» Articles » PMID: 36090789

Glia As a Key Factor in Cell Volume Regulation Processes of the Central Nervous System

Overview
Specialty Cell Biology
Date 2022 Sep 12
PMID 36090789
Authors
Affiliations
Soon will be listed here.
Abstract

Brain edema is a pathological condition with potentially fatal consequences, related to cerebral injuries such as ischemia, chronic renal failure, uremia, and diabetes, among others. Under these pathological states, the cell volume control processes are fully compromised, because brain cells are unable to regulate the movement of water, mainly regulated by osmotic gradients. The processes involved in cell volume regulation are homeostatic mechanisms that depend on the mobilization of osmolytes (ions, organic molecules, and polyols) in the necessary direction to counteract changes in osmolyte concentration in response to water movement. The expression and coordinated function of proteins related to the cell volume regulation process, such as water channels, ion channels, and other cotransport systems in the glial cells, and considering the glial cell proportion compared to neuronal cells, leads to consider the astroglial network the main regulatory unit for water homeostasis in the central nervous system (CNS). In the last decade, several studies highlighted the pivotal role of glia in the cell volume regulation process and water homeostasis in the brain, including the retina; any malfunction of this astroglial network generates a lack of the ability to regulate the osmotic changes and water movements and consequently exacerbates the pathological condition.

Citing Articles

Astrocyte aquaporin mediates a tonic water efflux maintaining brain homeostasis.

Pham C, Komaki Y, Deas-Just A, Le Gac B, Mouffle C, Franco C Elife. 2024; 13.

PMID: 39508543 PMC: 11542920. DOI: 10.7554/eLife.95873.


The missense mutation C667F in murine β-dystroglycan causes embryonic lethality, myopathy and blood-brain barrier destabilization.

Tan R, Sciandra F, Hubner W, Bozzi M, Reimann J, Schoch S Dis Model Mech. 2024; 17(6).

PMID: 38616731 PMC: 11212641. DOI: 10.1242/dmm.050594.


GABA Release from Astrocytes in Health and Disease.

Kilb W, Kirischuk S Int J Mol Sci. 2022; 23(24).

PMID: 36555501 PMC: 9784789. DOI: 10.3390/ijms232415859.

References
1.
Skatchkov S, Eaton M, Shuba Y, Kucheryavykh Y, Derst C, Veh R . Tandem-pore domain potassium channels are functionally expressed in retinal (Müller) glial cells. Glia. 2005; 53(3):266-76. DOI: 10.1002/glia.20280. View

2.
Vajda Z, Pedersen M, Fuchtbauer E, Wertz K, Stodkilde-Jorgensen H, Sulyok E . Delayed onset of brain edema and mislocalization of aquaporin-4 in dystrophin-null transgenic mice. Proc Natl Acad Sci U S A. 2002; 99(20):13131-6. PMC: 130598. DOI: 10.1073/pnas.192457099. View

3.
Cui B, Sun J, Xiang F, Liu L, Li W . Aquaporin 4 knockdown exacerbates streptozotocin-induced diabetic retinopathy through aggravating inflammatory response. Exp Eye Res. 2012; 98:37-43. DOI: 10.1016/j.exer.2012.02.013. View

4.
Jung J, Bhat R, Preston G, Guggino W, Baraban J, Agre P . Molecular characterization of an aquaporin cDNA from brain: candidate osmoreceptor and regulator of water balance. Proc Natl Acad Sci U S A. 1994; 91(26):13052-6. PMC: 45579. DOI: 10.1073/pnas.91.26.13052. View

5.
Kofuji P, Biedermann B, Siddharthan V, Raap M, Iandiev I, Milenkovic I . Kir potassium channel subunit expression in retinal glial cells: implications for spatial potassium buffering. Glia. 2002; 39(3):292-303. DOI: 10.1002/glia.10112. View