Evidence map›Paper›PMID 30104414›Full record

ArticleThe Journal of biological chemistry2018

TNF-α elicits phenotypic and functional alterations of vascular smooth muscle cells by miR-155-5p-dependent down-regulation of cGMP-dependent kinase 1.

Seunghwan Choi, Minsik Park, Joohwan Kim, Wonjin Park, Suji Kim, Dong-Keon Lee, Jong Yun Hwang, Jongseon Choe, Moo-Ho Won, Sungwoo Ryoo and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020
    Pooled it
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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

13 authors at 3 institutions in 2 countries.

Seunghwan ChoiFrom the Departments of Molecular and Cellular Biochemistry.
Minsik ParkFrom the Departments of Molecular and Cellular Biochemistry.
Joohwan KimFrom the Departments of Molecular and Cellular Biochemistry.
Wonjin ParkFrom the Departments of Molecular and Cellular Biochemistry.
Suji KimFrom the Departments of Molecular and Cellular Biochemistry.
Dong-Keon LeeFrom the Departments of Molecular and Cellular Biochemistry.
Jong Yun HwangObstetrics and Gynecology.
Jongseon ChoeImmunology, and.
Moo-Ho WonNeurobiology, Kangwon National University School of Medicine, Chuncheon, Gangwon-do 24341.
Sungwoo Ryoothe Department of Biology, College of Natural Sciences, Kangwon National University, Chuncheon, Gangwon-do 24341, and.
Kwon-Soo HaFrom the Departments of Molecular and Cellular Biochemistry.
Young-Guen Kwonthe Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Young-Myeong KimFrom the Departments of Molecular and Cellular Biochemistry, ymkim@kangwon.ac.kr.
Kangwon National University · KRBeijing Obstetrics and Gynecology Hospital · CNYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

cGMP-dependent protein kinase 1 (PKG1) plays an important role in nitric oxide (NO)/cGMP-mediated maintenance of vascular smooth muscle cell (VSMC) phenotype and vasorelaxation. Inflammatory cytokines, including tumor necrosis factor-α (TNFα), have long been understood to mediate several inflammatory vascular diseases. However, the underlying mechanism of TNFα-dependent inflammatory vascular disease is unclear. Here, we found that TNFα treatment decreased PKG1 expression in cultured VSMCs, which correlated with NF-κB-dependent biogenesis of miR-155-5p that targeted the 3'-UTR of PKG1 mRNA. TNFα induced VSMC phenotypic switching from a contractile to a synthetic state through the down-regulation of VSMC marker genes, suppression of actin polymerization, alteration of cell morphology, and elevation of cell proliferation and migration. All of these events were blocked by treatment with an inhibitor of miR-155-5p or PKG1, whereas transfection with miR-155-5p mimic or PKG1 siRNA promoted phenotypic modulation, similar to the response to TNFα. In addition, TNFα-induced miR-155-5p inhibited the vasorelaxant response of de-endothelialized mouse aortic vessels to 8-Br-cGMP by suppressing phosphorylation of myosin phosphatase and myosin light chain, both of which are downstream signal modulators of PKG1. Moreover, TNFα-induced VSMC phenotypic alteration and vasodilatory dysfunction were blocked by NF-κB inhibition. These results suggest that TNFα impairs NO/cGMP-mediated maintenance of the VSMC contractile phenotype and vascular relaxation by down-regulating PKG1 through NF-κB-dependent biogenesis of miR-155-5p. Thus, the NF-κB/miR-155-5p/PKG1 axis may be crucial in the pathogenesis of inflammatory vascular diseases, such as atherosclerotic intimal hyperplasia and preeclamptic hypertension.

Indexed as

3' Untranslated RegionsActinsAnimalsCell MovementCell ProliferationCells, CulturedCyclic GMP-Dependent Protein KinasesCyclic GMP-Dependent Protein Kinase Type IDown-RegulationMaleMice, Inbred C57BLMicroRNAsMuscle, Smooth, VascularNF-kappa BPolymerizationRNA, Messenger3' Untranslated RegionsActinsCyclic GMP-Dependent Protein KinasesCyclic GMP-Dependent Protein Kinase Type IMicroRNAsMirn155 microRNA, mouseNF-kappa BPrkg1 protein, mouseRNA, MessengerTumor Necrosis Factor-alphacGMP-dependent protein kinase 1microRNA (miRNA)NF-kappa B (NF-κB)protein kinase G (PKG)tumor necrosis factor (TNF)vascular smooth muscle cells

Identifiers

PMID30104414
PMCPMC6153283
OpenAlexW2887534122

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.