Journal article
Calcium Biology of the Transverse Tubules in Heart
Annals of the New York Academy of Sciences, Vol.1047(1), pp.99-111
06/2005
DOI: 10.1196/annals.1341.009
PMCID: PMC1484521
PMID: 16093488
Abstract
Ca
2+
sparks in heart muscle are activated on depolarization by the influx of Ca
2+
through dihydropyridine receptors in the sarcolemmal (SL) and transverse tubule (TT) membranes. The cardiac action potential is thus able to synchronize the [Ca
2+
]
i
transient as Ca
2+
release is activated throughout the cell. Increases in the amount of Ca
2+
within the sarcoplasmic reticulum (SR) underlie augmented Ca
2+
release globally and an increase in the sensitivity of the ryanodine receptors (RyRs) to be triggered by the local [Ca
2+
]
i
. In a similar manner, phosphorylation of the RyRs by protein kinase A (PKA) increases the sensitivity of the RyRs to be activated by local [Ca
2+
]
i
. Heart failure and other cardiac diseases are associated with changes in SR Ca
2+
content, phosphorylation state of the RyRs, [Ca
2+
]
i
signaling defects and arrhythmias. Additional changes in transverse tubules and nearby junctional SR may contribute to alterations in local Ca
2+
signaling. Here we briefly discuss how TT organization can influence Ca
2+
signaling and how changes in SR Ca
2+
release triggering can influence excitation–contraction (EC) coupling. High speed imaging methods are used in combination with single cell patch clamp experiments to investigate how abnormal Ca
2+
signaling may be regulated in health and disease. Three issues are examined in this presentation: (1) normal Ca
2+
-induced Ca
2+
release and Ca
2+
sparks, (2) abnormal SR Ca
2+
release in disease, and (3) the triggering and propagation of waves of elevated [Ca
2+
]
i
.
Details
- Title: Subtitle
- Calcium Biology of the Transverse Tubules in Heart
- Creators
- LONG-SHENG SONG - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USASILVIA GUATIMOSIM - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USALETICIA GÓMEZ-VIQUEZ - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USAERIC A SOBIE - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USAANDREW ZIMAN - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USAHALI HARTMANN - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USAW.J LEDERER - Medical Biotechnology Center and the Institute of Molecular Cardiology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USA
- Resource Type
- Journal article
- Publication Details
- Annals of the New York Academy of Sciences, Vol.1047(1), pp.99-111
- DOI
- 10.1196/annals.1341.009
- PMID
- 16093488
- PMCID
- PMC1484521
- NLM abbreviation
- Ann N Y Acad Sci
- ISSN
- 0077-8923
- eISSN
- 1749-6632
- Publisher
- Blackwell Publishing Ltd
- Language
- English
- Date published
- 06/2005
- Academic Unit
- Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Biochemistry and Molecular Biology; Internal Medicine
- Record Identifier
- 9984094607702771
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