Contribution of Anion Transporters to the Acidosis‐Induced Swelling and Intracellular Acidification of Glial Cells
: This study examines the contribution of anion transporters to the swelling and intracellular acidification of glial cells from an extracellular lactacidosis, a condition well‐known to accompany cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were exposed to lactacidosis in...
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| Veröffentlicht in: | Journal of neurochemistry 2000-07, Vol.75 (1), p.125-132 |
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| creator | Ringel, Florian Chang, Raymond C. C. Staub, Frank Baethmann, Alexander Plesnila, Nikolaus |
| description | : This study examines the contribution of anion
transporters to the swelling and intracellular acidification of glial cells
from an extracellular lactacidosis, a condition well‐known to accompany
cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were
exposed to lactacidosis in physiological or anion‐depleted media, and
different anion transport inhibitors were applied. Changes in cell volume and
intracellular pH (pHi) were simultaneously quantified by flow
cytometry. Extracellular lactacidosis (pH 6.2) led to an increase in cell
volume to 125.1 ± 2.5% of baseline within 60 min, whereas the
pHi dropped from the physiological value of 7.13 ± 0.05 to
6.32 ± 0.03. Suspension in Cl‐‐free or
HCO3‐/CO2‐free media or application of anion
transport inhibitors [0.1 mM bumetanide or 0.5 mM
4,4′‐diisothio‐cyanatostilbene‐2,2′‐disulfonic acid (DIDS)] did
not affect cell volume during baseline conditions but significantly reduced
cell swelling from lactacidosis. In addition, the Cl‐‐free or
HCO3‐/CO2‐free media and DIDS attenuated
intracellular acidosis on extracellular acidification. From these findings it
is concluded that besides the known activation of the
Na+/H+ exchanger, activation of the
Na+‐independent Cl‐/HCO3‐
exchanger and the Na+‐K+‐Cl‐ cotransporter contributes to acidosis‐induced glial swelling and the intracellular acidification. Inhibition of these processes may be of interest for future strategies in the treatment of cytotoxic brain edema from cerebral ischemia or traumatic brain injury. |
| doi_str_mv | 10.1046/j.1471-4159.2000.0750125.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71186864</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71186864</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5005-587b393ce3b6e7063847e640e6c7d9f0946bf8169fe87ab21b0b34aa764db72f3</originalsourceid><addsrcrecordid>eNqVkUuO1DAQhi0EYpqBKyALIXYJ5XfCrolgaDSCBcPash0H3ErHjZ1oZnYcgTNyEhI6PHaIlR_11V8lfQg9IVAS4PL5viRckYITUZcUAEpQAggV5c0dtPlduos2AJQWDDg9Qw9y3gMQySW5j84IVIJTITZobOIwpmCnMcQBxw5vh-VylcyQjzGNPmU8Rjx-9njrQhtzyN-_ftsN7eR8iz9c-74Pwydshhbv5iDj5o-pN-knHbrgzK_giz6YHjdzPT9E9zrTZ_9oPc_Rx9evrpo3xeX7i12zvSycABCFqJRlNXOeWekVSFZx5SUHL51q6w5qLm1XEVl3vlLGUmLBMm6Mkry1inbsHD075R5T_DL5POpDyMuGZvBxyloRUslK8n-CRElgQMUMvjiBLsWck-_0MYWDSbeagF7k6L1eDOjFgF7k6FWOvpmbH69TJnvw7V-tJxsz8HQFTHam72YJLuQ_HFeyrhfs5Qm7Dr2__Y8N9Nt3zfpgPwDc9qzu</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17603025</pqid></control><display><type>article</type><title>Contribution of Anion Transporters to the Acidosis‐Induced Swelling and Intracellular Acidification of Glial Cells</title><source>Wiley Free Content</source><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Ringel, Florian ; Chang, Raymond C. C. ; Staub, Frank ; Baethmann, Alexander ; Plesnila, Nikolaus</creator><creatorcontrib>Ringel, Florian ; Chang, Raymond C. C. ; Staub, Frank ; Baethmann, Alexander ; Plesnila, Nikolaus</creatorcontrib><description>: This study examines the contribution of anion
transporters to the swelling and intracellular acidification of glial cells
from an extracellular lactacidosis, a condition well‐known to accompany
cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were
exposed to lactacidosis in physiological or anion‐depleted media, and
different anion transport inhibitors were applied. Changes in cell volume and
intracellular pH (pHi) were simultaneously quantified by flow
cytometry. Extracellular lactacidosis (pH 6.2) led to an increase in cell
volume to 125.1 ± 2.5% of baseline within 60 min, whereas the
pHi dropped from the physiological value of 7.13 ± 0.05 to
6.32 ± 0.03. Suspension in Cl‐‐free or
HCO3‐/CO2‐free media or application of anion
transport inhibitors [0.1 mM bumetanide or 0.5 mM
4,4′‐diisothio‐cyanatostilbene‐2,2′‐disulfonic acid (DIDS)] did
not affect cell volume during baseline conditions but significantly reduced
cell swelling from lactacidosis. In addition, the Cl‐‐free or
HCO3‐/CO2‐free media and DIDS attenuated
intracellular acidosis on extracellular acidification. From these findings it
is concluded that besides the known activation of the
Na+/H+ exchanger, activation of the
Na+‐independent Cl‐/HCO3‐
exchanger and the Na+‐K+‐Cl‐ cotransporter contributes to acidosis‐induced glial swelling and the intracellular acidification. Inhibition of these processes may be of interest for future strategies in the treatment of cytotoxic brain edema from cerebral ischemia or traumatic brain injury.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.2000.0750125.x</identifier><identifier>PMID: 10854255</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford UK: Blackwell Science Ltd</publisher><subject>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology ; Animals ; Anions ; Antiporters - physiology ; Bicarbonates - administration & dosage ; Biological and medical sciences ; Brain edema ; Bumetanide - pharmacology ; Carbon Dioxide - administration & dosage ; Carrier Proteins - antagonists & inhibitors ; Carrier Proteins - physiology ; Cell Size - drug effects ; Chloride-Bicarbonate Antiporters ; Chlorides - administration & dosage ; Cl‐/HCO3‐ exchanger ; Culture Media ; Flow Cytometry ; Glioma - metabolism ; Glioma - pathology ; Hydrogen-Ion Concentration ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Lactacidosis ; Lactic Acid ; Medical sciences ; Na+‐K+‐Cl‐ cotransp ; orter‐C6 glioma cells ; Rats ; Sodium-Potassium-Chloride Symporters ; Traumas. Diseases due to physical agents ; traumatic brain injury ; Tumor Cells, Cultured</subject><ispartof>Journal of neurochemistry, 2000-07, Vol.75 (1), p.125-132</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5005-587b393ce3b6e7063847e640e6c7d9f0946bf8169fe87ab21b0b34aa764db72f3</citedby><cites>FETCH-LOGICAL-c5005-587b393ce3b6e7063847e640e6c7d9f0946bf8169fe87ab21b0b34aa764db72f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.2000.0750125.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.2000.0750125.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1476995$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10854255$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ringel, Florian</creatorcontrib><creatorcontrib>Chang, Raymond C. C.</creatorcontrib><creatorcontrib>Staub, Frank</creatorcontrib><creatorcontrib>Baethmann, Alexander</creatorcontrib><creatorcontrib>Plesnila, Nikolaus</creatorcontrib><title>Contribution of Anion Transporters to the Acidosis‐Induced Swelling and Intracellular Acidification of Glial Cells</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>: This study examines the contribution of anion
transporters to the swelling and intracellular acidification of glial cells
from an extracellular lactacidosis, a condition well‐known to accompany
cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were
exposed to lactacidosis in physiological or anion‐depleted media, and
different anion transport inhibitors were applied. Changes in cell volume and
intracellular pH (pHi) were simultaneously quantified by flow
cytometry. Extracellular lactacidosis (pH 6.2) led to an increase in cell
volume to 125.1 ± 2.5% of baseline within 60 min, whereas the
pHi dropped from the physiological value of 7.13 ± 0.05 to
6.32 ± 0.03. Suspension in Cl‐‐free or
HCO3‐/CO2‐free media or application of anion
transport inhibitors [0.1 mM bumetanide or 0.5 mM
4,4′‐diisothio‐cyanatostilbene‐2,2′‐disulfonic acid (DIDS)] did
not affect cell volume during baseline conditions but significantly reduced
cell swelling from lactacidosis. In addition, the Cl‐‐free or
HCO3‐/CO2‐free media and DIDS attenuated
intracellular acidosis on extracellular acidification. From these findings it
is concluded that besides the known activation of the
Na+/H+ exchanger, activation of the
Na+‐independent Cl‐/HCO3‐
exchanger and the Na+‐K+‐Cl‐ cotransporter contributes to acidosis‐induced glial swelling and the intracellular acidification. Inhibition of these processes may be of interest for future strategies in the treatment of cytotoxic brain edema from cerebral ischemia or traumatic brain injury.</description><subject>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology</subject><subject>Animals</subject><subject>Anions</subject><subject>Antiporters - physiology</subject><subject>Bicarbonates - administration & dosage</subject><subject>Biological and medical sciences</subject><subject>Brain edema</subject><subject>Bumetanide - pharmacology</subject><subject>Carbon Dioxide - administration & dosage</subject><subject>Carrier Proteins - antagonists & inhibitors</subject><subject>Carrier Proteins - physiology</subject><subject>Cell Size - drug effects</subject><subject>Chloride-Bicarbonate Antiporters</subject><subject>Chlorides - administration & dosage</subject><subject>Cl‐/HCO3‐ exchanger</subject><subject>Culture Media</subject><subject>Flow Cytometry</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Hydrogen-Ion Concentration</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Lactacidosis</subject><subject>Lactic Acid</subject><subject>Medical sciences</subject><subject>Na+‐K+‐Cl‐ cotransp</subject><subject>orter‐C6 glioma cells</subject><subject>Rats</subject><subject>Sodium-Potassium-Chloride Symporters</subject><subject>Traumas. Diseases due to physical agents</subject><subject>traumatic brain injury</subject><subject>Tumor Cells, Cultured</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkUuO1DAQhi0EYpqBKyALIXYJ5XfCrolgaDSCBcPash0H3ErHjZ1oZnYcgTNyEhI6PHaIlR_11V8lfQg9IVAS4PL5viRckYITUZcUAEpQAggV5c0dtPlduos2AJQWDDg9Qw9y3gMQySW5j84IVIJTITZobOIwpmCnMcQBxw5vh-VylcyQjzGNPmU8Rjx-9njrQhtzyN-_ftsN7eR8iz9c-74Pwydshhbv5iDj5o-pN-knHbrgzK_giz6YHjdzPT9E9zrTZ_9oPc_Rx9evrpo3xeX7i12zvSycABCFqJRlNXOeWekVSFZx5SUHL51q6w5qLm1XEVl3vlLGUmLBMm6Mkry1inbsHD075R5T_DL5POpDyMuGZvBxyloRUslK8n-CRElgQMUMvjiBLsWck-_0MYWDSbeagF7k6L1eDOjFgF7k6FWOvpmbH69TJnvw7V-tJxsz8HQFTHam72YJLuQ_HFeyrhfs5Qm7Dr2__Y8N9Nt3zfpgPwDc9qzu</recordid><startdate>200007</startdate><enddate>200007</enddate><creator>Ringel, Florian</creator><creator>Chang, Raymond C. C.</creator><creator>Staub, Frank</creator><creator>Baethmann, Alexander</creator><creator>Plesnila, Nikolaus</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>200007</creationdate><title>Contribution of Anion Transporters to the Acidosis‐Induced Swelling and Intracellular Acidification of Glial Cells</title><author>Ringel, Florian ; Chang, Raymond C. C. ; Staub, Frank ; Baethmann, Alexander ; Plesnila, Nikolaus</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5005-587b393ce3b6e7063847e640e6c7d9f0946bf8169fe87ab21b0b34aa764db72f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology</topic><topic>Animals</topic><topic>Anions</topic><topic>Antiporters - physiology</topic><topic>Bicarbonates - administration & dosage</topic><topic>Biological and medical sciences</topic><topic>Brain edema</topic><topic>Bumetanide - pharmacology</topic><topic>Carbon Dioxide - administration & dosage</topic><topic>Carrier Proteins - antagonists & inhibitors</topic><topic>Carrier Proteins - physiology</topic><topic>Cell Size - drug effects</topic><topic>Chloride-Bicarbonate Antiporters</topic><topic>Chlorides - administration & dosage</topic><topic>Cl‐/HCO3‐ exchanger</topic><topic>Culture Media</topic><topic>Flow Cytometry</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>Hydrogen-Ion Concentration</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Lactacidosis</topic><topic>Lactic Acid</topic><topic>Medical sciences</topic><topic>Na+‐K+‐Cl‐ cotransp</topic><topic>orter‐C6 glioma cells</topic><topic>Rats</topic><topic>Sodium-Potassium-Chloride Symporters</topic><topic>Traumas. Diseases due to physical agents</topic><topic>traumatic brain injury</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ringel, Florian</creatorcontrib><creatorcontrib>Chang, Raymond C. C.</creatorcontrib><creatorcontrib>Staub, Frank</creatorcontrib><creatorcontrib>Baethmann, Alexander</creatorcontrib><creatorcontrib>Plesnila, Nikolaus</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ringel, Florian</au><au>Chang, Raymond C. C.</au><au>Staub, Frank</au><au>Baethmann, Alexander</au><au>Plesnila, Nikolaus</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of Anion Transporters to the Acidosis‐Induced Swelling and Intracellular Acidification of Glial Cells</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2000-07</date><risdate>2000</risdate><volume>75</volume><issue>1</issue><spage>125</spage><epage>132</epage><pages>125-132</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>: This study examines the contribution of anion
transporters to the swelling and intracellular acidification of glial cells
from an extracellular lactacidosis, a condition well‐known to accompany
cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were
exposed to lactacidosis in physiological or anion‐depleted media, and
different anion transport inhibitors were applied. Changes in cell volume and
intracellular pH (pHi) were simultaneously quantified by flow
cytometry. Extracellular lactacidosis (pH 6.2) led to an increase in cell
volume to 125.1 ± 2.5% of baseline within 60 min, whereas the
pHi dropped from the physiological value of 7.13 ± 0.05 to
6.32 ± 0.03. Suspension in Cl‐‐free or
HCO3‐/CO2‐free media or application of anion
transport inhibitors [0.1 mM bumetanide or 0.5 mM
4,4′‐diisothio‐cyanatostilbene‐2,2′‐disulfonic acid (DIDS)] did
not affect cell volume during baseline conditions but significantly reduced
cell swelling from lactacidosis. In addition, the Cl‐‐free or
HCO3‐/CO2‐free media and DIDS attenuated
intracellular acidosis on extracellular acidification. From these findings it
is concluded that besides the known activation of the
Na+/H+ exchanger, activation of the
Na+‐independent Cl‐/HCO3‐
exchanger and the Na+‐K+‐Cl‐ cotransporter contributes to acidosis‐induced glial swelling and the intracellular acidification. Inhibition of these processes may be of interest for future strategies in the treatment of cytotoxic brain edema from cerebral ischemia or traumatic brain injury.</abstract><cop>Oxford UK</cop><pub>Blackwell Science Ltd</pub><pmid>10854255</pmid><doi>10.1046/j.1471-4159.2000.0750125.x</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of neurochemistry, 2000-07, Vol.75 (1), p.125-132 |
| issn | 0022-3042 1471-4159 |
| language | eng |
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| subjects | 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology Animals Anions Antiporters - physiology Bicarbonates - administration & dosage Biological and medical sciences Brain edema Bumetanide - pharmacology Carbon Dioxide - administration & dosage Carrier Proteins - antagonists & inhibitors Carrier Proteins - physiology Cell Size - drug effects Chloride-Bicarbonate Antiporters Chlorides - administration & dosage Cl‐/HCO3‐ exchanger Culture Media Flow Cytometry Glioma - metabolism Glioma - pathology Hydrogen-Ion Concentration Injuries of the nervous system and the skull. Diseases due to physical agents Lactacidosis Lactic Acid Medical sciences Na+‐K+‐Cl‐ cotransp orter‐C6 glioma cells Rats Sodium-Potassium-Chloride Symporters Traumas. Diseases due to physical agents traumatic brain injury Tumor Cells, Cultured |
| title | Contribution of Anion Transporters to the Acidosis‐Induced Swelling and Intracellular Acidification of Glial Cells |
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