Changes in the astrocytic aquaporin-4 and inwardly rectifying potassium channel expression in the brain of the amyotrophic lateral sclerosis SOD1G93Arat model

Glia ◽  
2012 ◽  
Vol 60 (12) ◽  
pp. 1991-2003 ◽  
Author(s):  
Danijela Bataveljić ◽  
Ljiljana Nikolić ◽  
Milena Milosević ◽  
Nataša Todorović ◽  
Pavle R. Andjus
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Potassium Channel ◽  
Aquaporin 4 ◽  
Inwardly Rectifying Potassium Channel ◽  
Channel Expression ◽  
Inwardly Rectifying ◽  
The Brain ◽  
Lateral Sclerosis

scholarly journals Novel Molecular Biomarkers at the Blood-Brain Barrier in ALS

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Danijela Bataveljic ◽  
Milena Milosevic ◽  
Lidija Radenovic ◽  
Pavle Andjus
Keyword(s):  
Membrane Proteins ◽  
Potassium Channel ◽  
Blood Brain Barrier ◽  
Disease Onset ◽  
Water Channel ◽  
Aquaporin 4 ◽  
Brain Barrier ◽  
Inwardly Rectifying Potassium Channel ◽  
Blood Brain ◽  
Inwardly Rectifying

Recently neuroinflammation has gained a particular focus as a key mechanism of ALS. Several studiesin vivoas well asin vitrohave nominated immunoglobulin G (IgG) isolated from ALS patients as an active contributor to disease onset and progression. We have shown that ALS IgG affects astroglial Ca2+excitability and induces downstream activation of phosphatidylinositol 3-kinase. These studies were hampered by a lack of knowledge of the pathway of entry of immune factors in the CNS. Our MRI data revealed the blood-brain barrier BBB leakage and T cell infiltration into brain parenchyma in ALS G93A rats. Since astrocyte ensheathes blood vessel wall contributing to BBB stability and plays an important role in ALS pathogenesis, we have studied astrocytic membrane proteins water channel aquaporin-4 and the inwardly rectifying potassium channel. In this review, we will summarize data related to BBB disruption with particular emphasis on impaired function of astrocytes in ALS. We will discuss implication of membrane proteins expressed on astrocytic endfeet, aquaporin-4, and inwardly rectifying potassium channel in the pathology of ALS. In addition to ALS-specific IgGs, these membrane proteins are proposed as novel biomarkers of the disease.

scholarly journals The epithelial potassium channel Kir7.1 is stimulated by progesterone

2021 ◽  
Vol 153 (10) ◽  
Author(s):  
Ida Björkgren ◽  
Sarah Mendoza ◽  
Dong Hwa Chung ◽  
Monika Haoui ◽  
Natalie True Petersen ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Progesterone Receptors ◽  
Current Clamp ◽  
Inwardly Rectifying Potassium Channel ◽  
Whole Cell Patch Clamp ◽  
Inwardly Rectifying ◽  
The Brain ◽  
Precise Molecular Mechanism

The choroid plexus (CP) epithelium secretes cerebrospinal fluid and plays an important role in healthy homeostasis of the brain. CP function can be influenced by sex steroid hormones; however, the precise molecular mechanism of such regulation is not well understood. Here, using whole-cell patch-clamp recordings from male and female murine CP cells, we show that application of progesterone resulted in specific and strong potentiation of the inwardly rectifying potassium channel Kir7.1, an essential protein that is expressed in CP and is required for survival. The potentiation was progesterone specific and independent of other known progesterone receptors expressed in CP. This effect was recapitulated with recombinant Kir7.1, as well as with endogenous Kir7.1 expressed in the retinal pigment epithelium. Current-clamp studies further showed a progesterone-induced hyperpolarization of CP cells. Our results provide evidence of a progesterone-driven control of tissues in which Kir7.1 is present.

The inwardly rectifying potassium channel subunit Kir2.2v (KCNJN1) maps to 17p11.2→p11.1

1997 ◽  
Vol 79 (1-2) ◽  
pp. 85-87 ◽  
Author(s):  
N. Namba ◽  
R. Mori ◽  
H. Tanaka ◽  
I. Kondo ◽  
K. Narahara ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Inwardly Rectifying Potassium Channel ◽  
Inwardly Rectifying

Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein

2008 ◽  
Vol 3 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jesús Ciriza ◽  
Marcos García-Ojeda ◽  
Inmaculada Martín-Burriel ◽  
Cendra Agulhon ◽  
Francisco Miana-Mena ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurotrophic Factor ◽  
Tetanus Toxin ◽  
Brain Derived Neurotrophic Factor ◽  
Trophic Factors ◽  
Low Concentrations ◽  
Neuro2a Cells ◽  
Genetic Fusion ◽  
The Brain ◽  
Lateral Sclerosis

AbstractNeurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.

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