Evidence map›Paper›PMID 31686316›Full record

ArticleMolecular and cellular biochemistry2020

CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells.

M D Khurshidul Zahid, Michael Rogowski, Christopher Ponce, Mahua Choudhury, Naima Moustaid-Moussa, Shaikh M Rahman

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 66 citations in OpenAlex.

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  17. The CEBPBTheranostics · 2024
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  19. The engagement of autophagy in maniac disease.CNS neuroscience & therapeutics · 2023
    Review
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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

6 authors at 2 institutions in 1 country.

M D Khurshidul ZahidDepartment of Nutritional Sciences & Obesity Research Institute, Texas Tech University, Lubbock, TX, 79409-1270, USA.
Michael RogowskiDepartment of Nutritional Sciences & Obesity Research Institute, Texas Tech University, Lubbock, TX, 79409-1270, USA.
Christopher PonceDepartment of Mathematics, Texas Tech University, Lubbock, TX, 79409-1270, USA.
Mahua ChoudhuryDepartment of Pharmaceutical Sciences, Irma Lerma Rangel College of Pharmacy, Texas A&M, Health Sciences Center, College Station, TX, 78363, USA.
Naima Moustaid-MoussaDepartment of Nutritional Sciences & Obesity Research Institute, Texas Tech University, Lubbock, TX, 79409-1270, USA.
Shaikh M RahmanDepartment of Nutritional Sciences & Obesity Research Institute, Texas Tech University, Lubbock, TX, 79409-1270, USA. shaikh.rahman@ttu.edu.
Texas Tech University · USTexas A&M Health Science Center · US

Funding

American Heart Association 09BGIA2060705
6 · The paper itself

Abstract

Atherosclerosis is associated with deregulated cholesterol metabolism and formation of macrophage foam cells. CCAAT/enhancer-binding protein beta (C/EBPβ) is a transcription factor, and its inhibition has recently been shown to prevent atherosclerosis development and foam cell formation. However, whether C/EBPβ regulates inflammation, endoplasmic reticulum (ER) stress, and apoptosis, in macrophage foam cells and its underlying molecular mechanism remains unknown. Here, we investigated the effect of C/EBPβ knockdown on proteins and genes implicated in inflammation, ER stress, apoptosis, and autophagy in macrophage foam cells. RAW264.7 macrophage cells were transfected with control and C/EBPβ-siRNA and then treated with nLDL and oxLDL. Key proteins and genes involved in inflammation, ER stress, apoptosis, and autophagy were analyzed by western blot and qPCR. We found that short interfering RNA (siRNA)-mediated knockdown of C/EBPβ attenuated atherogenic lipid-mediated induction of proteins and genes implicated in inflammation (P-NFkB-p65, NFkB-p65, and TNFα), ER stress (ATF4 and ATF6), and apoptosis (CHOP, caspase 1, 3, and 12). Interestingly, C/EBPβ knockdown upregulated the expression of autophagy proteins (LC3A/B-II, ATG5) and genes (LC3B, ATG5) but decreased the mammalian target of rapamycin (mTOR) protein phosphorylation and mTORC1 gene expression in oxLDL-loaded RAW264.7 macrophage cells. More importantly, treatment with rapamycin (inhibitor of mTOR) increased expression of proteins implicated in autophagy and cholesterol efflux in oxLDL-loaded RAW 264.7 macrophage cells. The present results suggest that C/EBPβ inactivation regulates macrophage foam cell formation in atherogenesis by reducing inflammation, ER stress, and apoptosis and by promoting autophagy and inactivating mTOR.

Indexed as

ApoptosisEndoplasmic Reticulum StressGene Expression RegulationAnimalsCCAAT-Enhancer-Binding Protein-betaFoam CellsGene Knockdown TechniquesInflammationLipoproteins, LDLMiceRAW 264.7 CellsCCAAT-Enhancer-Binding Protein-betaCebpb protein, mouseLipoproteins, LDLoxidized low density lipoproteinApoptosisAutophagyC/EBPβEndoplasmic reticulum stress (ERS)Macrophage foam cells

Identifiers

PMID31686316
OpenAlexW2989544643

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.