Evidence map›Paper›PMID 20007975›Full record

ArticleThe Journal of biological chemistry2010

Protein kinase C zeta mediates cigarette smoke/aldehyde- and lipopolysaccharide-induced lung inflammation and histone modifications.

Hongwei Yao, Jae-woong Hwang, Jorge Moscat, Maria T Diaz-Meco, Michael Leitges, Nandini Kishore, Xiong Li, Irfan Rahman

Open access · hybridAbstract 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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Protein Kinase Cζ Inhibitor Promotes Resolution of Bleomycin-Induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2016
    Article
  12. Article
  13. Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: implications for chronic obstructive pulmonary disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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  20. 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 3 institutions in 1 country.

Hongwei YaoDepartment of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, New York 14642, USA.
Jae-woong Hwang
Jorge Moscat
Maria T Diaz-Meco
Michael Leitges
Nandini Kishore
Xiong Li
Irfan Rahman
University of Cincinnati Medical Center · USUniversity of Rochester Medical Center · USPfizer (United States) · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI B Paige Lawrence · 1985 to 2026
$42.8M
MECHANISMS OF CIGARETTE SMOKE-INDUCED LUNG CELLULAR SENESCENCER01HL085613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2007 to 2017
$4.0M
CIRCADIAN-COUPLED CELLULAR AND LUNG FUNCTION IN COPDR01HL097751 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2009 to 2012
$1.9M
NHLBI NIH HHS R01 HL085613NHLBI NIH HHS R01-HL085613NHLBI NIH HHS R01 HL097751NHLBI NIH HHS R01-HL097751NIEHS NIH HHS P30 ES001247NIEHS NIH HHS P30-ES01247
6 · The paper itself

Abstract

Atypical protein kinase C (PKC) zeta is an important regulator of inflammation through activation of the nuclear factor-kappaB (NF-kappaB) pathway. Chromatin remodeling on pro-inflammatory genes plays a pivotal role in cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced abnormal lung inflammation. However, the signaling mechanism whereby chromatin remodeling occurs in CS- and LPS-induced lung inflammation is not known. We hypothesized that PKCzeta is an important regulator of chromatin remodeling, and down-regulation of PKCzeta ameliorates lung inflammation by CS and LPS exposures. We determined the role and molecular mechanism of PKCzeta in abnormal lung inflammatory response to CS and LPS exposures in PKCzeta-deficient (PKCzeta(-/-)) and wild-type mice. Lung inflammatory response was decreased in PKCzeta(-/-) mice compared with WT mice exposed to CS and LPS. Moreover, inhibition of PKCzeta by a specific pharmacological PKCzeta inhibitor attenuated CS extract-, reactive aldehydes (present in CS)-, and LPS-mediated pro-inflammatory mediator release from macrophages. The mechanism underlying these findings is associated with decreased RelA/p65 phosphorylation (Ser(311)) and translocation of the RelA/p65 subunit of NF-kappaB into the nucleus. Furthermore, CS/reactive aldehydes and LPS exposures led to activation and translocation of PKCzeta into the nucleus where it forms a complex with CREB-binding protein (CBP) and acetylated RelA/p65 causing histone phosphorylation and acetylation on promoters of pro-inflammatory genes. Taken together, these data suggest that PKCzeta plays an important role in CS/aldehyde- and LPS-induced lung inflammation through acetylation of RelA/p65 and histone modifications via CBP. These data provide new insights into the molecular mechanisms underlying the pathogenesis of chronic inflammatory lung diseases.

Indexed as

AcetylationActive Transport, Cell NucleusAldehydesAnimalsCell NucleusChromatin Assembly and DisassemblyEnzyme InhibitorsHistonesHumansInflammation MediatorsLipopolysaccharidesMacrophages, AlveolarMiceMice, KnockoutPhosphorylationPneumoniaAldehydesEnzyme InhibitorsHistonesInflammation MediatorsLipopolysaccharidesProtein Kinase CProtein Kinase C zetaRela protein, mouseTranscription Factor RelA

Identifiers

PMID20007975
PMCPMC2820769
OpenAlexW2072077225

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.