Evidence map›Paper›PMID 22733824›Full record

ArticleThe Journal of biological chemistry2012

MicroRNA-153 physiologically inhibits expression of amyloid-β precursor protein in cultured human fetal brain cells and is dysregulated in a subset of Alzheimer disease patients.

Justin M Long, Balmiki Ray, Debomoy K Lahiri

Abstract read
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In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

120 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  5. The Ubiquitin-Proteasome System in Brain Disorders: Pathogenic Pathways, Post-Translational Tweaks, and Therapeutic Frontiers.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
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60 more citing papers are in PubMed but not listed here.

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

3 authors.

Justin M LongDepartment of Psychiatry, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Balmiki Ray
Debomoy K Lahiri

Funding

Regulation of APP Pathway Gene Promoters in Alzheimer'sR01AG018379 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2000 to 2011
$3.1M
Mechanisms of Cholinesterase Inhibitors on Beta-amyloidR01AG018884 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2002 to 2012
$2.9M
NIA NIH HHS AG18379NIA NIH HHS AG18884NIA NIH HHS R01 AG018379NIA NIH HHS R01 AG018884
6 · The paper itself

Abstract

Regulation of amyloid-β (Aβ) precursor protein (APP) expression is complex. MicroRNAs (miRNAs) are expected to participate in the molecular network that controls this process. The composition of this network is, however, still undefined. Elucidating the complement of miRNAs that regulate APP expression should reveal novel drug targets capable of modulating Aβ production in AD. Here, we investigated the contribution of miR-153 to this regulatory network. A miR-153 target site within the APP 3'-untranslated region (3'-UTR) was predicted by several bioinformatic algorithms. We found that miR-153 significantly reduced reporter expression when co-transfected with an APP 3'-UTR reporter construct. Mutation of the predicted miR-153 target site eliminated this reporter response. miR-153 delivery in both HeLa cells and primary human fetal brain cultures significantly reduced APP expression. Delivery of a miR-153 antisense inhibitor to human fetal brain cultures significantly elevated APP expression. miR-153 delivery also reduced expression of the APP paralog APLP2. High functional redundancy between APP and APLP2 suggests that miR-153 may target biological pathways in which they both function. Interestingly, in a subset of human AD brain specimens with moderate AD pathology, miR-153 levels were reduced. This same subset also exhibited elevated APP levels relative to control specimens. Therefore, endogenous miR-153 inhibits expression of APP in human neurons by specifically interacting with the APP 3'-UTR. This regulatory interaction may have relevance to AD etiology, where low miR-153 levels may drive increased APP expression in a subset of AD patients.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAlzheimer DiseaseAmyloid beta-Protein PrecursorBrainFemaleFetusHeLa CellsHumansMaleMicroRNAsNerve Tissue Proteins3' Untranslated RegionsAmyloid beta-Protein PrecursorAPP protein, humanMicroRNAsMIRN153 microRNA, humanNerve Tissue Proteins

Identifiers

PMID22733824
PMCPMC3438960

What OpenQuestion holds

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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.