Evidence map›Paper›PMID 35411051›Full record

ArticleCell death & disease2022

Loss of RNA binding protein HuD facilitates the production of the senescence-associated secretory phenotype.

Seungyeon Ryu, Myeongwoo Jung, Chongtae Kim, Hoin Kang, Sukyoung Han, Seongho Cha, Seung Min Jeong, Eun Kyung Lee

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Inflammation: A New Look at an Old Problem.International journal of molecular sciences · 2022
    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

8 authors at 1 institution in 1 country.

Seungyeon RyuDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea.
Myeongwoo JungDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea.
Chongtae KimDepartment of Biochemistry, The Catholic University of Korea, Seoul, 06591, South Korea.
Hoin KangDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea.
Sukyoung HanDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea.
Seongho ChaDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea.
Seung Min JeongDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea.ORCID 0000-0002-9787-2539
Eun Kyung LeeDepartment of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, 06591, South Korea. leeek@catholic.ac.kr.ORCID 0000-0003-4207-2080
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HuD, an RNA binding protein, plays a role in the regulation of gene expression in certain types of cells, including neuronal cells and pancreatic β-cells, via RNA metabolism. Its aberrant expression is associated with the pathogenesis of several human diseases. To explore HuD-mediated gene regulation, stable cells expressing short hairpin RNA against HuD were established using mouse neuroblastoma Neuro2a (N2a) cells, which displayed enhanced phenotypic characteristics of cellular senescence. Two approaches, RNA immunoprecipitation (RNA IP)-NanoString profiling and cytokine array, were used to subsequently identify a subset of putative HuD targets that act as senescence-associated secretory phenotype (SASP), including C-C motif ligand 2 (CCL2), CCL20, C-X-C motif chemokine ligand 2 (CXCL2), and interleukin-6 (IL-6). Here, we further demonstrated that HuD regulates the expression of CCL2, a SASP candidate upregulated in cells following HuD knockdown, by binding to the 3'-untranslated region (UTR) of Ccl2 mRNA. Downregulation of HuD increased the level of CCL2 in N2a cells and the brain tissues of HuD knockout (KO) mice. Exposure to γ-irradiation induced cellular senescence in N2a cells and HuD knockdown facilitated stress-induced cellular senescence. Our results reveal that HuD acts as a novel regulator of CCL2 expression, and its aberrant expression may contribute to cellular senescence by regulating SASP production.

Indexed as

Insulin-Secreting CellsSenescence-Associated Secretory Phenotype3' Untranslated RegionsAnimalsCellular SenescenceELAV-Like Protein 4LigandsMiceMice, KnockoutRNA-Binding Proteins3' Untranslated RegionsElavl4 protein, mouseELAV-Like Protein 4LigandsRNA-Binding Proteins

Identifiers

PMID35411051
PMCPMC9001635
OpenAlexW4223470078

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.