Lead induces increased water permeability in astrocytes expressing aquaporin 4

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Fältnamn	Indikatorer	Metadata
000		04514naa a2200637 4500
001		oai:DiVA.org:kth-15185
003		SwePub
008		100805s2005 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:1947915
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-151852 URI
024	7	a https://doi.org/10.1016/j.neuroscience.2005.07.0272 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:19479152 URI
040		a (SwePub)kthd (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Gunnarson, E.u Karolinska Institutet4 aut
245	1 0	a Lead induces increased water permeability in astrocytes expressing aquaporin 4
264	1	b Elsevier BV,c 2005
338		a print2 rdacarrier
500		a QC 20150724
520		a The water channel aquaporin 4 (AQP4) is abundantly expressed in astrocytes. There is now compelling evidence that AQP4 may contribute to an unfavorable course in brain edema. Acute lead intoxication is a condition that causes brain damage preceded by brain edema. Here we report that lead increases AQP4 water permeability (P-f) in astrocytes. A rat astrocyte cell line that does not express aquaporin 4 was transiently transfected with aquaporin 4 tagged with green fluorescent protein (GFP). Using confocal laser scanning microscopy we measured water permeability in these cells and in AQP4-negative cells located on the same plate. AQP4-expressing astrocytes had a three-fold higher water permeability than astrocytes not expressing AQP4. Lead exposure induced a significant, 40%, increase in water permeability in astrocytes expressing AQP4, but had no effect on Pf in astrocytes not expressing AQP4. The increase in water permeability persisted after lead washout, while treatment with a lead chelator, meso-2,3-dimercaptosuccinic acid, abolished the lead-induced increase in Pf. The effect of lead was attenuated in the presence of a calcium (Ca2+)/ calmodulin-dependent protein kinase 11 (CaMKII) inhibitor, but not in the presence of a protein kinase C inhibitor. In cells expressing AQP4 where the consensus site for CaMKII phosphorylation was mutated, lead failed to increase water permeability. Lead exposure also increased Pf in rat astroglial cells in primary culture, which express endogenous AQP4. Lead had no effect on Pf in astrocytes transfected with aquaporin 3. In situ hybridization studies on rat brain after oral lead intake for three days showed no change in distribution of AQP4 mRNA. It is suggested that lead-triggered stimulation of water transport in AQP4-expressing astrocytes may contribute to the pathology of acute lead intoxication.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Cell- och molekylärbiologi0 (SwePub)301082 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Cell and Molecular Biology0 (SwePub)301082 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
650	7	a NATURVETENSKAPx Biologix Cellbiologi0 (SwePub)106042 hsv//swe
650	7	a NATURAL SCIENCESx Biological Sciencesx Cell Biology0 (SwePub)106042 hsv//eng
653		a glial cells
653		a lead
653		a toxicity
653		a water channel
653		a confocal microscopy
653		a primary culture
653		a protein-kinase-c
653		a brain edema
653		a rat-brain
653		a messenger-rna
653		a membrane
653		a domains
653		a channel protein
653		a cells
653		a encephalopathy
653		a mice
653		a mislocalization
700	1	a Axehult, G.4 aut
700	1	a Baturina, G.4 aut
700	1	a Zelenin, S.u Karolinska Institutet4 aut
700	1	a Zelenina, Marinau Karolinska Institutet,KTH,Cellens fysik4 aut0 (Swepub:kth)u14w09k8
700	1	a Aperia, A.u Karolinska Institutet4 aut
710	2	a Karolinska Institutetb Cellens fysik4 org
773	0	t Neuroscienced : Elsevier BVg 136:1, s. 105-114q 136:1<105-114x 0306-4522x 1873-7544
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-15185
856	4 8	u https://doi.org/10.1016/j.neuroscience.2005.07.027
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:1947915

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Av författaren/redakt...: Gunnarson, E.; Axehult, G.; Baturina, G.; Zelenin, S.; Zelenina, Marina; Aperia, A.

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