Evidence map›Paper›PMID 26577585›Full record

ArticlePflugers Archiv : European journal of physiology2016

Insulin augments serotonin-induced contraction via activation of the IR/PI3K/PDK1 pathway in the rat carotid artery.

Shun Watanabe, Takayuki Matsumoto, Mirai Oda, Kosuke Yamada, Junya Takagi, Kumiko Taguchi, Tsuneo Kobayashi

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 24 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Shun WatanabeDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.
Takayuki MatsumotoDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.
Mirai OdaDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.
Kosuke YamadaDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.
Junya TakagiDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.
Kumiko TaguchiDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.
Tsuneo KobayashiDepartment of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan. tkoba@hoshi.ac.jp.
Hoshi University · JPEbara (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperinsulinemia associated with type 2 diabetes may contribute to the development of vascular diseases. Although we recently reported that enhanced contractile responses to serotonin (5-hydroxytryptamine, 5-HT) are observed in the arteries of type 2 diabetes models, the causative factors and detailed signaling pathways involved remain unclear. The purpose of this study was to investigate whether high insulin would be an amplifier of 5-HT-induced contraction in rat carotid arteries and whether the contraction involves phosphoinositide 3-kinase (PI3K)/3-phosphoinositide-dependent protein kinase 1 (PDK1) signaling, an insulin-mediated signaling pathway. In rat carotid arteries organ-cultured with insulin (for 24 h), (1) the contractile responses to 5-HT were significantly greater (vs. vehicle), (2) the insulin-induced enhancement of 5-HT-induced contractions was largely suppressed by inhibitors of the insulin receptor (IR) (GSK1838705A), PI3K (LY294002), and PDK1 (GSK2334470), and (3) the levels of phosphorylated forms of both PDK1 and myosin phosphatase target subunit 1 (MYPT1) were greater upon 5-HT stimulation. In addition, in rat carotid arteries organ-cultured with an activator of PDK1 (PS48), the 5-HT-induced contraction was greater, and this was suppressed by PDK1 inhibition but not PI3K inhibition. In addition, MYPT1 and PDK1 phosphorylation upon 5-HT stimulation was enhanced (vs. vehicle). These results suggest that high insulin levels amplify 5-HT-induced contraction. Moreover, the present results indicated the direct linkage between IR/PI3K/PDK1 activation and 5-HT-induced contraction in rat carotid arteries for the first time.

Indexed as

VasoconstrictionAnimalsCarotid ArteriesInsulinMaleMuscle ContractionMuscle, Smooth, VascularPhosphatidylinositol 3-KinasesProtein Phosphatase 1Protein Serine-Threonine KinasesPyruvate Dehydrogenase Acetyl-Transferring KinaseRatsRats, WistarReceptor, InsulinSerotoninSignal TransductionInsulinPdk1 protein, ratPhosphatidylinositol 3-KinasesPpp1r12a protein, ratProtein Phosphatase 1Protein Serine-Threonine KinasesPyruvate Dehydrogenase Acetyl-Transferring KinaseReceptor, InsulinSerotoninInsulin receptorMyosin phosphatase target subunit 1Phosphoinositide 3-kinasePhosphoinositide-dependent kinase 1Vasoconstriction

Identifiers

PMID26577585
OpenAlexW2179090473

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.