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Atrial arrhythmogenicity in aged Scn5a+/∆KPQ mice modeling long QT type 3 syndrome and its relationship to $Na^{+}$ channel expression and cardiac conduction

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Enhanced eryptosis of erythrocytes from gene-targeted mice lacking annexin A7

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lang, Elisabeth Lang, Philipp A. Shumilina, Ekaterina Qadri, Syed M. Kucherenko, Yuliya Kempe, Daniela S. Föller, Michael Capasso, Anna Wieder, Thomas Gulbins, Erich Clemen, Christoph S. Herr, Claudia Noegel, Angelika A. Huber, Stephan M. Lang, Florian
Description	Country affiliation: Germany Author Affiliation: Lang E ( Department of Physiology, University of Tübingen, Gmelinstr. 5, 72076, Tübingen, Germany.)
Abstract	Annexin A7 is a ubiquitously expressed $Ca^{2+}-$ and phospholipid-binding protein. Erythrocytes from mice lacking annexin A7 $(anxA7^{−/−})$ are deformed and relatively resistant to osmotic swelling. In normal erythrocytes, hyperosmotic shock, $Cl^{−}$ removal, and energy depletion (glucose removal) trigger $PGE_{2}$ formation, which stimulates $Ca^{2+}-permeable$ cation channels, increases cytosolic $Ca^{2+}$ activity $([Ca^{2+}]_{i}),$ and thus triggers suicidal death of erythrocytes or eryptosis, characterized by scrambling of the cell membrane with phosphatidylserine exposure at the cell surface. The present experiments explored the influence of annexin A7 deficiency on eryptosis. In erythrocytes from annexin A7-deficient mice $(anxA7^{−/−})$ and wild-type mice $(anxA7^{+/+}),$ $PGE_{2}$ formation was determined utilizing an immunoassay, ion channel activity by whole-cell patch clamp recording, $[Ca^{2+}]_{i}$ by fluo3 fluorescence, and phosphatidylserine exposure by binding of annexin A5 in fluorescence activated cell sorter (FACS) analysis. Erythrocyte number and hematocrit were significantly smaller in blood from $anx7^{−/−}$ than in $anx7^{+/+}$ mice. $Cl^{−}-removal$ (replacement with gluconate) stimulated $PGE_{2}-formation,$ activated cation currents, increased $[Ca^{2+}]_{i},$ and triggered phosphatidylserine exposure, effects significantly more pronounced in $anx7^{−/−}$ than in $anx7^{+/+}$ erythrocytes. Hyperosmotic shock (addition of 400 mM sucrose) and glucose depletion (removal of glucose) similarly increased cytosolic $Ca^{2+}$ activity and triggered phosphatidylserine exposure, effects again significantly more pronounced in $anx7^{−/−}$ than in $anx7^{+/+}$ erythrocytes. The effects of $Cl^{−}$ removal on $PGE_{2}$ formation and the cation current, as well as the effect of hypertonic cell shrinkage on $[Ca^{2+}]_{i}$ and cell membrane scrambling, were blunted following inhibition of cyclooxygenase by aspirin or diclofenac. In conclusion, lack of annexin A7 sensitizes the erythrocytes for “proapoptotic” $Ca^{2+}$ overload, an effect shortening the life span of the affected erythrocytes and, thus, leading to anemia.
File Format	HTM / HTML
ISSN	00316768
Issue Number	3
Volume Number	460
e-ISSN	14322013
Journal	Pflügers Archiv - European Journal of Physiology
Language	English
Publisher	Springer
Publisher Date	2010-08-01
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Physiology Annexin A7 Physiology Erythrocytes Animals Cell Death Chlorides Energy Metabolism Mice Mice, Knockout Osmotic Pressure Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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