Evidence map›Paper›PMID 39331194›Full record

ArticleMolecular biology reports2024

The senescent marker p16INK4a enhances macrophage foam cells formation.

Wei Sheng Siew, Yin Quan Tang, Bey Hing Goh, Wei Hsum Yap

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. 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

4 authors.

Wei Sheng SiewSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya, 47500, Malaysia.ORCID https://orcid.org/0000-0002-8803-9035
Yin Quan TangSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya, 47500, Malaysia.ORCID https://orcid.org/0000-0001-7327-2830
Bey Hing GohSunway Biofunctional Molecules Discovery Centre, School of Medical and Life Sciences, Sunway University, Bandar Sunway, 47500, Selangor, Malaysia.ORCID https://orcid.org/0000-0003-1006-3649
Wei Hsum YapSchool of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya, 47500, Malaysia. weihsum.yap@taylors.edu.my.ORCID https://orcid.org/0000-0001-8116-6018

Funding

Malaysian Ministry of Higher Education FRGS/1/2019/SKK08/TAYLOR/02/2
6 · The paper itself

Abstract

backgroundThe senescence marker p16INK4a, which constitutes part of the genome 9p21.3 cardiovascular disease (CVD) risk allele, is believed to play a role in foam cells formation. This study aims to unravel the role of p16INK4a in mediating macrophage foam cells formation, cellular senescence, and autophagy lysosomal functions.

methodsThe mammalian expression plasmid pCMV-p16INK4a was used to induce p16INK4a overexpression in THP-1 macrophages. Next, wild-type and p16INK4a-overexpressed macrophages were incubated with oxidized LDL to induce foam cells formation. Lipids accumulation was evaluated using Oil-red-O staining and cholesterol efflux assay, as well as expression of scavenger receptors CD36 and LOX-1. Cellular senescence in macrophage foam cells were determined through analysis of senescence-associated β-galactosidase activity and other SASP factors expression. Meanwhile, autophagy induction was assessed through detection of autophagosome formation and LC3B/p62 markers expression.

resultsThe findings showed that p16INK4a enhanced foam cells formation with increased scavenger receptors CD36 and LOX-1 expression and reduced cholesterol efflux in THP-1 macrophages. Besides, β-galactosidase activity was enhanced, and SASP factors such as IL-1α, TNF-α, and MMP9 were up-regulated. In addition, p16INK4a is also shown to induce autophagy, as well as increasing autophagy markers LC3B and p62 expression.

conclusionsThis study provides insights on p16INK4a in mediating macrophages foam cells formation, cellular senescence, and foam cells formation.

Indexed as

AutophagyCD36 AntigensCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Foam CellsLipoproteins, LDLBiomarkersCholesterolHumansMacrophagesScavenger Receptors, Class ETHP-1 CellsBiomarkersCD36 AntigensCD36 protein, humanCDKN2A protein, humanCholesterolCyclin-Dependent Kinase Inhibitor p16Lipoproteins, LDLoxidized low density lipoproteinScavenger Receptors, Class EAutophagyCellular SenescenceMacrophage foam cellp16INK4a

Identifiers

PMID39331194

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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.