Evidence map›Paper›PMID 35805891›Full record

ArticleInternational journal of molecular sciences2022

The Regulatory Role of H19/miR-181a/ATG5 Signaling in Perinatal Nicotine Exposure-Induced Development of Neonatal Brain Hypoxic-Ischemic Sensitive Phenotype.

Yong Li, Yanyan Zhang, Andrew Walayat, Yingjie Fu, Bailin Liu, Lubo Zhang, Daliao Xiao

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Aging · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Cellular and Molecular Targets in Acute Ischemic Stroke.International journal of molecular sciences · 2022
    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

7 authors at 1 institution in 1 country.

Yong LiLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Yanyan ZhangLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Andrew WalayatLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Yingjie FuLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Bailin LiuLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Lubo ZhangLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.ORCID 0000-0002-9386-8938
Daliao XiaoLawrence D. Longo MD Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.ORCID 0000-0003-0147-2758
Loma Linda University · US

Funding

Maternal inhaled nicotine leads to aberrant development of hypertensive phenotypeR01HL135623 · NHLBI · LOMA LINDA UNIVERSITY · PI SHAO, XUESI MAX, XIAO, DALIAO · 2017 to 2021
$2.3M
miRNA as a novel therapeutic target in antenatal nicotine-induced ischemic heartR01HD088039 · NICHD · LOMA LINDA UNIVERSITY · PI XIAO, DALIAO · 2017 to 2021
$1.6M
Nicotine-mediated fetal programming of vascular dysfunction phenotypeR03DA041492 · NIDA · LOMA LINDA UNIVERSITY · PI XIAO, DALIAO · 2017 to 2018
$158k
NHLBI NIH HHS R01 HL135623NICHD NIH HHS R01 HD088039NIDA NIH HHS R03 DA041492NIH HHS HL135623, DA041492, HD088039The Regents of the University of California, Research Grants Program Office, Tobacco Related Disease Research Program (TRDRP) grant 29IR0437, T30FT0936
6 · The paper itself

Abstract

Nicotine exposure either from maternal cigarette smoking or e-cigarette vaping is one of the most common risk factors for neurodevelopmental disease in offspring. Previous studies revealed that perinatal nicotine exposure programs a sensitive phenotype to neonatal hypoxic-ischemic encephalopathy (HIE) in postnatal life, yet the underlying mechanisms remain undetermined. The goal of the present study was to determine the regulatory role of H19/miR-181a/ATG5 signaling in perinatal nicotine exposure-induced development of neonatal brain hypoxic-ischemic sensitive phenotype. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps. All experiments were conducted in offspring pups at postnatal day 9 (P9). Perinatal nicotine exposure significantly enhanced expression of miR-181a but attenuated autophagy-related protein 5 (ATG5) mRNA and protein levels in neonatal brains. Of interest, miR-181a mimicking administration in the absence of nicotine exposure also produced dose-dependent increased hypoxia/ischemia (H/I)-induced brain injury associated with a decreased ATG5 expression, closely resembling perinatal nicotine exposure-mediated effects. Locked nucleic acid (LNA)-miR-181a antisense reversed perinatal nicotine-mediated increase in H/I-induced brain injury and normalized aberrant ATG5 expression. In addition, nicotine exposure attenuated a long non-coding RNA (lncRNA) H19 expression level. Knockdown of H19 via siRNA increased the miR-181a level and enhanced H/I-induced neonatal brain injury. In conclusion, the present findings provide a novel mechanism that aberrant alteration of the H19/miR-181a/AGT5 axis plays a vital role in perinatal nicotine exposure-mediated ischemia-sensitive phenotype in offspring and suggests promising molecular targets for intervention and rescuing nicotine-induced adverse programming effects in offspring.

Indexed as

Brain InjuriesElectronic Nicotine Delivery SystemsHypoxia-Ischemia, BrainMicroRNAsRNA, Long NoncodingAnimalsAnimals, NewbornAutophagy-Related Protein 5BrainFemaleIschemiaNicotinePhenotypePregnancyRatsAutophagy-Related Protein 5H19 long non-coding RNAMicroRNAsNicotineRNA, Long NoncodingATG5lncRNA H19miR-181aneonatal HIEnicotine

Identifiers

PMID35805891
PMCPMC9266802
OpenAlexW4283274556

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.