Themes and Variations in ER/SR Calcium Release Channels: Structure and Function

Stathopulos, Peter B.; Seo, Min‐Duk; Enomoto, Masahiro; Amador, Fernando; Ishiyama, Noboru; Ikura, Mitsuhiko

doi:10.1152/physiol.00013.2012

Cited by 23 publications

(18 citation statements)

References 140 publications

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“…This is consistent with the prevailing view that myogenic responses can be mediated by endoplasmic reticulum IP 3 receptor activation (29). Notably, the evolutionarily-related ER/SR calcium channels (IP 3 receptors and ryanodine receptors) share a feed-forward mechanism whereby increased cytosolic calcium concentration induces further calcium release (30), possibly explaining the need to inhibit both receptor types to fully recapitulate the detrimental effects of the dF mutation.…”

Section: Discussionmentioning

confidence: 99%

Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets

Guo

Stoltz

Zhu

et al. 2014

Journal of Cystic Fibrosis

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BACKGROUND The most common CF-causing mutations interfere with CFTR trafficking from the endoplasmic reticulum (CFTR-F508del) or prematurely terminate transcription (CFTR-null). We suspected genotype-specific pattens of CFTR expression would have differential effects on smooth muscle cell calcium signaling and hence vascular tone. We hypothesized that compared to wild-type or CFTR-null aorta, aorta from CFTR-F508del (dF) piglets will have reduced endoplasmic reticulum calcium mobilization and decreased vasoconstriction. METHODS Aortic reactivity was assessed by myography, and ratiometric calcium imaging was performed in isolated vascular smooth muscle cells. RESULTS Aorta from dF piglets had reduced myogenic tone (P<0.001) and decreased constriction to KCl (P<0.05). Combined inhibition of ryanodine and IP3 receptors decreased wild-type and CFTR-null responses to levels seen in dF aorta. Compared to wild-type cells, dF-expressing smooth muscle cells had reduced calcium transients, while CFTR-null cells had decreased baseline intracellular calcium concentrations. CONCLUSIONS Expression of CFTR-F508del interferes with smooth muscle cell calcium handling and decreases aortic responsiveness.

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Section: Discussionmentioning

confidence: 99%

Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets

Guo

Stoltz

Zhu

et al. 2014

Journal of Cystic Fibrosis

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“…High-resolution structures of the RyR's 'little sister' , a slightly smaller but still huge channel, the inositol trisphosphate receptor (InsP3R), are now anticipated 12,18 . Because InsP3R is a closely related molecule controlling intracellular calcium release in virtually all cells 19,20 , we expect an unveiling of its structure in the future.…”

Section: Ivana Y Kuo and Barbara E Ehrlichmentioning

confidence: 99%

Muscling in on the ryanodine receptor

Kuo

Ehrlich

2015

Nat Struct Mol Biol

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“…Three mammalian isoforms of the ryanodine receptor are known: RYR1, predominant in skeletal muscle; RYR2, primarily expressed in heart muscle; and RYR3, found in the central nervous system and in skeletal and smooth muscle 29–31. From the early 1990s, mutations in the RYR1 gene on chromosome 19q13.1 have been associated with a predisposition to MH 32.…”

Section: Geneticsmentioning

confidence: 99%

Management of malignant hyperthermia: diagnosis and treatment

Schneiderbanger¹,

Johannsen²,

Roewer³

et al. 2014

TCRM

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Malignant hyperthermia is a potentially lethal inherited disorder characterized by disturbance of calcium homeostasis in skeletal muscle. Volatile anesthetics and/or the depolarizing muscle relaxant succinylcholine may induce this hypermetabolic muscular syndrome due to uncontrolled sarcoplasmic calcium release via functionally altered calcium release receptors, resulting in hypoxemia, hypercapnia, tachycardia, muscular rigidity, acidosis, hyperkalemia, and hyperthermia in susceptible individuals. Since the clinical presentation of malignant hyperthermia is highly variable, survival of affected patients depends largely on early recognition of the symptoms characteristic of malignant hyperthermia, and immediate action on the part of the attending anesthesiologist. Clinical symptoms of malignant hyperthermia, diagnostic criteria, and current therapeutic guidelines, as well as adequate management of anesthesia in patients susceptible to malignant hyperthermia, are discussed in this review.

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Themes and Variations in ER/SR Calcium Release Channels: Structure and Function

Cited by 23 publications

References 140 publications

Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets

Genotype-specific alterations in vascular smooth muscle cell function in cystic fibrosis piglets

Muscling in on the ryanodine receptor

Management of malignant hyperthermia: diagnosis and treatment

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