The molecular interaction of heart LIM protein (HLP) with RyR2 and caveolin-3 is essential for Ca 2+ -induced Ca 2+  release in the heart

Song, Dong Woo; Lee, Kyung‐Eun; Ryu, Jae Yong; Jeon, Hyesung; Kim, Do Han

doi:10.1016/j.bbrc.2015.06.045

Cited by 5 publications

(4 citation statements)

References 29 publications

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“…Its abundance in adult heart seems to remain high, and it was unaffected by aortic banding, an invasive procedure to induce cardiac hyper‐trophy (5), or isoproterenol infusion (22), which does not preclude the possibility that endogenous CRP4 is involved in the response to these adverse events. Recently, a molecular interaction between CRP4 with ryanodine receptor 2 (RyR2) and caveolin‐3 was reported in adult and neonatal ventricular CMs from rats (23). Knockdown of CRP4 affected the electrically evoked Ca 2+ release from the sarcoplasmic reticulum, suggesting that CRP4‐RyR2 complex formation in caveolin‐3–positive sarcolemmal caveolae may be necessary to enable an efficient excitation–contraction coupling (23).…”

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confidence: 99%

“…Recently, a molecular interaction between CRP4 with ryanodine receptor 2 (RyR2) and caveolin-3 was reported in adult and neonatal ventricular CMs from rats (23). Knockdown of CRP4 affected the electrically evoked Ca 2+ release from the sarcoplasmic reticulum, suggesting that CRP4-RyR2 complex formation in caveolin-3-positive sarcolemmal caveolae may be necessary to enable an efficient excitation-contraction coupling (23). Despite its high cardiac expression levels (5) and, although obviously closely related proteins such as CRP3/MLP appear to be important regulators of maladaptive cardiac remodeling, the significance of cardiac CRP4 in biology and pathophysiology have remained largely elusive so far.…”

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confidence: 99%

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Amplified pathogenic actions of angiotensin II in cysteine‐rich LIM‐only protein 4–negative mouse hearts

Straubinger

Boldt²,

Kuret

et al. 2017

FASEB j.

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LIM domain proteins have been identified as essential modulators of cardiac biology and pathology; however, it is unclear which role the cysteine-rich LIM-only protein (CRP)4 plays in these processes. In studying CRP4 mutant mice, we found that their hearts developed normally, but lack of CRP4 exaggerated multiple parameters of the cardiac stress response to the neurohormone angiotensin II (Ang II). Aiming to dissect the molecular details, we found a link between CRP4 and the cardioprotective cGMP pathway, as well as a multiprotein complex comprising well-known hypertrophy-associated factors. ignificant enrichment of the cysteine-rich intestinal protein (CRIP)1 in murine hearts lacking CRP4, as well as severe cardiac defects and premature death of CRIP1 and CRP4 morphant zebrafish embryos, further support the notion that depleting CRP4 is incompatible with a proper cardiac development and function. Together, amplified Ang II signaling identified CRP4 as a novel antiremodeling factor regulated, at least to some extent, by cardiac cGMP.-Straubinger, J., Boldt, K., Kuret, A., Deng, L., Krattenmacher, D., Bork, N., Desch, M., Feil, R., Feil, S., Nemer, M., Ueffing, M., Ruth, P., Just, S., Lukowski, R. Amplified pathogenic actions of angiotensin II in cysteine-rich LIM-only protein 4 negative mouse hearts.

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confidence: 99%

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confidence: 99%

Amplified pathogenic actions of angiotensin II in cysteine‐rich LIM‐only protein 4–negative mouse hearts

Straubinger

Boldt²,

Kuret

et al. 2017

FASEB j.

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“…Recently, many studies have provided evidence that the RyR2 colocalized with caveolin-3 [ 62 ]. RyR2 and caveolin-3-associated dihydropyridine receptor (DHPR) forms a triple complex with HLP family which is one member of the cysteine-rich protein (Crip) [ 63 ]. The RyR2 modulates Ca 2+ entry through caveolin-3-associated DHPR by regulating itself [ 15 ].…”

Section: Caveolin-3 and Electrical Signal Propagationmentioning

confidence: 99%

Caveolin-3 and Arrhythmias: Insights into the Molecular Mechanisms

Qiu

Wang

et al. 2022

JCM

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Caveolin-3 is a muscle-specific protein on the membrane of myocytes correlated with a variety of cardiovascular diseases. It is now clear that the caveolin-3 plays a critical role in the cardiovascular system and a significant role in cardiac protective signaling. Mutations in the gene encoding caveolin-3 cause a broad spectrum of clinical phenotypes, ranging from persistent elevations in the serum levels of creatine kinase in asymptomatic humans to cardiomyopathy. The influence of Caveolin-3(CAV-3) mutations on current density parallels the effect on channel trafficking. For example, mutations in the CAV-3 gene promote ventricular arrhythmogenesis in long QT syndrome 9 by a combined decrease in the loss of the inward rectifier current (IK1) and gain of the late sodium current (INa-L). The functional significance of the caveolin-3 has proved that caveolin-3 overexpression or knockdown contributes to the occurrence and development of arrhythmias. Caveolin-3 overexpression could lead to reduced diastolic spontaneous Ca2+ waves, thus leading to the abnormal L-Type calcium channel current-induced ventricular arrhythmias. Moreover, CAV-3 knockdown resulted in a shift to more negative values in the hyperpolarization-activated cyclic nucleotide channel 4 current (IHCN4) activation curve and a significant decrease in IHCN4 whole-cell current density. Recent evidence indicates that caveolin-3 plays a significant role in adipose tissue and is related to obesity development. The role of caveolin-3 in glucose homeostasis has attracted increasing attention. This review highlights the underlining mechanisms of caveolin-3 in arrhythmia. Progress in this field may contribute to novel therapeutic approaches for patients prone to developing arrhythmia.

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“…Among the caveolin isoforms, caveoline-1 (Cav1) and caveoline-2 (Cav2) are expressed in most cell types. Cav1 is involved in cholesterol transport and signal transduction, whereas caveoline-3 (Cav3) is specific to skeletal, smooth, and cardiac muscle and results in muscular disorders when defective [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Anesthesia for patients with PTRF mutations: a case report

et al. 2018

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BackgroundPolymeraze I and transcript release factor (PTRF) mutations are a newly recognized disease, which cause congenital generalized lipodystrophy associated with myopathy.Case presentationA 29-year-old man (height 126 cm; weight 22 kg) with a PTRF mutation was scheduled for mandibular dentigerous cystectomy. His primary symptoms were lipodystrophy, myopathy, long QT syndrome, refractory nephrosis, and abnormal lipid metabolism. Defibrillator pads were applied soon after the patient entered the operating room. Anesthesia was induced using continuous administration of dexmedetomidine (4 μg/kg/h) for 15 min; midazolam (7 mg) was added while monitoring the bispectral index and his vital signs. Remifentanil and rocuronium were administered before endotracheal intubation. The surgeon used local anesthesia, and dexmedetomidine and remifentanil were titrated throughout the surgery. The surgery was performed uneventfully, and the patient was extubated following the administration of sugammadex and flumazenil.ConclusionPatients with PTRF mutations require careful anesthetic planning. We planned to administer lipid-free, non-inhalational agents for the induction and maintenance of anesthesia. The anesthetic method used for this minor surgery was safe and effective.

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The molecular interaction of heart LIM protein (HLP) with RyR2 and caveolin-3 is essential for Ca 2+ -induced Ca 2+ release in the heart

Cited by 5 publications

References 29 publications

Amplified pathogenic actions of angiotensin II in cysteine‐rich LIM‐only protein 4–negative mouse hearts

Amplified pathogenic actions of angiotensin II in cysteine‐rich LIM‐only protein 4–negative mouse hearts

Caveolin-3 and Arrhythmias: Insights into the Molecular Mechanisms

Anesthesia for patients with PTRF mutations: a case report

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