Evidence map›Paper›PMID 32466437›Full record

ArticleCells2020

Role of microRNA 690 in Mediating Angiotensin II Effects on Inflammation and Endoplasmic Reticulum Stress.

Kalhara R Menikdiwela, Latha Ramalingam, Mostafa M Abbas, Halima Bensmail, Shane Scoggin, Nishan S Kalupahana, Asha Palat, Preethi Gunaratne, Naima Moustaid-Moussa

Open access · goldAbstract read
In one paragraph

Article in Cells, 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
1.4field-weighted citation impact, top 19% 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, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Specific microRNA Signature Kinetics inInternational journal of molecular sciences · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Endoplasmic Reticulum (ER) Stress in Part Mediates Effects of Angiotensin II in Pancreatic Beta Cells.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    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

9 authors at 4 institutions in 3 countries.

Kalhara R MenikdiwelaDepartment of Nutritional Sciences, Obesity Research Institute, Texas Tech University, Lubbock, TX 79409, USA.
Latha RamalingamDepartment of Nutritional Sciences, Obesity Research Institute, Texas Tech University, Lubbock, TX 79409, USA.
Mostafa M AbbasQatar Computing Research Institute, Hamad Bin Khalifa University, Doha 34110, Qatar.
Halima BensmailQatar Computing Research Institute, Hamad Bin Khalifa University, Doha 34110, Qatar.
Shane ScogginDepartment of Nutritional Sciences, Obesity Research Institute, Texas Tech University, Lubbock, TX 79409, USA.
Nishan S KalupahanaDepartment of Nutritional Sciences, Obesity Research Institute, Texas Tech University, Lubbock, TX 79409, USA.
Asha PalatBiology and Biochemistry, University of Houston, Houston, TX 77204, USA.
Preethi GunaratneBiology and Biochemistry, University of Houston, Houston, TX 77204, USA.
Naima Moustaid-MoussaDepartment of Nutritional Sciences, Obesity Research Institute, Texas Tech University, Lubbock, TX 79409, USA.
Texas Tech University · USHamad bin Khalifa University · QAUniversity of Houston · USUniversity of Peradeniya · LK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overactivation of the renin-angiotensin system (RAS) during obesity disrupts adipocyte metabolic homeostasis and induces endoplasmic reticulum (ER) stress and inflammation; however, underlying mechanisms are not well known. We propose that overexpression of angiotensinogen (Agt), the precursor protein of RAS in adipose tissue or treatment of adipocytes with Angiotensin II (Ang II), RAS bioactive hormone, alters specific microRNAs (miRNA), that target ER stress and inflammation leading to adipocyte dysfunction. Epididymal white adipose tissue (WAT) from B6 wild type (Wt) and transgenic male mice overexpressing Agt (Agt-Tg) in adipose tissue and adipocytes treated with Ang II were used. Small RNA sequencing and microarray in WAT identified differentially expressed miRNAs and genes, out of which miR-690 and mitogen-activated protein kinase kinase 3 (MAP2K3) were validated as significantly up- and down-regulated, respectively, in Agt-Tg, and in Ang II-treated adipocytes compared to respective controls. Additionally, the direct regulatory role of miR-690 on MAP2K3 was confirmed using mimic, inhibitors and dual-luciferase reporter assay. Downstream protein targets of MAP2K3 which include p38, NF-κB, IL-6 and CHOP were all reduced. These results indicate a critical post-transcriptional role for miR-690 in inflammation and ER stress. In conclusion, miR-690 plays a protective function and could be a useful target to reduce obesity.

Indexed as

Endoplasmic Reticulum Stress3T3-L1 CellsAdipocytesAdipose Tissue, WhiteAngiotensin IIAnimalsBase SequenceBiomarkersGene Expression RegulationInflammationMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMicroRNAsRenin-Angiotensin SystemAngiotensin IIBiomarkersMicroRNAsMIRN690 microRNA, mouseadipocytesendoplasmic reticulum (ER) stressinflammationmiR-690obesityrenin–angiotensin system (RAS)

Identifiers

PMID32466437
PMCPMC7348980
OpenAlexW3031491730

What OpenQuestion 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 OpenQuestion graph.