NO-sGC pathway modulates Ca2+ release and muscle contraction in zebrafish skeletal muscle
Vertebrate skeletal muscle contraction and relaxation is a complex process that depends on Ca2+ ions to promote the interaction of actin and myosin. This process can be modulated by nitric oxide (NO), a gas molecule synthesized endogenously by (nitric oxide synthase) NOS isoforms. At nanomolar conce...
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| Hauptverfasser: | , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
23 August 2017
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| In: |
Frontiers in physiology
Year: 2017, Jahrgang: 8 |
| ISSN: | 1664-042X |
| DOI: | 10.3389/fphys.2017.00607 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: http://dx.doi.org/10.3389/fphys.2017.00607 Verlag, kostenfrei, Volltext: https://www.frontiersin.org/articles/10.3389/fphys.2017.00607/full 
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| Verfasserangaben: | Zhou Xiyuan, Rainer H.A. Fink and Matias Mosqueira |
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| 245 | 1 | 0 | |a NO-sGC pathway modulates Ca2+ release and muscle contraction in zebrafish skeletal muscle |c Zhou Xiyuan, Rainer H.A. Fink and Matias Mosqueira |
| 246 | 3 | 3 | |a NO-sGC pathway modulates Ca 2+ release and muscle contraction in zebrafish skeletal muscle |
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| 520 | |a Vertebrate skeletal muscle contraction and relaxation is a complex process that depends on Ca2+ ions to promote the interaction of actin and myosin. This process can be modulated by nitric oxide (NO), a gas molecule synthesized endogenously by (nitric oxide synthase) NOS isoforms. At nanomolar concentrations NO activates soluble guanylate cyclase (sGC), which in turn activates protein kinase G via conversion of GTP into cyclic GMP. Alternatively, NO post-translationally modifies proteins via S-nitrosylation of the thiol group of cysteine. However, the mechanisms of action of NO on Ca2+ homeostasis during muscle contraction are not fully understood and we hypothesize that NO exerts its effects on Ca2+ homeostasis in skeletal muscles mainly through negative modulation of Ca2+ release and Ca2+ uptake via the NO-sGC-PKG pathway. To address this, we used 5-7 days-post fecundation-larvae of zebrafish, a well-established animal model for physiological and pathophysiological muscle activity. We evaluated the response of muscle contraction and Ca2+ transients in presence of SNAP, a NO-donor or L-NAME, an unspecific NOS blocker in combination with specific blockers of key proteins of Ca2+ homeostasis. We also evaluate the expression of NOS in combination with dihydropteridine receptor, ryanodine receptor and sarco/endoplasmic reticulum Ca2+ ATPase. We concluded that endogenous NO reduced force production through negative modulation of Ca2+ transients via the NO-sGC pathway. This effect could be reversed using an unspecific NOS blocker or sGC blocker. | ||
| 650 | 4 | |a : skeletal muscle | |
| 650 | 4 | |a Calcium transient | |
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| 650 | 4 | |a Nitric Oxide | |
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