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1

Kir4.1, Kir2.1 and aquaporin-4 mRNA level in the brain and retina of rat with toxic liver failure

100%
Obara M., Pannicke T., Bringmann A., Reichenbach A., Albrecht J.
Acta Neurobiologiae Experimentalis
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2007
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tom 67
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nr 3
2

Decreased expression of the Kir4.1 channel in the brain of rats with hepatic encephalopathy and in ammonia- and glutamine-treated cultured astrocytes

86%
Obara-Michlewska M., Pannicke T., Bringman A., Reichenbach A., Wrzosek A., Szewczyk A., Albrecht J.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
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nr 1
Hepatic encephalopathy (HE) is a neuropsychiatric disorder associated with hyperammonemia. Swelling of astrocytes is a primary cause of brain edema in patients and in animal models of HE. Hyperammonemic brain edema is aggravated by hypoosmotic imbalance due to hyponatremia, and is thought to be related not only to ammonia itself, but in the first instance to glutamine (Gln), which is synthesized in astrocytes in excess from ammonia and glutamate (Albrecht and Norenberg, 2006). This study addressed two questions 1) whether and in what degree is the impairment of ion and water homeostasis in astrocytes related to altered potassium transport, 2) if such disturbances occur, in what degree can they be ascribed to Gln accumulation? To this end we investigated the expression of the major potassium transport vehicles: glial inwardly rectifying potassium channels (Kir4.1, Kir2.1) and the Na+-K+-2Cl- cotransporter-1 (NKCC1), in brain of rats with experimentally induced HE and in rat cortical astrocytes treated in culture with ammonia or Gln. Thioacetamide-induced HE decreased the Kir4.1 expression in the rat cerebral cortex at both the mRNA and protein level, while the mRNA level of Kir2.1 and NKCC1 remained unaltered. In primary cortical astrocytes, Gln, but not ammonia, induced a decrease in the levels of Kir4.1 mRNA and protein. Kir2.1 and NKCC1 mRNA levels in cultured astrocytes were unchanged upon Gln administration. Treatment of cultured astrocytes with ammonia or Gln resulted in the reduction of the hypoosmolarity-induced potasium (86Rb) efflux from the cells. Treatment with Gln induced also a decrease in the astrocytic uptake of glutamate (D-[3H]-aspartate). The results suggest that decreased expression of Kir4.1 contributes to disturbances in ion and water homeostasis and impaired Glu clearance accompanying HE, and further bespeak the role of Gln in the pathogenesis of HE. However, direct correlation between Kir4.1 downregulation and impairment of potassium fluxes awaits to be confirmed. Experiments using siRNA duplexes, selectively downregulating Kir4.1 in cultured astrocytes, are conducted to further investigate the involvement of Kir4.1 in astrocytic cell swelling and volume regulation.
3

Ammonia alters the expression of the inwardly rectifying potassium channel kir 4.1 in vivo and in vitro

86%
Obara-Michalewska M., Podstawka K., Pannicke T., Bringmann A., Reichenbach A., Albrecht J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Ammonia is a major pathogenic factor in hepatic encephalopathy (HE). Cerebral edema resulting from astrocytic swelling is a major complication of HE. This study addresses a hypothesis linking brain edema to the dysfunction of inwardly rectifying potassium channels ñ the major route of potassium clearance by astrocytes. We measured the effect of thioacetamide (TAA)-induced HE and in vitro treatment of cultured astrocytes with ammonia, on the expression of Kir 4.1, the most common of the channels. Three TAA administrations (250 mg/kg, ip) at 24 h intervals induce liver failure associated with edematous changes in the cerebral cortex. Real-time PCR and Western-blot analysis revealed a markedly decreased expression of Kir4.1 mRNA and protein, respectively, in the cerebral cortex of the TAA-treated rats. Treatment of cerebral cortical astrocytes with 5mM ammonium chloride for 72 h, which induced astrocytic swelling as measured with the [3H]OMG (Kletzien method for cell volume measurement), likewise decreased Kir4.1 expression at the mRNA and protein level. However, a considerable variation has been observed with different preparations used, and the degree of correlation between cell swelling and Kir4.1 expression remains to be established. Treatment of cultured astrocytes with 5 mM glutamine for 72 h reproduced the effects of ammonia on Kir4.1 mRNA expression, adding credence to the current view that the cell swelling-inducing effect of ammonia is mediated by glutamine (Albrecht and Norenberg 2006, Hepatology). Supported by the Ministry of Science and High Education, grant no S005/P-N/2007/01
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