Evidence map›Paper›PMID 25961161›Full record

ArticleMolecules (Basel, Switzerland)2015

Antiproliferative Activity of Hinokitiol, a Tropolone Derivative, Is Mediated via the Inductions of p-JNK and p-PLCγ1 Signaling in PDGF-BB-Stimulated Vascular Smooth Muscle Cells.

Po-Sheng Yang, Meng-Jiy Wang, Thanasekaran Jayakumar, Duen-Suey Chou, Ching-Ya Ko, Ming-Jen Hsu, Cheng-Ying Hsieh

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. STIM1 Knockout Enhances PDGF-Mediated CaInternational journal of molecular sciences · 2018
    Article
  9. Article
  10. Article
  11. 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

7 authors at 2 institutions in 1 country.

Po-Sheng YangDepartment of Surgery, MacKay Memorial Hospital and Mackay Medical College, No. 92, Sec. 2, Zhongshan N. Rd., Taipei City 10449, Taiwan. psyangd0039@gmail.com.
Meng-Jiy WangDepartment of Pharmacology, School of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei 110, Taiwan. mjwang@mail.ntust.edu.tw.
Thanasekaran JayakumarDepartment of Pharmacology, School of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei 110, Taiwan. tjaya_2002@yahoo.co.in.
Duen-Suey ChouDepartment of Pharmacology, School of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei 110, Taiwan. fird@tmu.edu.tw.
Ching-Ya KoDepartment of Pharmacology, School of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei 110, Taiwan. smallko1022@hotmail.com.
Ming-Jen HsuDepartment of Pharmacology, School of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei 110, Taiwan. aspirin@tmu.edu.tw.
Cheng-Ying HsiehDepartment of Pharmacology, School of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei 110, Taiwan. hsiehcy@tmu.edu.tw.
Taipei Medical University · TWMackay Junior College of Medicine, Nursing and Management · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal proliferation of vascular smooth muscle cells (VSMCs) is important in the pathogenesis of vascular disorders such as atherosclerosis and restenosis. Hinokitiol, a tropolone derivative found in Chamacyparis taiwanensis, has been found to exhibit anticancer activity in a variety of cancers through inhibition of cell proliferation. In the present study, the possible anti-proliferative effect of hinokitiol was investigated on VSMCs. Our results showed that hinokitiol significantly attenuated the PDGF-BB-stimulated proliferation of VSMCs without cytotoxicity. Hinokitiol suppressed the expression of proliferating cell nuclear antigen (PCNA), a maker for cell cycle arrest, and caused G0/G1 phase arrest in cell cycle progression. To investigate the mechanism underlying the anti-proliferative effect of hinokitiol, we examined the effects of hinokitiol on phosphorylations of Akt, ERK1/2, p38 and JNK1/2. Phospholipase C (PLC)-γ1 phosphorylation, its phosphorylated substrates and p27kip1 expression was also analyzed. Pre-treatment of VSMCs with hinikitiol was found to significantly inhibit the PDGF-BB-induced phosphorylations of JNK1/2 and PLC-γ1, however no effects on Akt, ERK1/2, and p38. The up-regulation of p27kip1 was also observed in hinokitiol-treated VSMCs. Taken together, our results suggest that hinokitiol inhibits PDGF-BB-induced proliferation of VSMCs by inducing cell cycle arrest, suppressing JNK1/2 phosphorylation and PLC-γ1, and stimulating p27kip1 expression. These findings suggest that hinokitiol may be beneficial for the treatment of vascular-related disorders and diseases.

Indexed as

AnimalsBecaplerminCell Cycle CheckpointsCell ProliferationCyclin-Dependent Kinase Inhibitor p27G1 PhaseMaleMAP Kinase Signaling SystemMonoterpenesMuscle, Smooth, VascularMyocytes, Smooth Musclep38 Mitogen-Activated Protein KinasesPhospholipase C gammaPhosphorylationProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktBecaplerminbeta-thujaplicinCyclin-Dependent Kinase Inhibitor p27Monoterpenesp38 Mitogen-Activated Protein KinasesPhospholipase C gammaProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-sisTropolone

Identifiers

PMID25961161
PMCPMC6272725
OpenAlexW1589641772

What Socratic 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 Socratic graph.