Evidence map›Paper›PMID 34071138›Full record

ArticleInternational journal of molecular sciences2021

The Effects of Insulin on Immortalized Rat Schwann Cells, IFRS1.

Tomokazu Saiki, Nobuhisa Nakamura, Megumi Miyabe, Mizuho Ito, Tomomi Minato, Kazunori Sango, Tatsuaki Matsubara, Keiko Naruse

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. In Vitro Models for Peripheral Nerve Regeneration.Advanced healthcare materials · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
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

8 authors at 2 institutions in 1 country.

Tomokazu SaikiDepartment of Pharmacy, Aichi Gakuin University Dental Hospital, Nagoya 464-8651, Japan.
Nobuhisa NakamuraDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.ORCID 0000-0003-3265-5194
Megumi MiyabeDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Mizuho ItoDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Tomomi MinatoDepartment of Clinical Laboratory, Aichi Gakuin University Dental Hospital, Nagoya 464-8651, Japan.
Kazunori SangoDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.ORCID 0000-0002-9750-9596
Tatsuaki MatsubaraDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Keiko NaruseDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Aichi Gakuin University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 21592506
6 · The paper itself

Abstract

Schwann cells play an important role in peripheral nerve function, and their dysfunction has been implicated in the pathogenesis of diabetic neuropathy and other demyelinating diseases. The physiological functions of insulin in Schwann cells remain unclear and therefore define the aim of this study. By using immortalized adult Fischer rat Schwann cells (IFRS1), we investigated the mechanism of the stimulating effects of insulin on the cell proliferation and expression of myelin proteins (myelin protein zero (MPZ) and myelin basic protein (MBP). The application of insulin to IFRS1 cells increased the proliferative activity and induced phosphorylation of Akt and ERK, but not P38-MAPK. The proliferative potential of insulin-stimulated IFRS1 was significantly suppressed by the addition of LY294002, a PI3 kinase inhibitor. The insulin-stimulated increase in MPZ expression was significantly suppressed by the addition of PD98059, a MEK inhibitor. Furthermore, insulin-increased MBP expression was significantly suppressed by the addition of LY294002. These findings suggest that both PI3-K/Akt and ERK/MEK pathways are involved in insulin-induced cell growth and upregulation of MPZ and MBP in IFRS1 Schwann cells.

Indexed as

AnimalsCell DivisionCell Line, TransformedChromonesDiabetic NeuropathiesExtracellular Signal-Regulated MAP KinasesFlavonoidsGene Expression RegulationInsulinMitogen-Activated Protein Kinase KinasesMorpholinesMyelin ProteinsPhosphatidylinositol 3-KinasesPhosphorylationProtein Processing, Post-TranslationalProto-Oncogene Proteins c-akt2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAkt1 protein, ratChromonesExtracellular Signal-Regulated MAP KinasesFlavonoidsInsulinMitogen-Activated Protein Kinase KinasesMorpholinesMyelin ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, InsulinAktextracellular-signal-regulated kinase (ERK)insulinmyelin associated glycoproteinmyelin basic proteinmyelin protein zeroSchwann cells

Identifiers

PMID34071138
PMCPMC8197103
OpenAlexW3165342905

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.