ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2015
Nature of extracellular signal that triggers RhoA/ROCK activation for the basal internal anal sphincter tone in humans.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
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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.
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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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Evidence for the presence and release of BDNF in the neuronal and non-neuronal structures of the internal anal sphincter.Neurogastroenterology and motility · 2022Article
- Review
- BDNF rescues aging-associated internal anal sphincter dysfunction.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- BDNF augments rat internal anal sphincter smooth muscle tone via RhoA/ROCK signaling and nonadrenergic noncholinergic relaxation via increased NO release.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Downregulation of thromboxane A2 and angiotensin II type 1 receptors associated with aging-related decrease in internal anal sphincter tone.Scientific reports · 2019Article
- Is the Lower Esophageal Sphincter Tone Related to a Gas?Cellular and molecular gastroenterology and hepatology · 2018Article
- In vivo magnetofection: a novel approach for targeted topical delivery of nucleic acids for rectoanal motility disorders.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Role of differentially expressed microRNA-139-5p in the regulation of phenotypic internal anal sphincter smooth muscle tone.Scientific reports · 2017Article
- Ca2+/calmodulin/MLCK pathway initiates, and RhoA/ROCK maintains, the internal anal sphincter smooth muscle tone.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Aging-associated changes in microRNA expression profile of internal anal sphincter smooth muscle: Role of microRNA-133a.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles.Journal of neurogastroenterology and motility · 2016Review
- Role of microRNAs in gastrointestinal smooth muscle fibrosis and dysfunction: novel molecular perspectives on the pathophysiology and therapeutic targeting.American journal of physiology. Gastrointestinal and liver physiology · 2016Review
Corrections and comments
- Erratum issuedCorrigendum.2015
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The extracellular signal that triggers activation of rho-associated kinase (RhoA/ROCK), the major molecular determinant of basal internal anal sphincter (IAS) smooth muscle tone, is not known. Using human IAS tissues, we identified the presence of the biosynthetic machineries for angiotensin II (ANG II), thromboxane A2 (TXA2), and prostaglandin F2α (PGF2α). These end products of the renin-angiotensin system (RAS) (ANG II) and arachidonic acid (TXA2 and PGF2α) pathways and their effects in human IAS vs. rectal smooth muscle (RSM) were studied. A multipronged approach utilizing immunocytochemistry, Western blot analyses, and force measurements was implemented. Additionally, in a systematic analysis of the effects of respective inhibitors along different steps of biosynthesis and those of antagonists, their end products were evaluated either individually or in combination. To further describe the molecular mechanism for the IAS tone via these pathways, we monitored RhoA/ROCK activation and its signal transduction cascade. Data showed characteristically higher expression of biosynthetic machineries of RAS and AA pathways in the IAS compared with the RSM. Additionally, specific inhibition of the arachidonic acid (AA) pathway caused ~80% decrease in the IAS tone, whereas that of RAS lead to ~20% decrease. Signal transduction studies revealed that the end products of both AA and RAS pathways cause increase in the IAS tone via activation of RhoA/ROCK. Both AA and RAS (via the release of their end products TXA2, PGF2α, and ANG II, respectively), provide extracellular signals which activate RhoA/ROCK for the maintenance of the basal tone in human IAS.
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Registered trials
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 OpenQuestion graph.