CARDIAC CALSEQUESTRIN AS A POSSIBLE TARGET FOR ARRHYTHMIA

Authors

  • Harapriya Chakravarty Birla Institute of Technology
  • Ashoke Sharon Birla Institute of Technology

Abstract

The term arrhythmia encapsulates all the conditions which result in the change in rhythm of the heart. It is classified broadly into two classes;
tachycardia, with increased and rhythm of heart and bradycardia, with decreased rhythm of the heart. In most cases, the arrhythmias are not serious
and asymptomatic, however, in some cases it leads to heart attack which becomes fatal. The present review focuses on stepwise understanding of
functioning of the heart and its excitation-contraction (EC) coupling followed by the mechanism of arrhythmia and the present line of medications.
The systematic flow of blood in and out of the cardiac chambers is due to the rhythmic contraction and relaxation of cardiac muscle, i.e. the EC
coupling of cardiac myocyte. Any disruption in the ion flow during the EC coupling causes arrhythmia. Ca
ions act as the trigger for the excitationcontraction
coupling,;
therefore,
understanding its movement
is an essential
to
understand the rhythm
disorders
of
the heart.
Calsequestrin (CASQ)

is
the most
abundant
calcium
buffering
protein
present
in the sarcoplasmic
reticulum
of
skeletal
and
cardiac
muscles. This
review
further focuses

on
CASQ;
its structure
and functions. Moreover,
it describes
the
association of CASQ
with
arrhythmia.
With
the
calcium binding
the CASQ
attains
its

linear
polymeric
structure
on the neutralization
of its
highly
electronegative
surface.
The protein
binds
calcium
with high
capacity and intermediate

affinity
which
releases
and
uptakes
calcium
reversibly
during the
EC coupling.
Mutation in
CASQ
genes has
been
associated
with
catecholaminergic

polymorphic
ventricular
tachycardia,
and moreover,
there
are
quite
a few
molecules which
are
known
to
bind
to
CASQ
and bring about changes
in
ionic
buffering
properties.
Therefore
under suitable
optimized
conditions CASQ
could
be
chosen
as a
novel
target
for
cardiac
arrhythmia.
Scrutinizing
the
scope
of CASQ
this review
presents
the first in depth study
suggesting cardiac
CASQ
as a possible target
for
arrhythmia.
2+
Keywords: Calsequestrin, Arrhythmia, Tachycardia, Bradycardia, Catecholaminergic polymorphic ventricular tachycardia, Excitation-contraction
coupling.

Downloads

Download data is not yet available.

Author Biography

Ashoke Sharon, Birla Institute of Technology

Associate Professor

References

REFERENCES

Zipes DP, Wellens HJ. Sudden cardiac death. Circulation

;98(21):2334-51.

de Luna AB, Coumel P, Leclercq JF. Ambulatory sudden cardiac death:

Mechanisms of production of fatal arrhythmia on the basis of data from

cases. Am Heart J 1989;117(1):151-9.

Gatzoulis MA, Balaji S, Webber SA, Siu SC, Hokanson JS, Poile C, et al.

Risk factors for arrhythmia and sudden cardiac death late after repair of

tetralogy of Fallot: A multicentre study. Lancet 2000;356(9234):975-81.

Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac

arrhythmias. N Engl J Med 2001;345(20):1473-82.

Ebashi S. Excitation-contraction coupling. Annu Rev Physiol

;38:293-313.

Bers DM. Cardiac excitation-contraction coupling. Nature

;415(6868):198-205.

Lee YS, Keener JP. A calcium-induced calcium release mechanism

mediated by calsequestrin. J Theor Biol 2008;253(4):668-79.

Park H, Wu S, Dunker AK, Kang C. Polymerization of calsequestrin.

Implications for Ca

regulation. J Biol Chem 2003;278(18):16176-82.

Mitchell RD, Simmerman HK, Jones LR. Ca

+

binding effects on protein

conformation and protein interactions of canine cardiac calsequestrin.

J Biol Chem 1988;263(3):1376-81.

+

Bal NC, Sharon A, Gupta SC, Jena N, Shaikh S, Gyorke S, et al. The

catecholaminergic polymorphic ventricular tachycardia mutation

R33Q disrupts the N-terminal structural motif that regulates reversible

calsequestrin polymerization. J Biol Chem 2010;285(22):17188-96.

Lahat H, Pras E, Olender T, Avidan N, Ben-Asher E, Man O, et al.

A missense mutation in a highly conserved region of CASQ2

is associated with autosomal recessive catecholamine-induced

polymorphic ventricular tachycardia in Bedouin families from Israel.

Am J Hum Genet 2001;69(6):1378-84.

Valle G, Galla D, Nori A, Priori S, Gyorke S, De Filippis V, et al.

Catecholaminergic polymorphic ventricular tachycardia-related

mutations R33Q and L167H alter calcium sensitivity of human cardiac

calsequestrin. Biochem J 2008;413:291-303.

Rizzi N, Liu N, Napolitano C, Nori A, Turcato F, Colombi B,

et al. Unexpected structural and functional consequences of the

R33Q homozygous mutation in cardiac calsequestrin a complex

arrhythmogenic cascade in a knock in mouse model. Circ Res

;103(3):298-306.

di Barletta MR, Viatchenko-Karpinski S, Nori A, Memmi M,

Terentyev D, Turcato F, et al. Clinical phenotype and functional

characterization of CASQ2 mutations associated with catecholaminergic

polymorphic ventricular tachycardia. Circulation 2006;114(10):1012-9.

Kim E, Youn B, Kemper L, Campbell C, Milting H, Varsanyi M, et al.

Characterization of human cardiac calsequestrin and its deleterious

mutants. J Mol Biol 2007;373(4):1047-57.

Kalyanasundaram A, Bal NC, Franzini-Armstrong C, Knollmann BC,

Periasamy M. The calsequestrin mutation CASQ2 D307H does not

affect protein stability and targeting to the junctional sarcoplasmic

reticulum but compromises its dynamic regulation of calcium buffering.

J Biol Chem 2010;285(5):3076-83.

Dirksen WP, Lacombe VA, Chi M, Kalyanasundaram A, ViatchenkoKarpinski

S, Terentyev

D,

et

al.

A

mutation

in

calsequestrin,

CASQ2

D307H, impairs sarcoplasmic

reticulum

Ca

handling and

causes complex ventricular arrhythmias in mice. Cardiovasc Res

;75(1):69-78.

+

Bal NC, Jena N, Sopariwala D, Balaraju T, Shaikh S, Bal C, et al.

Probing cationic selectivity of cardiac calsequestrin and its CPVT

mutants. Biochem J 2011;435(2):391-9.

Subra AK, Nissen MS, Lewis KM, Muralidharan AK, Sanchez EJ,

Milting H, et al. Molecular mechanisms of pharmaceutical drug binding

into calsequestrin. Int J Mol Sci 2012;13(11):14326-43.

Pinnell J, Turner S, Howell S. Cardiac muscle physiology. Contin Educ

Anaesth Crit Care Pain 2007;7(3):85-8.

Bartos DC, Grandi E, Ripplinger CM. Ion channels in the heart. Compr

Physiol 2015;5(3):1423-64.

Serrano MJ. Available from: http://www.slideshare.net/specialclass/

editd-anti-arrhythmic.

Dulhunty AF. Excitation-contraction coupling from the 1950s into the

new millennium. Clin Exp Pharmacol Physiol 2006;33(9):763-72.

Faggioni M, Kryshtal DO, Knollmann BC. Calsequestrin mutations

and catecholaminergic polymorphic ventricular tachycardia. Pediatr

Cardiol 2012;33(6):959-67.

Hoffman BF, Rosen MR. Cellular mechanisms for cardiac arrhythmias.

Circ Res 1981;49(1):1-15.

Gaztañaga L, Marchlinski FE, Betensky BP. Mechanisms of cardiac

arrhythmias. Rev Esp Cardiol (Engl Ed) 2012;65(2):174-85.

Mangoni ME, Nargeot J. Genesis and regulation of the heart

automaticity. Physiol Rev 2008;88(3):919-82.

Issa Z, Miller J, Zipes D. Electrophysiological mechanisms of

cardiac arrhythmias. Clinical Arrhythmology and Electrophysiology:

A Companion to Brawnwald’s Heart Disease. Filadelfia: Saunders;

p. 1-26.

Zipes DP. Mechanisms of clinical arrhythmias. J Cardiovasc

Electrophysiol 2003;14(8):902-12.

Driessen HE, Bourgonje VJ, van Veen TA, Vos MA. New antiarrhythmic

targets to control intracellular calcium handling. Neth Heart J

;22(5):198-213.

Clusin WT. Calcium and cardiac arrhythmias: DADs, EADs, and

alternans. Crit Rev Clin Lab Sci 2003;40(3):337-75.

Kar A. Medicinal Chemistry. New Delhi: New Age International; 2005.

Thireau J, Pasquié JL, Martel E, Le Guennec JY, Richard S. New drugs

vs. old concepts: A fresh look at antiarrhythmics. Pharmacol Ther

;132(2):125-45.

Fogoros RN. Introduction to antiarrhythmic drugs. Antiarrhythmic Drugs:

A Practical Guide. 2

ed. Pittsburgh, PA: Blackwell; 2008. p. 36-51.

Vaughan Williams EM. A classification of antiarrhythmic

nd

actions reassessed after a decade of new drugs. J Clin Pharmacol

;24(4):129-47.

Elliott WJ, Ram CV. Calcium channel blockers. J Clin Hypertens

(Greenwich) 2011;13(9):687-9.

Buckley N, Dawson A, Whyte I. Calcium channel blockers. Medicine

;35(11):599-602.

Olson KR, Erdman AR, Woolf AD, Scharman EJ, Christianson G,

Caravati EM, et al. Calcium channel blocker ingestion: An evidencebased

consensus guideline for

out-of-hospital management.

Clin

Toxicol

;43(7):797-822.

Howarth D, Dawson A, Smith A, Buckley N, Whyte I. Calcium channel

blocking drug overdose: An Australian series. Hum Exp Toxicol

;13(3):161-6.

Bourgonje V, Vos M, Ozdemir S, Acsai K, Doisne N, Van der Nagel R,

et al. Combined Na/Ca exchanger and L-type calcium channel block by

SEA-0400 suppresses Torsade de pointes arrhythmias with maintained

haemodynamics. Cardiovasc Res 2012;93:S105.

Bourgonje VJ, Schoenmakers M, Beekman JD, van der Nagel R,

Houtman MJ, Miedema LF, et al. Relevance of calmodulin/CaMKII

activation for arrhythmogenesis in the AV block dog. Heart Rhythm

;9(11):1875-83.

Zhou Q, Xiao J, Jiang D, Wang R, Vembaiyan K, Wang A, et al.

Carvedilol and its new analogs suppress arrhythmogenic store overloadinduced

Ca

release. Nat Med 2011;17(8):1003-9.

Kobayashi S, Yano M, Uchinoumi H, Suetomi T, Susa T, Ono M,

+

et al. Dantrolene, a therapeutic agent for malignant hyperthermia,

inhibits catecholaminergic polymorphic ventricular tachycardia in a

RyR2R2474S/+ knock in mouse model. Circ J 2010;74(12):2579-84.

Marai I, Boulos M, Khoury A. Pharmacological and nonpharmacological

therapies

of catecholaminergic

polymorphic

ventricular

tachycardia.

Int

J Cardiovasc

Res 2014;3:2. DOI:

http://

www.dx. doi. org/10.4172/2324, 2014. 8602.

MacLennan DH, Wong PT. Isolation of a calcium-sequestering

protein from sarcoplasmic reticulum. Proc Natl Acad Sci U S A

;68(6):1231-5.

MacLennan DH, Campbell KP, Reithmeier RA. Calsequestrin. Calcium

Cell Function 1983;4:151-73.

Asian J Pharm Clin Res, Vol 9, Issue 1, 2016, 53-64

Chakravarty and Sharon

Scott B, Simmerman H, Collins J, Nadal-Ginard B, Jones L. Complete

amino acid sequence of canine cardiac calsequestrin deduced by cDNA

cloning. J Biol Chem 1988;263(18):8958-64.

Fliegel L, Newton E, Burns K, Michalak M. Molecular cloning of

cDNA encoding a 55-kDa multifunctional thyroid hormone binding

protein of skeletal muscle sarcoplasmic reticulum. J Biol Chem

;265(26):15496-502.

Damiani E, Volpe P, Margreth A. Coexpression of two isoforms of

calsequestrin in rabbit slow-twitch muscle. J Muscle Res Cell Motil

;11(6):522-30.

Beard NA, Laver DR, Dulhunty AF. Calsequestrin and the calcium

release channel of skeletal and cardiac muscle. Prog Biophys Mol Biol

;85(1):33-69.

Park H, Park IY, Kim E, Youn B, Fields K, Dunker AK, et al. Comparing

skeletal and cardiac calsequestrin structures and their calcium binding

a proposed mechanism for coupled calcium binding and protein

polymerization. J Biol Chem 2004;279(17):18026-33.

Liu N, Napolitano C, Priori SG. Catecholaminergic polymorphic

ventricular tachycardia. In: Electrical Diseases of the Heart. New York:

Springer; 2013. p. 551-60.

Györke S, Hagen BM, Terentyev D, Lederer WJ. Chain-reaction Ca

signaling in the heart. J Clin Invest 2007;117(7):1758-62.

Ikemoto N, Bhatnagar GM, Nagy B, Gergely J. Interaction of divalent

cations with the 55,000-dalton protein component of the sarcoplasmic

reticulum studies of fluorescence and circular dichroism. J Biol Chem

;247(23):7835-7.

Volpe P, Martini A, Furlan S, Meldolesi J. Calsequestrin is a component

of smooth muscles: The skeletal- and cardiac-muscle isoforms are both

present, although in highly variable amounts and ratios. Biochem J

;301:465-9.

Fliegel L, Leberer E, Green NM, MacLennan DH. The fast-twitch

muscle calsequestrin isoform predominates in rabbit slow-twitch soleus

muscle. FEBS Lett 1989;242(2):297-300.

Park KW, Goo JH, Chung HS, Kim H, Kim DH, Park WJ. Cloning

of the genes encoding mouse cardiac and skeletal calsequestrins:

Expression pattern during embryogenesis. Gene 1998;217(1-2):25-30.

Rodriguez MM, Chen CH, Smith BL, Mochly-Rosen D. Characterization

of the binding and phosphorylation of cardiac calsequestrin by epsilon

protein kinase C. FEBS Lett 1999;454(3):240-6.

Scott BT, Simmerman HK, Collins JH, Nadal-Ginard B, Jones LR.

Complete amino acid sequence of canine cardiac calsequestrin deduced

by cDNA cloning. J Biol Chem 1988;263(18):8958-64.

Slupsky JR, Ohnishi M, Carpenter MR, Reithmeier RA. Characterization

of cardiac calsequestrin. Biochemistry 1987;26(20):6539-44.

Treves S, Vilsen B, Chiozzi P, Andersen JP, Zorzato F. Molecular cloning,

functional expression and tissue distribution of the cDNA encoding

frog skeletal muscle calsequestrin. Biochem J 1992;283:767-72.

Yazaki PJ, Salvatori S, Dahms AS. Amino acid sequence of chicken

calsequestrin deduced from cDNA: Comparison of calsequestrin and

aspartactin. Biochem Biophys Res Commun 1990;170(3):1089-95.

Sanchez EJ, Lewis KM, Danna BR, Kang C. High-capacity Ca

binding

of human skeletal calsequestrin. J Biol Chem 2012;287(14):11592-601.

Wang S, Trumble WR, Liao H, Wesson CR, Dunker AK, Kang CH.

Crystal structure of calsequestrin from rabbit skeletal muscle

sarcoplasmic reticulum. Nat Struct Biol 1998;5(6):476-83.

He Z, Dunker AK, Wesson CR, Trumble WR. Ca

induced folding and

aggregation of skeletal muscle sarcoplasmic reticulum calsequestrin.

The involvement of the trifluoperazine-binding site. J Biol Chem

;268(33):24635-41.

+

Burley SK, Petsko GA. Aromatic-aromatic interaction: A mechanism of

protein structure stabilization. Science 1985;229(4708):23-8.

Ostwald TJ, MacLennan DH, Dorrington KJ. Effects of cation

binding on the conformation of calsequestrin and the high affinity

calcium-binding protein of sarcoplasmic reticulum. J Biol Chem

;249(18):5867-71.

+

+

Ikemoto N, Nagy B, Bhatnagar GM, Gergely J. Studies on a

metal-binding protein of the sarcoplasmic reticulum. J Biol Chem

;249(8):2357-65.

Zhang L, Kelley J, Schmeisser G, Kobayashi YM, Jones LR. Complex

formation between junctin, triadin, calsequestrin, and the ryanodine

receptor. Proteins of the cardiac junctional sarcoplasmic reticulum

membrane. J Biol Chem 1997;272(37):23389-97.

Beard NA, Sakowska MM, Dulhunty AF, Laver DR. Calsequestrin

is an inhibitor of skeletal muscle ryanodine receptor calcium release

channels. Biophys J 2002;82:310-20.

Bal NC, Jena N, Chakravarty H, Kumar A, Chi M, Balaraju T, et al.

The C-terminal calcium-sensitive disordered motifs regulate isoformspecific

polymerization

characteristics

of

calsequestrin.

Biopolymers

;103(1):15-22.

Gaburjakova M, Bal NC, Gaburjakova J, Periasamy M. Functional

interaction between calsequestrin and ryanodine receptor in the heart.

Cell Mol Life Sci 2013;70(16):2935-45.

Dunker AK, Lawson JD, Brown CJ, Williams RM, Romero P,

Oh JS, et al. Intrinsically disordered protein. J Mol Graph Model

;19(1):26-59.

Shin JH, Lee HK, Rhim SC, Cho KJ, Choi CG, Suh DC. Spinal epidural

extraskeletal Ewing sarcoma: MR findings in two cases. AJNR Am J

Neuroradiol 2001;22:795-8.

Beard NA, Dulhunty AF. C-terminal residues of skeletal muscle

calsequestrin are essential for calcium binding and for skeletal

ryanodine receptor inhibition. Skelet Muscle 2015;5(1):6.

Zhou Y, Xue S, Yang JJ. Calciomics: Integrative studies of Ca

-binding

proteins and their interactomes in biological systems. Metallomics

;5(1):29-42.

Cozens B, Reithmeier RA. Size and shape of rabbit skeletal muscle

calsequestrin. J Biol Chem 1984;259(10):6248-52.

Park H, Park IY, Kim E, Youn B, Fields K, Dunker AK, et al. Comparing

skeletal and cardiac calsequestrin structures and their calcium binding:

A proposed mechanism for coupled calcium binding and protein

polymerization. J Biol Chem 2004;279(17): 18026-33.

Zheng H, Chordia MD, Cooper DR, Chruszcz M, Müller P, Sheldrick GM,

et al. Validation of metal-binding sites in macromolecular structures

with the check my metal web server. Nat Protoc 2014;9(1):156-70.

Kumar A, Chakravarty H, Bal NC, Balaraju T, Jena N, Misra G, et al.

Identification of calcium binding sites on calsequestrin 1 and their

implications for polymerization. Mol Biosyst 2013;9(7):1949-57.

Charlier HA, Olson RD, Thornock CM, Mercer WK,

Olson DR, Broyles TS, et al. Investigations of calsequestrin as

a target for anthracyclines: Comparison of functional effects of

daunorubicin, daunorubicinol, and trifluoperazine. Mol Pharmacol

;67(5):1505-12.

Sanchez EJ, Hayes RP, Barr JT, Lewis KM, Webb BN, Subramanian AK,

et al. Potential role of cardiac calsequestrin in the lethal arrhythmic

effects of cocaine. Drug Alcohol Depend 2013;133(2):344-51.

Olson RD, Li X, Palade P, Shadle SE, Mushlin PS, Gambliel HA,

et al. Sarcoplasmic reticulum calcium release is stimulated and

inhibited by daunorubicin and daunorubicinol. Toxicol Appl Pharmacol

;169(2):168-76.

Mushlin PS, Cusack BJ, Boucek RJ, Andrejuk T, Li X, Olson RD.

Time related increases in cardiac concentrations of doxorubicinol could

interact with doxorubicin to depress myocardial contractile function. Br

J Pharmacol 1993;110(3):975-82.

Pessah IN, Durie EL, Schiedt MJ, Zimanyi I. Anthraquinone-sensitized

Ca

release channel from rat cardiac sarcoplasmic reticulum: Possible

receptor-mediated mechanism of doxorubicin cardiomyopathy. Mol

Pharmacol 1990;37(4):503-14.

+

Kang C, Nissen MS, Sanchez EJ, Lam KS, Milting H. Potential

adverse interaction of human cardiac calsequestrin. Eur J Pharmacol

;646(1-3):12-21.

Published

01-01-2016

How to Cite

Chakravarty, H., and A. Sharon. “CARDIAC CALSEQUESTRIN AS A POSSIBLE TARGET FOR ARRHYTHMIA”. Asian Journal of Pharmaceutical and Clinical Research, vol. 9, no. 1, Jan. 2016, pp. 53-64, https://innovareacademics.in/journals/index.php/ajpcr/article/view/9820.

Issue

Section

Review Article(s)