PGE in the regulation of programmed erythrocyte death
Hyperosmotic shock, energy depletion, or removal of extracellular Cl(-) activates Ca(2+)-permeable cation channels in erythrocyte membranes. Subsequent Ca(2+) entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by mac...
Gespeichert in:
| Veröffentlicht in: | Cell death and differentiation 2005-05, Vol.12 (5), p.415-428 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 428 |
|---|---|
| container_issue | 5 |
| container_start_page | 415 |
| container_title | Cell death and differentiation |
| container_volume | 12 |
| creator | Lang, P A Kempe, D S Myssina, S Tanneur, V Birka, C Laufer, S Lang, F Wieder, T Huber, S M |
| description | Hyperosmotic shock, energy depletion, or removal of extracellular Cl(-) activates Ca(2+)-permeable cation channels in erythrocyte membranes. Subsequent Ca(2+) entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl(-) removal triggered the release of prostaglandin E(2) (PGE(2)). In whole-cell recording, activation of the cation channels by Cl(-) removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A(2) inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl(-) removal. PGE(2) (but not thromboxane) induced cation channel activation, increase in cytosolic Ca(2+) concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE(2)-induced PS exposure was not. In conclusion, hyperosmotic shock or Cl(-) removal stimulates erythrocyte PS exposure through PGE(2) formation and subsequent activation of Ca(2+)-permeable cation channels. |
| doi_str_mv | 10.1038/sj.cdd.4401561 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_67893288</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67893288</sourcerecordid><originalsourceid>FETCH-LOGICAL-n161t-15d689cdd13f83110ba2ccd558aec37255fb6d454bef37bdfc7ef5adf1595cdf3</originalsourceid><addsrcrecordid>eNo9kDtPwzAUhS0EoqWwsoE8sSXY8TMjqkpBqgQDzJFjX7ep8ii2M_TfE6mF6Z7h09F3LkL3lOSUMP0c97l1LuecUCHpBZpTrmQmOGGXU2aCZCXhaoZuYtwTQqQq5TWaUaG4LHkxR-JzvcJNj9MOcIDt2JrUDD0ePD6EYRtM14HDEI5pFwZ7TIAdmLS7RVfetBHuzneBvl9XX8u3bPOxfl--bLKeSpoyKpzU5eRHmdeMUlKbwlonhDZgmSqE8LV0XPAaPFO181aBF8Z5KkphnWcL9HTqnWR-Roip6ppooW1ND8MYK6l0yQqtJ_DxDI71ZFwdQtOZcKz-hk7AwwnoTRoD_APnx7FfWRJfoQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67893288</pqid></control><display><type>article</type><title>PGE in the regulation of programmed erythrocyte death</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>SpringerLink Journals - AutoHoldings</source><creator>Lang, P A ; Kempe, D S ; Myssina, S ; Tanneur, V ; Birka, C ; Laufer, S ; Lang, F ; Wieder, T ; Huber, S M</creator><creatorcontrib>Lang, P A ; Kempe, D S ; Myssina, S ; Tanneur, V ; Birka, C ; Laufer, S ; Lang, F ; Wieder, T ; Huber, S M</creatorcontrib><description>Hyperosmotic shock, energy depletion, or removal of extracellular Cl(-) activates Ca(2+)-permeable cation channels in erythrocyte membranes. Subsequent Ca(2+) entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl(-) removal triggered the release of prostaglandin E(2) (PGE(2)). In whole-cell recording, activation of the cation channels by Cl(-) removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A(2) inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl(-) removal. PGE(2) (but not thromboxane) induced cation channel activation, increase in cytosolic Ca(2+) concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE(2)-induced PS exposure was not. In conclusion, hyperosmotic shock or Cl(-) removal stimulates erythrocyte PS exposure through PGE(2) formation and subsequent activation of Ca(2+)-permeable cation channels.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/sj.cdd.4401561</identifier><identifier>PMID: 15746942</identifier><language>eng</language><publisher>England</publisher><subject>Ankyrins - metabolism ; Annexins - metabolism ; Apoptosis - drug effects ; Calcium - metabolism ; Calcium Channels - drug effects ; Calpain - metabolism ; Cell Size - drug effects ; Chlorides - metabolism ; Cyclooxygenase Inhibitors - pharmacology ; Cytosol - drug effects ; Diclofenac - pharmacology ; Enzyme Inhibitors - pharmacology ; Erythrocytes - drug effects ; Flow Cytometry ; Humans ; Models, Biological ; Osmotic Pressure - drug effects ; Patch-Clamp Techniques ; Phosphatidylserines - metabolism ; Phospholipases A - metabolism ; Prostaglandins E - pharmacology ; Prostaglandins E - secretion ; Quinacrine - pharmacology ; Saline Solution, Hypertonic</subject><ispartof>Cell death and differentiation, 2005-05, Vol.12 (5), p.415-428</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15746942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lang, P A</creatorcontrib><creatorcontrib>Kempe, D S</creatorcontrib><creatorcontrib>Myssina, S</creatorcontrib><creatorcontrib>Tanneur, V</creatorcontrib><creatorcontrib>Birka, C</creatorcontrib><creatorcontrib>Laufer, S</creatorcontrib><creatorcontrib>Lang, F</creatorcontrib><creatorcontrib>Wieder, T</creatorcontrib><creatorcontrib>Huber, S M</creatorcontrib><title>PGE in the regulation of programmed erythrocyte death</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><description>Hyperosmotic shock, energy depletion, or removal of extracellular Cl(-) activates Ca(2+)-permeable cation channels in erythrocyte membranes. Subsequent Ca(2+) entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl(-) removal triggered the release of prostaglandin E(2) (PGE(2)). In whole-cell recording, activation of the cation channels by Cl(-) removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A(2) inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl(-) removal. PGE(2) (but not thromboxane) induced cation channel activation, increase in cytosolic Ca(2+) concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE(2)-induced PS exposure was not. In conclusion, hyperosmotic shock or Cl(-) removal stimulates erythrocyte PS exposure through PGE(2) formation and subsequent activation of Ca(2+)-permeable cation channels.</description><subject>Ankyrins - metabolism</subject><subject>Annexins - metabolism</subject><subject>Apoptosis - drug effects</subject><subject>Calcium - metabolism</subject><subject>Calcium Channels - drug effects</subject><subject>Calpain - metabolism</subject><subject>Cell Size - drug effects</subject><subject>Chlorides - metabolism</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Cytosol - drug effects</subject><subject>Diclofenac - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Erythrocytes - drug effects</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Models, Biological</subject><subject>Osmotic Pressure - drug effects</subject><subject>Patch-Clamp Techniques</subject><subject>Phosphatidylserines - metabolism</subject><subject>Phospholipases A - metabolism</subject><subject>Prostaglandins E - pharmacology</subject><subject>Prostaglandins E - secretion</subject><subject>Quinacrine - pharmacology</subject><subject>Saline Solution, Hypertonic</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kDtPwzAUhS0EoqWwsoE8sSXY8TMjqkpBqgQDzJFjX7ep8ii2M_TfE6mF6Z7h09F3LkL3lOSUMP0c97l1LuecUCHpBZpTrmQmOGGXU2aCZCXhaoZuYtwTQqQq5TWaUaG4LHkxR-JzvcJNj9MOcIDt2JrUDD0ePD6EYRtM14HDEI5pFwZ7TIAdmLS7RVfetBHuzneBvl9XX8u3bPOxfl--bLKeSpoyKpzU5eRHmdeMUlKbwlonhDZgmSqE8LV0XPAaPFO181aBF8Z5KkphnWcL9HTqnWR-Roip6ppooW1ND8MYK6l0yQqtJ_DxDI71ZFwdQtOZcKz-hk7AwwnoTRoD_APnx7FfWRJfoQ</recordid><startdate>200505</startdate><enddate>200505</enddate><creator>Lang, P A</creator><creator>Kempe, D S</creator><creator>Myssina, S</creator><creator>Tanneur, V</creator><creator>Birka, C</creator><creator>Laufer, S</creator><creator>Lang, F</creator><creator>Wieder, T</creator><creator>Huber, S M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200505</creationdate><title>PGE in the regulation of programmed erythrocyte death</title><author>Lang, P A ; Kempe, D S ; Myssina, S ; Tanneur, V ; Birka, C ; Laufer, S ; Lang, F ; Wieder, T ; Huber, S M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-n161t-15d689cdd13f83110ba2ccd558aec37255fb6d454bef37bdfc7ef5adf1595cdf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Ankyrins - metabolism</topic><topic>Annexins - metabolism</topic><topic>Apoptosis - drug effects</topic><topic>Calcium - metabolism</topic><topic>Calcium Channels - drug effects</topic><topic>Calpain - metabolism</topic><topic>Cell Size - drug effects</topic><topic>Chlorides - metabolism</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Cytosol - drug effects</topic><topic>Diclofenac - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Erythrocytes - drug effects</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Models, Biological</topic><topic>Osmotic Pressure - drug effects</topic><topic>Patch-Clamp Techniques</topic><topic>Phosphatidylserines - metabolism</topic><topic>Phospholipases A - metabolism</topic><topic>Prostaglandins E - pharmacology</topic><topic>Prostaglandins E - secretion</topic><topic>Quinacrine - pharmacology</topic><topic>Saline Solution, Hypertonic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lang, P A</creatorcontrib><creatorcontrib>Kempe, D S</creatorcontrib><creatorcontrib>Myssina, S</creatorcontrib><creatorcontrib>Tanneur, V</creatorcontrib><creatorcontrib>Birka, C</creatorcontrib><creatorcontrib>Laufer, S</creatorcontrib><creatorcontrib>Lang, F</creatorcontrib><creatorcontrib>Wieder, T</creatorcontrib><creatorcontrib>Huber, S M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lang, P A</au><au>Kempe, D S</au><au>Myssina, S</au><au>Tanneur, V</au><au>Birka, C</au><au>Laufer, S</au><au>Lang, F</au><au>Wieder, T</au><au>Huber, S M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PGE in the regulation of programmed erythrocyte death</atitle><jtitle>Cell death and differentiation</jtitle><addtitle>Cell Death Differ</addtitle><date>2005-05</date><risdate>2005</risdate><volume>12</volume><issue>5</issue><spage>415</spage><epage>428</epage><pages>415-428</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Hyperosmotic shock, energy depletion, or removal of extracellular Cl(-) activates Ca(2+)-permeable cation channels in erythrocyte membranes. Subsequent Ca(2+) entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl(-) removal triggered the release of prostaglandin E(2) (PGE(2)). In whole-cell recording, activation of the cation channels by Cl(-) removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A(2) inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl(-) removal. PGE(2) (but not thromboxane) induced cation channel activation, increase in cytosolic Ca(2+) concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE(2)-induced PS exposure was not. In conclusion, hyperosmotic shock or Cl(-) removal stimulates erythrocyte PS exposure through PGE(2) formation and subsequent activation of Ca(2+)-permeable cation channels.</abstract><cop>England</cop><pmid>15746942</pmid><doi>10.1038/sj.cdd.4401561</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1350-9047 |
| ispartof | Cell death and differentiation, 2005-05, Vol.12 (5), p.415-428 |
| issn | 1350-9047 1476-5403 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67893288 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | Ankyrins - metabolism Annexins - metabolism Apoptosis - drug effects Calcium - metabolism Calcium Channels - drug effects Calpain - metabolism Cell Size - drug effects Chlorides - metabolism Cyclooxygenase Inhibitors - pharmacology Cytosol - drug effects Diclofenac - pharmacology Enzyme Inhibitors - pharmacology Erythrocytes - drug effects Flow Cytometry Humans Models, Biological Osmotic Pressure - drug effects Patch-Clamp Techniques Phosphatidylserines - metabolism Phospholipases A - metabolism Prostaglandins E - pharmacology Prostaglandins E - secretion Quinacrine - pharmacology Saline Solution, Hypertonic |
| title | PGE in the regulation of programmed erythrocyte death |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T13%3A58%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=PGE%20in%20the%20regulation%20of%20programmed%20erythrocyte%20death&rft.jtitle=Cell%20death%20and%20differentiation&rft.au=Lang,%20P%20A&rft.date=2005-05&rft.volume=12&rft.issue=5&rft.spage=415&rft.epage=428&rft.pages=415-428&rft.issn=1350-9047&rft.eissn=1476-5403&rft_id=info:doi/10.1038/sj.cdd.4401561&rft_dat=%3Cproquest_pubme%3E67893288%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67893288&rft_id=info:pmid/15746942&rfr_iscdi=true |