Histidine-rich Ca binding protein: a regulator of sarcoplasmic reticulum calcium sequestration and cardiac function

Gregory, Kimberly N.; Ginsburg, Kenneth S.; Bódi, Ilona; Hahn, Harvey S.; Marreez, Yehia; Song, Qiujing; Padmanabhan, Prabhu; Mitton, Bryan; Waggoner, Jeanne G.; Monte, Federica del

doi:10.1016/j.yjmcc.2006.02.003

Cited by 58 publications

(92 citation statements)

References 31 publications

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“…These findings confound our understanding of HRC's role in cardiac muscle function as both downregulation and overexpression of HRC produced similar effects on SR Ca 2ϩ storage. Results from the HRC overexpression mouse model (297) show important differences compared with results from acute gene transfer (223). In contrast to the acute HRC overexpression in rat myocytes, transgenic mice had slow Ca 2ϩ reuptake by SERCA2a and slow Ca 2ϩ extrusion by NCX.…”

Section: Fkbp126/calstabin2mentioning

confidence: 93%

“…Interestingly, HRC null and overexpression transgenic mouse models have been generated and showed an increase in triadin expression with no change in SR load (297,398). These findings confound our understanding of HRC's role in cardiac muscle function as both downregulation and overexpression of HRC produced similar effects on SR Ca 2ϩ storage.…”

Section: Fkbp126/calstabin2mentioning

confidence: 99%

“…In contrast to the acute HRC overexpression in rat myocytes, transgenic mice had slow Ca 2ϩ reuptake by SERCA2a and slow Ca 2ϩ extrusion by NCX. This in turn slowed the Ca 2ϩ transient decay rate but not cellular contractile function (297). Chronic HRC overexpression also caused the development of cardiac hypertrophy and an age-dependent transition to congestive heart failure (297).…”

Section: Fkbp126/calstabin2mentioning

confidence: 99%

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Designing Heart Performance by Gene Transfer

Davis¹,

Westfall²,

Townsend³

et al. 2008

Physiological Reviews

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The birth of molecular cardiology can be traced to the development and implementation of high-fidelity genetic approaches for manipulating the heart. Recombinant viral vector-based technology offers a highly effective approach to genetically engineer cardiac muscle in vitro and in vivo. This review highlights discoveries made in cardiac muscle physiology through the use of targeted viral-mediated genetic modification. Here the history of cardiac gene transfer technology and the strengths and limitations of viral and nonviral vectors for gene delivery are reviewed. A comprehensive account is given of the application of gene transfer technology for studying key cardiac muscle targets including Ca2+handling, the sarcomere, the cytoskeleton, and signaling molecules and their posttranslational modifications. The primary objective of this review is to provide a thorough analysis of gene transfer studies for understanding cardiac physiology in health and disease. By comparing results obtained from gene transfer with those obtained from transgenesis and biophysical and biochemical methodologies, this review provides a global view of cardiac structure-function with an eye towards future areas of research. The data presented here serve as a basis for discovery of new therapeutic targets for remediation of acquired and inherited cardiac diseases.

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Section: Fkbp126/calstabin2mentioning

confidence: 93%

Section: Fkbp126/calstabin2mentioning

confidence: 99%

Section: Fkbp126/calstabin2mentioning

confidence: 99%

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Designing Heart Performance by Gene Transfer

Davis¹,

Westfall²,

Townsend³

et al. 2008

Physiological Reviews

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“…Of these 25 genes, 5 are expressed in cardiac tissue: U1 small nuclear ribonucleoprotein (SNRP70); histidine-rich calcium-binding protein (HRC); transient receptor potential cation channel, subfamily M, member 4 (TRPM4); transcriptional enhancer 4 (TEAD2); and potassium voltage-gated channel, Shaker-related subfamily, member7 (KCNA7) (11,(14)(15)(16)(17)(18). Previously, KCNA7 was excluded as a possible candidate gene (16).…”

Section: Pfhbi Disease Is Linked To a Mutation In Trpm4mentioning

confidence: 99%

Impaired endocytosis of the ion channel TRPM4 is associated with human progressive familial heart block type I

Kruse¹,

Schulze‐Bahr²,

Corfield³

et al. 2009

J. Clin. Invest.

297

339

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Progressive familial heart block type I (PFHBI) is a progressive cardiac bundle branch disease in the His-Purkinje system that exhibits autosomal-dominant inheritance. In 3 branches of a large South African Afrikaner pedigree with an autosomal-dominant form of PFHBI, we identified the mutation c.19G→A in the transient receptor potential cation channel, subfamily M, member 4 gene (TRPM4) at chromosomal locus 19q13.3. This mutation predicted the amino acid substitution p.E7K in the TRPM4 amino terminus. TRPM4 encodes a Ca 2+ -activated nonselective cation (CAN) channel that belongs to the transient receptor potential melastatin ion channel family. Quantitative analysis of TRPM4 mRNA content in human cardiac tissue showed the highest expression level in Purkinje fibers. Cellular expression studies showed that the c.19G→A missense mutation attenuated deSUMOylation of the TRPM4 channel. The resulting constitutive SUMOylation of the mutant TRPM4 channel impaired endocytosis and led to elevated TRPM4 channel density at the cell surface. Our data therefore revealed a gain-of-function mechanism underlying this type of familial heart block.

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“…On the other hand, calumenin knockdown by siRNA in myocytes does not affect SR Ca 2+ storage capacity (9) or total Ca2+ buffering capacity due to the fact that calumenin is a minor protein in the SR compared to CSQ (11,29 The functional role of calumenin in Ca 2+ cycling in the SR is similar to that of HRC (7,30). HRC is distributed throughout the SR in a similar expression pattern as that of calumenin.…”

Section: Calumenin In Ec Couplingmentioning

confidence: 99%