Evidence map›Paper›PMID 18682699›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2008

Targeting mRNA stability arrests inflammatory bone loss.

Chetan S Patil, Min Liu, Wenpu Zhao, Derek D Coatney, Fei Li, Elizabeth A VanTubergen, Nisha J D'Silva, Keith L Kirkwood

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.8field-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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Tristetraprolin regulates the skeletal phenotype and osteoclastogenic potential through monocytic myeloid-derived suppressor cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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  10. Enhanced stability of tristetraprolin mRNA protects mice against immune-mediated inflammatory pathologies.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Cell- and Gene- Based Therapeutics for Periodontal Regeneration.International journal of preventive medicine · 2015
    Review
  12. Post-transcriptional control of cytokine gene expression in health and disease.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Article
  13. Article
  14. 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

8 authors at 2 institutions in 1 country.

Chetan S PatilDepartment of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Min Liu
Wenpu Zhao
Derek D Coatney
Fei Li
Elizabeth A VanTubergen
Nisha J D'Silva
Keith L Kirkwood
University of Michigan–Ann Arbor · USUniversity at Buffalo, State University of New York · US

Funding

Negative Regulation of Innate Immune Responses through MAPK PhosphatasesR01DE018290 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIRKWOOD, KEITH L · 2007 to 2011
$1.8M
Altering Cytokine mRNA Stability in Periodontal Bone LossR21DE017966 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIRKWOOD, KEITH L · 2007 to 2008
$393k
NIDCR NIH HHS DE017966NIDCR NIH HHS DE018290NIDCR NIH HHS R01 DE018290NIDCR NIH HHS R21 DE017966
6 · The paper itself

Abstract

Many proinflammatory cytokines contain adenylate-uridylate-rich elements (AREs) within the 3'-untranslated region (UTR) that confer rapid mRNA destabilization. During the inflammatory response, cytokine mRNA are stabilized via complex interactions with RNA-binding proteins controlled by phosphorylation via multiple signaling pathways including the mitogen-activated protein kinases (MAPKs). In the absence of inflammation, a key cytokine-regulating RNA-binding protein, tristetraprolin (TTP), shuttles mRNA transcripts to degradation machinery in order to maintain low levels of inflammatory cytokines. Using this general model of mRNA decay, over expression of TTP was evaluated in an experimental model of inflammatory bone loss to determine whether altering cytokine mRNA stability has an impact in pathological bone resorption. Using adenoviral-delivered TTP, significant reductions of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and prostaglandin (PG)E(2) were observed in vitro through a mechanism consistent with targeting mRNA stability. In vivo analysis indicates a significant protective effect from inflammation-induced bone loss and inflammatory infiltrate in animals overexpressing TTP compared with reporter controls. These findings provide experimental evidence that mRNA stability is a valid therapeutic target in inflammatory bone loss.

Indexed as

AdenoviridaeAnimalsBone Diseases, MetabolicCell LineDinoprostoneGenetic TherapyHeLa CellsHumansInflammationInterleukin-6MiceRatsRNA StabilityTristetraprolinTumor Necrosis Factor-alphaDinoprostoneInterleukin-6TristetraprolinTumor Necrosis Factor-alpha

Identifiers

PMID18682699
PMCPMC2752748
OpenAlexW2091795818

What OpenQuestion holds

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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.