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Article ; Online: Windows to cell function and dysfunction: signatures written in the boundary layers.

Smith, Peter J S / Collis, Leon P / Messerli, Mark A

BioEssays : news and reviews in molecular, cellular and developmental biology

2010 Volume 32, Issue 6, Page(s) 514–523

Abstract: The medium surrounding cells either in culture or in tissues contains a chemical mix varying with cell state. As solutes move in and out of the cytoplasmic compartment they set up characteristic signatures in the cellular boundary layers. These layers ... ...

Abstract	The medium surrounding cells either in culture or in tissues contains a chemical mix varying with cell state. As solutes move in and out of the cytoplasmic compartment they set up characteristic signatures in the cellular boundary layers. These layers are complex physical and chemical environments the profiles of which reflect cell physiology and provide conduits for intercellular messaging. Here we review some of the most relevant characteristics of the extracellular/intercellular space. Our initial focus is primarily on cultured cells but we extend our consideration to the far more complex environment of tissues, and discuss how chemical signatures in the boundary layer can or may affect cell function. Critical to the entire essay are the methods used, or being developed, to monitor chemical profiles in the boundary layers. We review recent developments in ultramicro electrochemical sensors and tailored optical reporters suitable for the task in hand.
MeSH term(s)	Cell Physiological Phenomena/physiology ; Cells, Cultured ; Extracellular Space/metabolism ; Models, Biological
Language	English
Publishing date	2010-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.200900173
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Article ; Online: Ion trapping with fast-response ion-selective microelectrodes enhances detection of extracellular ion channel gradients.

Messerli, Mark A / Collis, Leon P / Smith, Peter J S

Biophysical journal

2009 Volume 96, Issue 4, Page(s) 1597–1605

Abstract: Previously, functional mapping of channels has been achieved by measuring the passage of net charge and of specific ions with electrophysiological and intracellular fluorescence imaging techniques. However, functional mapping of ion channels using ... ...

Abstract	Previously, functional mapping of channels has been achieved by measuring the passage of net charge and of specific ions with electrophysiological and intracellular fluorescence imaging techniques. However, functional mapping of ion channels using extracellular ion-selective microelectrodes has distinct advantages over the former methods. We have developed this method through measurement of extracellular K+ gradients caused by efflux through Ca2+-activated K+ channels expressed in Chinese hamster ovary cells. We report that electrodes constructed with short columns of a mechanically stable K+-selective liquid membrane respond quickly and measure changes in local [K+] consistent with a diffusion model. When used in close proximity to the plasma membrane (<4 microm), the ISMs pose a barrier to simple diffusion, creating an ion trap. The ion trap amplifies the local change in [K+] without dramatically changing the rise or fall time of the [K+] profile. Measurement of extracellular K+ gradients from activated rSlo channels shows that rapid events, 10-55 ms, can be characterized. This method provides a noninvasive means for functional mapping of channel location and density as well as for characterizing the properties of ion channels in the plasma membrane.
MeSH term(s)	Animals ; CHO Cells ; Cell Membrane/physiology ; Computer Simulation ; Cricetinae ; Cricetulus ; Diffusion ; Extracellular Space/chemistry ; Ion Channel Gating/physiology ; Microelectrodes ; Monte Carlo Method ; Patch-Clamp Techniques ; Potassium/analysis ; Potassium/metabolism ; Potassium Channels, Calcium-Activated/physiology
Chemical Substances	Potassium Channels, Calcium-Activated ; Potassium (RWP5GA015D)
Language	English
Publishing date	2009-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2008.11.025
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Article ; Online: Simultaneous single neuron recording of O2 consumption, [Ca2+]i and mitochondrial membrane potential in glutamate toxicity.

Gleichmann, Marc / Collis, Leon P / Smith, Peter J S / Mattson, Mark P

Journal of neurochemistry

2009 Volume 109, Issue 2, Page(s) 644–655

Abstract: In order to determine the sequence of cellular processes in glutamate toxicity, we simultaneously recorded O(2) consumption, cytosolic Ca(2+) concentration ([Ca(2+)](i)), and mitochondrial membrane potential (mDeltapsi) in single cortical neurons. Oxygen ...

Abstract	In order to determine the sequence of cellular processes in glutamate toxicity, we simultaneously recorded O(2) consumption, cytosolic Ca(2+) concentration ([Ca(2+)](i)), and mitochondrial membrane potential (mDeltapsi) in single cortical neurons. Oxygen consumption was measured using an amperometric self-referencing platinum electrode adjacent to neurons in which [Ca(2+)](i) and mDeltapsi were monitored with Fluo-4 and TMRE(+), respectively, using a spinning disk laser confocal microscope. Excitotoxic doses of glutamate caused an elevation of [Ca(2+)](i) followed seconds afterwards by an increase in O(2) consumption which reached a maximum level within 1-5 min. A modest increase in mDeltapsi occurred during this time period, and then, shortly before maximal O(2) consumption was reached, the mDeltapsi, as indicated by TMRE(+) fluorescence, dissipated. Maximal O(2) consumption lasted up to 5 min and then declined together with mDeltapsi and ATP levels, while [Ca(2+)](i) further increased. mDeltapsi and [Ca(2+)](i) returned to baseline levels when neurons were treated with an NMDA receptor antagonist shortly after the [Ca(2+)](i) increased. Our unprecedented spatial and time resolution revealed that this sequence of events is identical in all neurons, albeit with considerable variability in magnitude and kinetics of changes in O(2) consumption, [Ca(2+)](i), and mDeltapsi. The data obtained using this new method are consistent with a model where Ca(2+) influx causes ATP depletion, despite maximal mitochondrial respiration, minutes after glutamate receptor activation.
MeSH term(s)	Animals ; Calcium/metabolism ; Cations, Divalent/metabolism ; Cell Survival/drug effects ; Cell Survival/physiology ; Cells, Cultured ; Cerebral Cortex/cytology ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Cytosol/metabolism ; Glutamic Acid/toxicity ; Membrane Potential, Mitochondrial/drug effects ; Membrane Potential, Mitochondrial/physiology ; Mitochondrial Membranes/drug effects ; Mitochondrial Membranes/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Oxygen Consumption/drug effects ; Oxygen Consumption/physiology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Cations, Divalent ; Glutamic Acid (3KX376GY7L) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2009-02-16
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2009.05997.x
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Article: Windows to cell function and dysfunction: Signatures written in the boundary layers

Smith, Peter J.S / Collis, Leon P / Messerli, Mark A

BioEssays. 2010 June, v. 32, no. 6

2010

Abstract	The medium surrounding cells either in culture or in tissues contains a chemical mix varying with cell state. As solutes move in and out of the cytoplasmic compartment they set up characteristic signatures in the cellular boundary layers. These layers are complex physical and chemical environments the profiles of which reflect cell physiology and provide conduits for intercellular messaging. Here we review some of the most relevant characteristics of the extracellular/intercellular space. Our initial focus is primarily on cultured cells but we extend our consideration to the far more complex environment of tissues, and discuss how chemical signatures in the boundary layer can or may affect cell function. Critical to the entire essay are the methods used, or being developed, to monitor chemical profiles in the boundary layers. We review recent developments in ultramicro electrochemical sensors and tailored optical reporters suitable for the task in hand.
Language	English
Dates of publication	2010-06
Size	p. 514-523.
Publishing place	Wiley-VCH Verlag
Document type	Article
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.200900173
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Article: Simultaneous single neuron recording of O₂ consumption, [Ca²⁺]i and mitochondrial membrane potential in glutamate toxicity

Gleichmann, Marc / Collis, Leon P / Smith, Peter J.S / Mattson, Mark P

Journal of neurochemistry. 2009 Apr., v. 109, no. 2

2009

Abstract: In order to determine the sequence of cellular processes in glutamate toxicity, we simultaneously recorded O₂ consumption, cytosolic Ca²⁺ concentration ([Ca²⁺]i), and mitochondrial membrane potential (mΔψ) in single cortical neurons. Oxygen consumption ... ...

Abstract	In order to determine the sequence of cellular processes in glutamate toxicity, we simultaneously recorded O₂ consumption, cytosolic Ca²⁺ concentration ([Ca²⁺]i), and mitochondrial membrane potential (mΔψ) in single cortical neurons. Oxygen consumption was measured using an amperometric self-referencing platinum electrode adjacent to neurons in which [Ca²⁺]i and mΔψ were monitored with Fluo-4 and TMRE⁺, respectively, using a spinning disk laser confocal microscope. Excitotoxic doses of glutamate caused an elevation of [Ca²⁺]i followed seconds afterwards by an increase in O₂ consumption which reached a maximum level within 1-5 min. A modest increase in mΔψ occurred during this time period, and then, shortly before maximal O₂ consumption was reached, the mΔψ, as indicated by TMRE⁺ fluorescence, dissipated. Maximal O₂ consumption lasted up to 5 min and then declined together with mΔψ and ATP levels, while [Ca²⁺]i further increased. mΔψ and [Ca²⁺]i returned to baseline levels when neurons were treated with an NMDA receptor antagonist shortly after the [Ca²⁺]i increased. Our unprecedented spatial and time resolution revealed that this sequence of events is identical in all neurons, albeit with considerable variability in magnitude and kinetics of changes in O₂ consumption, [Ca²⁺]i, and mΔψ. The data obtained using this new method are consistent with a model where Ca²⁺ influx causes ATP depletion, despite maximal mitochondrial respiration, minutes after glutamate receptor activation.
Keywords	oxygen consumption
Language	English
Dates of publication	2009-04
Size	p. 644-655.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2009.05997.x
Database	NAL-Catalogue (AGRICOLA)

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Article: beta2-Adrenergic receptor agonists stimulate L-type calcium current independent of PKA in newborn rabbit ventricular myocytes.

Collis, Leon P / Srivastava, Shekhar / Coetzee, William A / Artman, Michael

American journal of physiology. Heart and circulatory physiology

2007 Volume 293, Issue 5, Page(s) H2826–35

Abstract: Selective stimulation of beta(2)-adrenergic receptors (ARs) in newborn rabbit ventricular myocardium invokes a positive inotropic effect that is lost during postnatal maturation. The underlying mechanisms for this age-related stimulatory response remain ... ...

Abstract	Selective stimulation of beta(2)-adrenergic receptors (ARs) in newborn rabbit ventricular myocardium invokes a positive inotropic effect that is lost during postnatal maturation. The underlying mechanisms for this age-related stimulatory response remain unresolved. We examined the effects of beta(2)-AR stimulation on L-type Ca(2+) current (I(Ca,L)) during postnatal development. I(Ca,L) was measured (37 degrees C; either Ca(2+) or Ba(2+) as the charge carrier) using the whole-cell patch-clamp technique in newborn (1 to 5 days old) and adult rabbit ventricular myocytes. Ca(2+) transients were measured concomitantly by dialyzing the cell with indo-1. Activation of beta(2)-ARs (with either 100 nM zinterol or 1 microM isoproterenol in the presence of the beta(1)-AR antagonist, CGP20712A) stimulated I(Ca,L) twofold in newborns but not in adults. The beta(2)-AR-mediated increase in Ca(2+) transient amplitude in newborns was due exclusively to the augmentation of I(Ca,L). Zinterol increased the rate of inactivation of I(Ca,L) and increased the Ca(2+) flux integral. The beta(2)-AR inverse agonist, ICI-118551 (500 nM), but not the beta(1)-AR antagonist, CGP20712A (500 nM), blocked the response to zinterol. Unexpectedly, the PKA blockers, H-89 (10 microM), PKI 6-22 amide (10 microM), and Rp-cAMP (100 microM), all failed to prevent the response to zinterol but completely blocked responses to selective beta(1)-AR stimulation of I(Ca,L) in newborns. Our results demonstrate that in addition to the conventional beta(1)-AR/cAMP/PKA pathway, newborn rabbit myocardium exhibits a novel beta(2)-AR-mediated, PKA-insensitive pathway that stimulates I(Ca,L). This striking developmental difference plays a major role in the age-related differences in inotropic responses to beta(2)-AR agonists.
MeSH term(s)	Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists/administration & dosage ; Animals ; Animals, Newborn ; Calcium/metabolism ; Calcium Channels, L-Type/drug effects ; Calcium Channels, L-Type/physiology ; Calcium Signaling/drug effects ; Calcium Signaling/physiology ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dose-Response Relationship, Drug ; Ion Channel Gating/drug effects ; Ion Channel Gating/physiology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/physiology ; Rabbits ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists ; Calcium Channels, L-Type ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2007-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00101.2007
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Article ; Online: Comparative gene expression profiling in human-induced pluripotent stem cell--derived cardiocytes and human and cynomolgus heart tissue.

Puppala, Dinesh / Collis, Leon P / Sun, Sunny Z / Bonato, Vinicius / Chen, Xian / Anson, Blake / Pletcher, Mathew / Fermini, Bernard / Engle, Sandra J

Toxicological sciences : an official journal of the Society of Toxicology

2013 Volume 131, Issue 1, Page(s) 292–301

Abstract: Cardiotoxicity is one of the leading causes of drug attrition. Current in vitro models insufficiently predict cardiotoxicity, and there is a need for alternative physiologically relevant models. Here we describe the gene expression profile of human- ... ...

Abstract	Cardiotoxicity is one of the leading causes of drug attrition. Current in vitro models insufficiently predict cardiotoxicity, and there is a need for alternative physiologically relevant models. Here we describe the gene expression profile of human-induced pluripotent stem cell-derived cardiocytes (iCC) postthaw over a period of 42 days in culture and compare this profile to human fetal and adult as well as adult cynomolgus nonhuman primate (NHP, Macaca fascicularis) heart tissue. Our results indicate that iCC express relevant cardiac markers such as ion channels (SCN5A, KCNJ2, CACNA1C, KCNQ1, and KCNH2), tissue-specific structural markers (MYH6, MYLPF, MYBPC3, DES, TNNT2, and TNNI3), and transcription factors (NKX2.5, GATA4, and GATA6) and lack the expression of stem cell markers (FOXD3, GBX2, NANOG, POU5F1, SOX2, and ZFP42). Furthermore, we performed a functional evaluation of contractility of the iCC and showed functional and pharmacological correlations with myocytes isolated from adult NHP hearts. These results suggest that stem cell-derived cardiocytes may represent a novel in vitro model to study human cardiac toxicity with potential ex vivo and in vivo translation.
MeSH term(s)	Animals ; Calcium Signaling/drug effects ; Cell Culture Techniques ; Cell Differentiation ; Drug Evaluation, Preclinical ; Drug-Related Side Effects and Adverse Reactions ; Gene Expression Profiling ; Humans ; Macaca fascicularis ; Myocardium/metabolism ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Pluripotent Stem Cells/cytology ; Transcriptome/drug effects
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfs282
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Article: Modulation of extracellular proton fluxes from retinal horizontal cells of the catfish by depolarization and glutamate.

Kreitzer, Matthew A / Collis, Leon P / Molina, Anthony J A / Smith, Peter J S / Malchow, Robert Paul

The Journal of general physiology

2007 Volume 130, Issue 2, Page(s) 169–182

Abstract: Self-referencing H(+)-selective microelectrodes were used to measure extracellular proton fluxes from cone-driven horizontal cells isolated from the retina of the catfish (Ictalurus punctatus). The neurotransmitter glutamate induced an alkalinization of ... ...

Abstract	Self-referencing H(+)-selective microelectrodes were used to measure extracellular proton fluxes from cone-driven horizontal cells isolated from the retina of the catfish (Ictalurus punctatus). The neurotransmitter glutamate induced an alkalinization of the area adjacent to the external face of the cell membrane. The effect of glutamate occurred regardless of whether the external solution was buffered with 1 mM HEPES, 3 mM phosphate, or 24 mM bicarbonate. The AMPA/kainate receptor agonist kainate and the NMDA receptor agonist N-methyl-D-aspartate both mimicked the effect of glutamate. The effect of kainate on proton flux was inhibited by the AMPA/kainate receptor blocker CNQX, and the effect of NMDA was abolished by the NMDA receptor antagonist DAP-5. Metabotropic glutamate receptor agonists produced no alteration in proton fluxes from horizontal cells. Depolarization of cells either by increasing extracellular potassium or directly by voltage clamp also produced an alkalinization adjacent to the cell membrane. The effects of depolarization on proton flux were blocked by 10 microM nifedipine, an inhibitor of L-type calcium channels. The plasmalemma Ca(2+/)H(+) ATPase (PMCA) blocker 5(6)-carboxyeosin also significantly reduced proton flux modulation by glutamate. Our results are consistent with the hypothesis that glutamate-induced extracellular alkalinizations arise from activation of the PMCA pump following increased intracellular calcium entry into cells. This process might help to relieve suppression of photoreceptor neurotransmitter release that results from exocytosed protons from photoreceptor synaptic terminals. Our findings argue strongly against the hypothesis that protons released by horizontal cells act as the inhibitory feedback neurotransmitter that creates the surround portion of the receptive fields of retinal neurons.
MeSH term(s)	Animals ; Calcium/physiology ; Catfishes ; Excitatory Amino Acid Agonists/pharmacology ; Glutamic Acid/physiology ; Hydrogen-Ion Concentration ; Kainic Acid/pharmacology ; Membrane Potentials/physiology ; Microelectrodes ; N-Methylaspartate/pharmacology ; Patch-Clamp Techniques ; Potassium/pharmacology ; Protons ; Retinal Horizontal Cells/drug effects ; Retinal Horizontal Cells/metabolism ; Sodium-Hydrogen Exchangers/physiology
Chemical Substances	Excitatory Amino Acid Agonists ; Protons ; Sodium-Hydrogen Exchangers ; Glutamic Acid (3KX376GY7L) ; N-Methylaspartate (6384-92-5) ; Potassium (RWP5GA015D) ; Kainic Acid (SIV03811UC) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2007-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3118-5
ISSN	1540-7748 ; 0022-1295
ISSN (online)	1540-7748
ISSN	0022-1295
DOI	10.1085/jgp.200709737
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Article: Role for malic enzyme, pyruvate carboxylation, and mitochondrial malate import in glucose-stimulated insulin secretion.

Heart, Emma / Cline, Gary W / Collis, Leon P / Pongratz, Rebecca L / Gray, Joshua P / Smith, Peter J S

American journal of physiology. Endocrinology and metabolism

2009 Volume 296, Issue 6, Page(s) E1354–62

Abstract: Pyruvate cycling has been implicated in glucose-stimulated insulin secretion (GSIS) from pancreatic beta-cells. The operation of some pyruvate cycling pathways is proposed to necessitate malate export from the mitochondria and NADP(+)-dependent ... ...

Abstract	Pyruvate cycling has been implicated in glucose-stimulated insulin secretion (GSIS) from pancreatic beta-cells. The operation of some pyruvate cycling pathways is proposed to necessitate malate export from the mitochondria and NADP(+)-dependent decarboxylation of malate to pyruvate by cytosolic malic enzyme (ME1). Evidence in favor of and against a role of ME1 in GSIS has been presented by others using small interfering RNA-mediated suppression of ME1. ME1 was also proposed to account for methyl succinate-stimulated insulin secretion (MSSIS), which has been hypothesized to occur via succinate entry into the mitochondria in exchange for malate and subsequent malate conversion to pyruvate. In contrast to rat, mouse beta-cells lack ME1 activity, which was suggested to explain their lack of MSSIS. However, this hypothesis was not tested. In this report, we demonstrate that although adenoviral-mediated overexpression of ME1 greatly augments GSIS in rat insulinoma INS-1 832/13 cells, it does not restore MSSIS, nor does it significantly affect GSIS in mouse islets. The increase in GSIS following ME1 overexpression in INS-1 832/13 cells did not alter the ATP-to-ADP ratio but was accompanied by increases in malate and citrate levels. Increased malate and citrate levels were also observed after INS-1 832/13 cells were treated with the malate-permeable analog dimethyl malate. These data suggest that although ME1 overexpression augments anaplerosis and GSIS in INS-1 832/13 cells, it is not likely involved in MSSIS and GSIS in pancreatic islets.
MeSH term(s)	Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Calcium/metabolism ; Cell Line, Tumor ; Citric Acid/metabolism ; Cytosol/enzymology ; Gene Expression Regulation, Enzymologic ; Glucose/metabolism ; Glucose/pharmacology ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/metabolism ; Malate Dehydrogenase/genetics ; Malate Dehydrogenase/metabolism ; Malates/metabolism ; Male ; Mice ; Mice, Inbred Strains ; Mitochondria/metabolism ; Oxygen Consumption/physiology ; Pyruvate Carboxylase/metabolism ; Rats ; Succinates/metabolism ; Succinates/pharmacology
Chemical Substances	Insulin ; Malates ; Succinates ; Citric Acid (2968PHW8QP) ; Adenosine Diphosphate (61D2G4IYVH) ; malic acid (817L1N4CKP) ; Adenosine Triphosphate (8L70Q75FXE) ; Malate Dehydrogenase (EC 1.1.1.37) ; malate dehydrogenase (decarboxylating) (EC 1.1.1.39) ; Pyruvate Carboxylase (EC 6.4.1.1) ; Glucose (IY9XDZ35W2) ; Calcium (SY7Q814VUP) ; monomethyl succinate (YA2V724S0A)
Language	English
Publishing date	2009-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.90836.2008
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Article ; Online: Expression of a sorcin missense mutation in the heart modulates excitation-contraction coupling.

Collis, Leon P / Meyers, Marian B / Zhang, Jie / Phoon, Colin K L / Sobie, Eric A / Coetzee, William A / Fishman, Glenn I

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2007 Volume 21, Issue 2, Page(s) 475–487

Abstract: Sorcin is a Ca2+ binding protein implicated in the regulation of intracellular Ca2+ cycling and cardiac excitation-contraction coupling. Structural and human genetic studies suggest that a naturally occurring sequence variant encoding L112-sorcin ... ...

Abstract	Sorcin is a Ca2+ binding protein implicated in the regulation of intracellular Ca2+ cycling and cardiac excitation-contraction coupling. Structural and human genetic studies suggest that a naturally occurring sequence variant encoding L112-sorcin disrupts an E-F hand Ca2+ binding domain and may be responsible for a heritable form of hypertension and hypertrophic heart disease. We generated transgenic mice overexpressing L112-sorcin in the heart and characterized the effects on Ca2+ regulation and cardiac function both in vivo and in dissociated cardiomyocytes. Hearts of sorcin(F112L) transgenic mice were mildly dilated but ventricular function was preserved and systemic blood pressure was normal. Sorcin(F112L) myocytes were smaller than control cells and displayed complex alterations in Ca2+ regulation and contractility, including a slowed inactivation of L-type Ca2+ current, enhanced Ca2+ spark width, duration, and frequency, and increased Na+-Ca2+ exchange activity. In contrast, mice with cardiac-specific overexpression of wild-type sorcin displayed directionally opposite effects on L-type Ca2+ channel function and Ca2+ spark behavior. These data further define the role of sorcin in cardiac excitation-contraction coupling and highlight its negative regulation of SR calcium release. Our results also suggest that additional factors may be responsible for the development of cardiac hypertrophy and hypertension in humans expressing the L112-sorcin sequence variant.
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/physiology ; Computer Simulation ; Humans ; Immunoblotting ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Confocal ; Mutation, Missense ; Myocardial Contraction/physiology ; Myocardium/cytology ; Myocardium/metabolism ; Sarcoplasmic Reticulum/metabolism
Chemical Substances	Calcium-Binding Proteins ; Sri protein, mouse ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2007-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.06-6292com
Database	MEDical Literature Analysis and Retrieval System OnLINE

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