Evidence map›Paper›PMID 36045747›Full record

ArticleFrontiers in physiology2022

nNOS-derived NO modulates force production and iNO-derived NO the excitability in C2C12-derived 3D tissue engineering skeletal muscle

Matias Mosqueira, Lisa-Mareike Scheid, Dominik Kiemel, Talisa Richardt, Mona Rheinberger, Dirk Ollech, Almut Lutge, Tim Heißenberg, Lena Pfitzer, Lisa Engelskircher and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Matias MosqueiraCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Lisa-Mareike ScheidCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Dominik KiemelCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Talisa RichardtCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Mona RheinbergerCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Dirk OllechCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Almut LutgeCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Tim HeißenbergCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Lena PfitzerCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Lisa EngelskircherCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Umut YildizCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Isabel PorthCardio-Ventilatory Muscle Physiology Laboratory, Institute of Physiology and Pathophysiology, Heidelberg University Hospital, Heidelberg, Germany.
Heidelberg University · DEUniversity Hospital Heidelberg · DEScience for Life Laboratory · SEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) is a bioactive gas produced by one of the three NO synthases: neuronal NOS (nNOS), inducible (iNOS), and endothelial NOS (eNOS). NO has a relevant modulatory role in muscle contraction; this takes place through two major signaling pathways: (i) activation of soluble guanylate cyclase and, thus, protein kinase G or (ii) nitrosylation of sulfur groups of cysteine. Although it has been suggested that nNOS-derived NO is the responsible isoform in muscle contraction, the roles of eNOS and iNOS and their signaling pathways have not yet been clarified. To elucidate the action of each pathway, we optimized the generation of myooids, an engineered skeletal muscle tissue based on the C2C12 cell line. In comparison with diaphragm strips from wild-type mice, 180 myooids were analyzed, which expressed all relevant excitation-contraction coupling proteins and both nNOS and iNOS isoforms. Along with the biochemical results, myooids treated with NO donor (SNAP) and unspecific NOS blocker (L-NAME) revealed a comparable NO modulatory effect on force production as was observed in the diaphragm strips. Under the effects of pharmacological tools, we analyzed the myooids in response to electrical stimulation of two possible signaling pathways and NO sources. The nNOS-derived NO exerted its negative effect on force production

Indexed as

C2C12calciumforcemyooidnitric oxidetissue engineering

Identifiers

PMID36045747
PMCPMC9421439
OpenAlexW4291513108

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.