A review of recent insights into the role of the sarcoplasmic reticulum and Ca entry in uterine smooth muscle

Noble, Karen; Matthew, A; Burdyga, Theodor; Wray, Susan

doi:10.1016/j.ejogrb.2009.02.010

Cited by 52 publications

(49 citation statements)

References 138 publications

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“…Thus the pattern of spontaneous contractions compared with controls was less frequent but longer lasting, and with many of the contractions having a spiked appearance (518). This pattern was also found in portal vein from knockout mice (671).…”

Section: Functional Effectsmentioning

confidence: 55%

Sarcoplasmic Reticulum Function in Smooth Muscle

Wray

Burdyga

2010

Physiological Reviews

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154

134

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The sarcoplasmic reticulum (SR) of smooth muscles presents many intriguing facets and questions concerning its roles, especially as these change with development, disease, and modulation of physiological activity. The SR's function was originally perceived to be synthetic and then that of a Ca store for the contractile proteins, acting as a Ca amplification mechanism as it does in striated muscles. Gradually, as investigators have struggled to find a convincing role for Ca-induced Ca release in many smooth muscles, a role in controlling excitability has emerged. This is the Ca spark/spontaneous transient outward current coupling mechanism which reduces excitability and limits contraction. Release of SR Ca occurs in response to inositol 1,4,5-trisphosphate, Ca, and nicotinic acid adenine dinucleotide phosphate, and depletion of SR Ca can initiate Ca entry, the mechanism of which is being investigated but seems to involve Stim and Orai as found in nonexcitable cells. The contribution of the elemental Ca signals from the SR, sparks and puffs, to global Ca signals, i.e., Ca waves and oscillations, is becoming clearer but is far from established. The dynamics of SR Ca release and uptake mechanisms are reviewed along with the control of luminal Ca. We review the growing list of the SR's functions that still includes Ca storage, contraction, and relaxation but has been expanded to encompass Ca homeostasis, generating local and global Ca signals, and contributing to cellular microdomains and signaling in other organelles, including mitochondria, lysosomes, and the nucleus. For an integrated approach, a review of aspects of the SR in health and disease and during development and aging are also included. While the sheer versatility of smooth muscle makes it foolish to have a “one model fits all” approach to this subject, we have tried to synthesize conclusions wherever possible.

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Section: Functional Effectsmentioning

confidence: 55%

Sarcoplasmic Reticulum Function in Smooth Muscle

Wray

Burdyga

2010

Physiological Reviews

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154

134

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“…Although the role for InsP 3 is undisputed, ryanodine provides a more controversial story. Taggart and Wray (1998) found that ryanodine had little, if any, effect in isolated rat uterus, and a recent review (Noble et al, 2009) concluded that in intact myometrium, from a variety of species, ryanodine receptors appear to have little function. However, Barata et al (2004) demonstrated a role for cADPR and hence ryanodine receptors in intracellular calcium and contraction of isolated human myometrial cells.…”

Section: Discussionmentioning

confidence: 99%

“…It is now well established that a rise in intracellular calcium in uterine smooth muscle causes activation of myosin light chain kinase and phosphorylation of myosin light chain, leading to contraction. This rise in calcium, as in many different cell types, is traditionally believed to be from two sources: extracellular calcium entry though plasma membrane calcium channels and release of calcium from the sarcoplasmic reticulum (Noble et al, 2009). Release from the sarcoplasmic reticulum is mediated through the action of agonists on plasma membrane G protein-coupled receptors predominantly leading to the production of the second messenger inositol 1,4,5-trisphosphate (InsP 3 ).…”

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confidence: 99%

A Functional Role for Nicotinic Acid Adenine Dinucleotide Phosphate in Oxytocin-Mediated Contraction of Uterine Smooth Muscle from Rat

Aley

Noh²,

Gào³

et al. 2010

The Journal of Pharmacology and Experimental Therapeutics

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Conventionally, G protein-coupled receptors are thought to increase calcium via inositol 1,4,5-trisphosphate (InsP 3 ). More recent evidence shows that an alternative second messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), also has a role to play, causing researchers to question established calcium releasing pathways. With the recent development, by our group, of cell-permeant NAADP (NAADP-aceteoxymethyl ester) and a selective NAADP receptor antagonist (Ned-19; 1-(3-((4-(2-fluorophenyl)piperazin-1-yl)methyl)-4-methoxyphenyl)-2,3,4,9-tetrahydro-1H-pyrido [3,4-b]indole-3-carboxylic acid), the ability to investigate this signaling pathway has improved. Therefore, we investigated a role for NAADP in oxytocin-mediated responses in the rat uterus. Oxytocin-and NAADP-mediated effects were investigated by using contractile measurements of whole uterine strips from rat in organ baths. Responses were correlated to calcium release in cultured rat uterine smooth muscle cells measured by fluorescence microscopy. Inhibition of both oxytocin-induced contraction and calcium release by the traditional NAADP-signaling disrupter bafilomycin and the NAADP receptor antagonist Ned-19 clearly demonstrated a role for NAADP in oxytocin-induced signaling. A cell-permeant form of NAADP was able to produce both uterine contractions and calcium release. This response was unaffected by depletion of sarcoplasmic reticulum stores with thapsigargin, but was abolished by both bafilomycin and Ned-19. Crucially, oxytocin stimulated an increase in NAADP in rat uterine tissue. The present study demonstrates directly that NAADP signaling plays a role in rat uterine contractions. Moreover, investigation of this signaling pathway highlights yet another component of oxytocin-mediated signaling, stressing the need to consider the action of new components as they are discovered, even in signaling pathways that are thought to be well established.

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“…is a negative regulator of calcium ion import into the sarcoplasmic reticulum and its role in regulating the frequency and amplitude of contractions in rat myometrium has been described [19] but there is little information on the function of this protein in human uterine activity.…”

Section: Discussionmentioning

confidence: 99%

Phosphorylation of proteins during human myometrial contractions: A phosphoproteomic approach

Hudson

Bernal

2017

Biochemical and Biophysical Research Communications

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms . Other yet unknown phosphorylation or de-phosphorylation events may contribute to myometrial contraction and relaxation. In this study we have performed a global phosphoproteomic analysis of human myometrial tissue using tandem mass tagging to detect changes in the phosphorylation status of individual myometrial proteins during spontaneous and oxytocin-driven phasic contractions. We were able to detect 22 individual phosphopeptides whose relative ratio changed (fold > 2 or < 0.5) in response to spontaneous or oxytocin-stimulated contraction.The most significant changes in phosphorylation were to MYLK on serine 1760, a site associated with reductions in calmodulin binding and subsequent kinase activity.Phosphorylated MYLK (ser1760) increased significantly during spontaneous (9.83 ± 3.27 fold, P < 0.05) and oxytocin -induced (18.56 ± 8.18 fold, P < 0.01) contractions and we were able to validate these data using immunoblotting. Pathway analysis suggested additional proteins involved in calcium signalling, cGMP-PRKG signalling, adrenergic signalling and oxytocin signalling were also phosphorylated during contractions. This study demonstrates that a global phosphoproteomic analysis of myometrial tissue is a sensitive approach to detect changes in the phosphorylation of proteins during myometrial contractions, and provides a platform for further validation of these changes and for identification of their functional significance.

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A review of recent insights into the role of the sarcoplasmic reticulum and Ca entry in uterine smooth muscle

Cited by 52 publications

References 138 publications

Sarcoplasmic Reticulum Function in Smooth Muscle

Sarcoplasmic Reticulum Function in Smooth Muscle

A Functional Role for Nicotinic Acid Adenine Dinucleotide Phosphate in Oxytocin-Mediated Contraction of Uterine Smooth Muscle from Rat

Phosphorylation of proteins during human myometrial contractions: A phosphoproteomic approach

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