMDA (N-methyl-D-aspartate) receptors, GABAA (γ-aminobutyric acid A) receptors and TRP (transient receptor potential) channels are described to gain a comprehensive understanding of the current state of the field as well as to provide a basis for future thought and experimentation.

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