Chloride (Cl-) is the most abundant free anion in animal cells, along with sodium and potassium are responsible for osmotic pressure and acid-base balance, and determines fundamental biological functions in all tissues. Cl- is not in electrochemical equilibrium in most cell types, for example, in epithelial cells, sympathetic ganglion cells, primary sensory neurons, immature central nervous system neurons, leukocytes and both smooth and cardiac muscle cells, [Cl-]i is maintained above equilibrium. In contrast, in some cells, particularly mature cortical neurons are associated with the active Cl- extrusion mechanisms (i.e. Cl- extruders), [Cl-]i is maintained at a value lower than that predicted for a passive Cl- distribution across the plasma membrane.
Development and regulation of Cl- homeostasis depends on the coordination of several processes. Cotransporters, or symporters, utilize electric potential and/or chemical gradients to move two or more protons and ions in the same direction across the cell membrane, whereas, chloride can move against its concentration gradient by piggybacking another ion that moves down its gradient. Exchangers, or antiporters, do effectively the same thing but by coupling the transport of two or more ion species across the membrane in opposite directions. Impaired Cl- transport affects diverse processes ranging from neuron excitability to water secretion, which underlie pathological conditions such as epilepsy, deafness, imbalance, brain edema and ischemia, pain and neurogenic inflammation, hypertrophy or heart failure-induced remodeling, chronic kidney disease and cystic fibrosis, etc. Further investigation to explore how the molecular mechanisms of nociception occur via membrane-bound Cl- ion channels or cotransporters is vital in developing a new class of therapeutics.
This Research Topic is specifically interested in original research communications, perspectives, commentaries, and reviews on, but not limited to:
• The signaling role for Cl- in new cell types;
• The new molecular structure and function of transporters or channels that involved in Cl- transport;
• The new roles in diseases of Cl- transporters / channels;
• The basic thermodynamic and kinetics aspects of Cl- transport;
new signal transduction mechanisms of Cl- transporters / channels regulation;
• The new methods for studying Cl- regulation, spanning from fluorescent dyes or fluorescent chloride reporters in single cells to knock-out models.
Chloride (Cl-) is the most abundant free anion in animal cells, along with sodium and potassium are responsible for osmotic pressure and acid-base balance, and determines fundamental biological functions in all tissues. Cl- is not in electrochemical equilibrium in most cell types, for example, in epithelial cells, sympathetic ganglion cells, primary sensory neurons, immature central nervous system neurons, leukocytes and both smooth and cardiac muscle cells, [Cl-]i is maintained above equilibrium. In contrast, in some cells, particularly mature cortical neurons are associated with the active Cl- extrusion mechanisms (i.e. Cl- extruders), [Cl-]i is maintained at a value lower than that predicted for a passive Cl- distribution across the plasma membrane.
Development and regulation of Cl- homeostasis depends on the coordination of several processes. Cotransporters, or symporters, utilize electric potential and/or chemical gradients to move two or more protons and ions in the same direction across the cell membrane, whereas, chloride can move against its concentration gradient by piggybacking another ion that moves down its gradient. Exchangers, or antiporters, do effectively the same thing but by coupling the transport of two or more ion species across the membrane in opposite directions. Impaired Cl- transport affects diverse processes ranging from neuron excitability to water secretion, which underlie pathological conditions such as epilepsy, deafness, imbalance, brain edema and ischemia, pain and neurogenic inflammation, hypertrophy or heart failure-induced remodeling, chronic kidney disease and cystic fibrosis, etc. Further investigation to explore how the molecular mechanisms of nociception occur via membrane-bound Cl- ion channels or cotransporters is vital in developing a new class of therapeutics.
This Research Topic is specifically interested in original research communications, perspectives, commentaries, and reviews on, but not limited to:
• The signaling role for Cl- in new cell types;
• The new molecular structure and function of transporters or channels that involved in Cl- transport;
• The new roles in diseases of Cl- transporters / channels;
• The basic thermodynamic and kinetics aspects of Cl- transport;
new signal transduction mechanisms of Cl- transporters / channels regulation;
• The new methods for studying Cl- regulation, spanning from fluorescent dyes or fluorescent chloride reporters in single cells to knock-out models.
