Evidence map›Paper›PMID 20685657›Full record

ArticleThe Journal of biological chemistry2010

Interferon-gamma-mediated inhibition of serum response factor-dependent smooth muscle-specific gene expression.

Zengdun Shi, Don C Rockey

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–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

17 citing papers in PubMed.

  1. Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Fibroblast-specific Stat1 deletion enhances the myofibroblast phenotype during tissue repair.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2020
    Article
  6. Article
  7. Article
  8. Upregulation of the actin cytoskeleton via myocardin leads to increased expression of type 1 collagen.Laboratory investigation; a journal of technical methods and pathology · 2017
    Article
  9. The Molecular Basis of Portal Hypertension.Transactions of the American Clinical and Climatological Association · 2017
    Review
  10. Article
  11. Article
  12. The mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis in mice.International journal of physiology, pathophysiology and pharmacology · 2016
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Preproendothelin-1 expression is negatively regulated by IFNγ during hepatic stellate cell activation.American journal of physiology. Gastrointestinal and liver physiology · 2012
    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

2 authors.

Zengdun ShiDepartment of Internal Medicine, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390, USA.
Don C Rockey

Funding

PATHOGENESIS OF HEPATIC FIBROSIS AND PORTAL HYPERTENSIONR01DK050574 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ROCKEY, DON C. · 1996 to 2010
$3.0M
Regulation of Stellate Cell ContractilityR01DK063308 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ROCKEY, DON C. · 2004 to 2008
$1.7M
NIDDK NIH HHS R01 DK050574NIDDK NIH HHS R01 DK063308NIDDK NIH HHS R01 DK 50574NIDDK NIH HHS R01 DK 60338
6 · The paper itself

Abstract

IFNγ exerts multiple biological effects on effector cells by regulating many downstream genes, including smooth muscle-specific genes. However, the molecular mechanisms underlying IFNγ-induced inhibition of smooth muscle-specific gene expression remain unclear. In this study, we have shown that serum response factor (SRF), a common transcriptional factor important in cell proliferation, migration, and differentiation, is targeted by IFNγ in a STAT1-dependent manner. We show that the molecular mechanism by which IFNγ regulates SRF is via activation of the 2-5A-RNase L system, which triggers SRF mRNA decay and reduced SRF expression. As a result, decreased SRF expression reduces expression of SRF target genes such as smooth muscle α-actin and smooth muscle myosin heavy chain. Additionally, IFNγ reduced p300 and acetylated histone-3 binding in both smooth muscle α-actin and SRF promoters, epigenetically decreasing smooth muscle α-actin and SRF transcriptional activation. Our data reveal that SRF is a novel IFNγ-regulated gene and further elucidate the molecular pathway between IFNγ, IFNγ-regulated genes, and SRF and its target genes.

Indexed as

Gene Expression RegulationActinsAnimalsCells, CulturedEndoribonucleasesHepatic Stellate CellsHumansInterferon-gammaMiceMice, Inbred BALB CMice, KnockoutMuscle, SmoothPromoter Regions, GeneticRatsRats, Sprague-DawleyRNA, Messenger2-5A-dependent ribonucleaseActinsEndoribonucleasesInterferon-gammaRNA, MessengerSerum Response FactorSTAT1 Transcription Factor

Identifiers

PMID20685657
PMCPMC2952243

What OpenQuestion holds

Textmetadata
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.