Evidence map›Paper›PMID 32211403›Full record

ArticleFrontiers in cell and developmental biology2020

Downregulation of Lysosomal Acid Ceramidase Mediates HMGB1-Induced Migration and Proliferation of Mouse Coronary Arterial Myocytes.

Xinxu Yuan, Owais M Bhat, Hannah Lohner, Yang Zhang, Pin-Lan Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. 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
1.5field-weighted citation impact, top 20% 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, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Cell Senescence and Central Regulators of Immune Response.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Involvement of Ceramide Metabolism in Cerebral Ischemia.Frontiers in molecular biosciences · 2022
    Review
  10. Article
  11. Review
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

5 authors at 2 institutions in 1 country.

Xinxu YuanDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Owais M BhatDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Hannah LohnerDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Yang ZhangDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, United States.
Pin-Lan LiDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Virginia Commonwealth University · USUniversity of Houston · US

Funding

Regulation of Lysosomes in Autophagy in Coronary Arterial MyocytesR01HL057244 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2001 to 2021
$6.7M
Subendothelial Exosomes in Coronary Microvascular DysfunctionR01HL075316 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2004 to 2024
$6.7M
Hypertension and glomerular injury in hyperhomocysteinemia - role of inflammatory exosomesR01DK054927 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 1998 to 2023
$6.7M
Lysosome Trafficking Dysregulation of Arterial Myocytes in AtherogenesisR01HL122937 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN, ZHANG, YANG · 2014 to 2024
$4.0M
Lysosome dysfunction in podocytopathy and associated hypertensionR01DK120491 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2018 to 2022
$2.4M
MECHANISM OF CORONARY ENDOTHELIUM MEDIATED VASODILATIONR29HL057244 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LI, PIN-LAN · 1997 to 2000
$101k
NHLBI NIH HHS R01 HL057244NHLBI NIH HHS R01 HL075316NHLBI NIH HHS R01 HL122937NHLBI NIH HHS R29 HL057244NIDDK NIH HHS R01 DK054927NIDDK NIH HHS R01 DK120491
6 · The paper itself

Abstract

High-mobility group box 1 protein (HMGB1) has been reported to trigger lysosome destabilization causing a wide of inflammatory diseases. The present study tested whether a lysosomal enzyme, acid ceramidase (AC), plays a critical role in HMGB1-induced alteration in ceramide metabolism and whether such HMGB1-AC interaction is associated with abnormal migration and proliferation of vascular smooth muscle cells (SMCs). We first observed that the expression of AC in the medial layer of mouse coronary arterial wall and colocalization of AC with a lysosome marker Lamp-1. In primary cultured coronary arterial myocytes (CAMs), AC expression and colocalization with Lamp-1 were significantly up-regulated by AC inducer, genistein, but down-regulated by AC inhibitor, N-oleoylethanolamine (NOE). HMGB1 dose-dependently decreased the colocalization of AC with Lamp-1 and reduced mRNA and protein expressions of AC in CAMs, but reversed by genistein. Consistently, HMGB1 significantly induced increases in the levels of long-chain ceramides in CAMs, which were not further enhanced by NOE but blocked by genistein. More importantly, HMGB1 promoted migration and proliferation of CAMs, which were not further increased by NOE but reduced by genistein. Lastly, CAMs isolated from smooth muscle-specific AC knockout mice (AC gene

Indexed as

cell migrationcell proliferationceramidecoronary arterylysosomes

Identifiers

PMID32211403
PMCPMC7076051
OpenAlexW3012545885

What OpenQuestion holds

Textmetadata
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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.