The Experts below are selected from a list of 169572 Experts worldwide ranked by ideXlab platform
David A. Jacobson - One of the best experts on this subject based on the ideXlab platform.
-
The Two-Pore-Domain Potassium Channels, TASK-1 and TASK-3, regulate Pancreatic Beta-Cell Membrane Potential in Response to pH and Anesthetics
Biophysical Journal, 2011Co-Authors: Prasanna K. Dadi, Louis H. Philipson, David A. JacobsonAbstract:Glucose stimulation of the pancreatic β-Cell depolarizes the Membrane Potential to allow activation of voltage dependent calcium channels resulting in action Potential (AP) firing, calcium influx, and insulin secretion. Two-pore-domain potassium (K2P) channels regulate the Membrane Potential from where AP firing occurs in many neurons. However, a role of K2P channels in regulating the pancreatic β-Cell Membrane Potential is unknown and thus we addressed expression and function of the TASK K2P channels in the mouse β-Cell. We find that TASK-1 and TASK-3 channels are expressed in mouse β-Cells. Furthermore, β-Cell TASK-like currents are sensitive to external pH, showing inhibition with acidic pH and stimulation with alkaline pH. Interestingly, glucose regulates β-Cell intraCellular pH causing acidic conditions in low glucose and alkaline conditions in high glucose, which may serve to regulate β-Cell TASK channel activity. Increasing glucose from 2 to 14 mM caused polarization of the β-Cell Membrane Potential whereas reducing glucose from 14 to 2 mM caused Membrane depolarization by 6.1 +/- 2.2 mV when KATP was inhibited with tolbutamide. Similarly extraCellular alkalinization (pH 8) resulted in polarization of the β-Cell Membrane Potential by 9.19 +/-2.0 mV, whereas extraCellular acidification (pH 6) caused Membrane depolarization by 9.84 +/-2.9 mV. Anesthetic compounds that activate (halothane) or inhibit (lidocaine) TASK channels were evaluated for their ability to regulate β-Cell Membrane Potential. Treatment of islets with lidocaine depolarized the β-Cell Membrane Potential by 6.2 +/- 1.5 mV and halothane treatment resulted in β-Cell Membrane polarization. Both lidocaine and halothane have been shown to cause perturbations in human glucose homeostasis. Thus, this data implicate important roles for TASK channels in regulating the β-Cell Membrane Potential, which may influence anesthetic and pH/glucose induced modulation of insulin secretion.
Justin Boy Kaye - One of the best experts on this subject based on the ideXlab platform.
-
A synthetic transMembrane segment derived from TRPV4 channel self-assembles into potassium-like channels to regulate vascular smooth muscle Cell Membrane Potential.
Journal of materials chemistry. B, 2014Co-Authors: Jinhang Zhu, Min Zhu, Feifei Jiang, Jin Zhang, Mingkui Zhong, Justin Boy KayeAbstract:Synthetic ion channels represent a new approach to mimicking natural ion channels and developing therapeutic drugs to restore ion channel dysfunction. The large superfamily of transient receptor Potential (TRP) channels involved in numerous biological processes is an important and potent therapeutic target for various human diseases. In the present study, a synthetic peptide whose sequence is from the fourth transMembrane segment of TRPV4 is found that is capable of self-assembling into potassium (K+)-like ion channels designated as TRP-PK1 in the Membranes of liposomes and live Cells. TRP-PK1 effectively mediates K+ flow across the Cell Membrane to regulate the Membrane Potential. TRP-PK1 is also able to relax agonist-induced vessel contraction and regulate the resting blood pressure by hyperpolarizing the vascular smooth muscle Cell Membrane Potential. TRP-PK1 represents a novel lead compound for mimicking K+ channels and treating hypertension, heart rate disorder and other K+ channel dysfunction-induced diseases. The present study also sheds new light onto the mimic ion channel function and the significant utilization of natural biological sources.
Hiroshi Imahori - One of the best experts on this subject based on the ideXlab platform.
-
Utilization of Photoinduced Charge-Separated State of Donor–Acceptor-Linked Molecules for Regulation of Cell Membrane Potential and Ion Transport
Journal of the American Chemical Society, 2012Co-Authors: Tomohiro Numata, Tatsuya Murakami, Fumiaki Kawashima, Nobuhiro Morone, John E. Heuser, Yuta Takano, Kei Ohkubo, Shunichi Fukuzumi, Yasuo Mori, Hiroshi ImahoriAbstract:The control of ion transport across Cell Membranes by light is an attractive strategy that allows targeted, fast control of precisely defined events in the biological Membrane. Here we report a novel general strategy for the control of Membrane Potential and ion transport by using charge-separation molecules and light. Delivery of charge-separation molecules to the plasma Membrane of PC12 Cells by a membranous nanocarrier and subsequent light irradiation led to depolarization of the Membrane Potential as well as inhibition of the potassium ion flow across the Membrane. Photoregulation of the Cell Membrane Potential and ion transport by using charge-separation molecules is highly promising for control of Cell functions.
-
utilization of photoinduced charge separated state of donor acceptor linked molecules for regulation of Cell Membrane Potential and ion transport
Journal of the American Chemical Society, 2012Co-Authors: Tomohiro Numata, Tatsuya Murakami, Fumiaki Kawashima, Nobuhiro Morone, John E. Heuser, Yuta Takano, Kei Ohkubo, Shunichi Fukuzumi, Yasuo Mori, Hiroshi ImahoriAbstract:The control of ion transport across Cell Membranes by light is an attractive strategy that allows targeted, fast control of precisely defined events in the biological Membrane. Here we report a novel general strategy for the control of Membrane Potential and ion transport by using charge-separation molecules and light. Delivery of charge-separation molecules to the plasma Membrane of PC12 Cells by a membranous nanocarrier and subsequent light irradiation led to depolarization of the Membrane Potential as well as inhibition of the potassium ion flow across the Membrane. Photoregulation of the Cell Membrane Potential and ion transport by using charge-separation molecules is highly promising for control of Cell functions.
Prasanna K. Dadi - One of the best experts on this subject based on the ideXlab platform.
-
The Two-Pore-Domain Potassium Channels, TASK-1 and TASK-3, regulate Pancreatic Beta-Cell Membrane Potential in Response to pH and Anesthetics
Biophysical Journal, 2011Co-Authors: Prasanna K. Dadi, Louis H. Philipson, David A. JacobsonAbstract:Glucose stimulation of the pancreatic β-Cell depolarizes the Membrane Potential to allow activation of voltage dependent calcium channels resulting in action Potential (AP) firing, calcium influx, and insulin secretion. Two-pore-domain potassium (K2P) channels regulate the Membrane Potential from where AP firing occurs in many neurons. However, a role of K2P channels in regulating the pancreatic β-Cell Membrane Potential is unknown and thus we addressed expression and function of the TASK K2P channels in the mouse β-Cell. We find that TASK-1 and TASK-3 channels are expressed in mouse β-Cells. Furthermore, β-Cell TASK-like currents are sensitive to external pH, showing inhibition with acidic pH and stimulation with alkaline pH. Interestingly, glucose regulates β-Cell intraCellular pH causing acidic conditions in low glucose and alkaline conditions in high glucose, which may serve to regulate β-Cell TASK channel activity. Increasing glucose from 2 to 14 mM caused polarization of the β-Cell Membrane Potential whereas reducing glucose from 14 to 2 mM caused Membrane depolarization by 6.1 +/- 2.2 mV when KATP was inhibited with tolbutamide. Similarly extraCellular alkalinization (pH 8) resulted in polarization of the β-Cell Membrane Potential by 9.19 +/-2.0 mV, whereas extraCellular acidification (pH 6) caused Membrane depolarization by 9.84 +/-2.9 mV. Anesthetic compounds that activate (halothane) or inhibit (lidocaine) TASK channels were evaluated for their ability to regulate β-Cell Membrane Potential. Treatment of islets with lidocaine depolarized the β-Cell Membrane Potential by 6.2 +/- 1.5 mV and halothane treatment resulted in β-Cell Membrane polarization. Both lidocaine and halothane have been shown to cause perturbations in human glucose homeostasis. Thus, this data implicate important roles for TASK channels in regulating the β-Cell Membrane Potential, which may influence anesthetic and pH/glucose induced modulation of insulin secretion.
Jinhang Zhu - One of the best experts on this subject based on the ideXlab platform.
-
A synthetic transMembrane segment derived from TRPV4 channel self-assembles into potassium-like channels to regulate vascular smooth muscle Cell Membrane Potential.
Journal of materials chemistry. B, 2014Co-Authors: Jinhang Zhu, Min Zhu, Feifei Jiang, Jin Zhang, Mingkui Zhong, Justin Boy KayeAbstract:Synthetic ion channels represent a new approach to mimicking natural ion channels and developing therapeutic drugs to restore ion channel dysfunction. The large superfamily of transient receptor Potential (TRP) channels involved in numerous biological processes is an important and potent therapeutic target for various human diseases. In the present study, a synthetic peptide whose sequence is from the fourth transMembrane segment of TRPV4 is found that is capable of self-assembling into potassium (K+)-like ion channels designated as TRP-PK1 in the Membranes of liposomes and live Cells. TRP-PK1 effectively mediates K+ flow across the Cell Membrane to regulate the Membrane Potential. TRP-PK1 is also able to relax agonist-induced vessel contraction and regulate the resting blood pressure by hyperpolarizing the vascular smooth muscle Cell Membrane Potential. TRP-PK1 represents a novel lead compound for mimicking K+ channels and treating hypertension, heart rate disorder and other K+ channel dysfunction-induced diseases. The present study also sheds new light onto the mimic ion channel function and the significant utilization of natural biological sources.