Evidence map›Paper›PMID 19531482›Full record

ArticleThe Journal of biological chemistry2009

cAMP stringently regulates human cathelicidin antimicrobial peptide expression in the mucosal epithelial cells by activating cAMP-response element-binding protein, AP-1, and inducible cAMP early repressor.

Krishnendu Chakraborty, Palash Chandra Maity, Alok Kumar Sil, Yoshifumi Takeda, Santasabuj Das

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 56 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Krishnendu ChakrabortyDepartment of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33 C.I.T. Road, Scheme XM, Beliaghata, Kolkata 700010.
Palash Chandra MaityDepartment of Microbiology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata 700019.
Alok Kumar SilDepartment of Microbiology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata 700019.
Yoshifumi TakedaCollaborative Research Center of Okayama University for Infectious Diseases, National Institute of Cholera and Enteric Diseases, P-33 C.I.T. Road, Scheme XM, Beliaghata, Kolkata 700010, India.
Santasabuj DasDepartment of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33 C.I.T. Road, Scheme XM, Beliaghata, Kolkata 700010.
National Institute of Cholera and Enteric Diseases · INUniversity of Calcutta · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Little is known about the regulation of the innate host defense peptide cathelicidin at the mucosal surfaces. Expression is believed to be transcriptionally regulated, and several cis-acting elements have been identified in the cathelicidin putative promoter. However, the trans-acting factors have not been clearly defined. We have recently reported that bacterial exotoxins suppress cathelicidin expression in sodium butyrate-differentiated intestinal epithelial cells (ECs), and this may be mediated through inducible cAMP early repressor. Here we have shown that cAMP-signaling pathways transcriptionally regulate cathelicidin expression in various ECs. cAMP-response element-binding protein (CREB) and AP-1 (activator protein-1) bind to the cathelicidin putative promoter in vitro. Additionally, transcriptional complexes containing CREB, AP-1, and cathelicidin upstream regulatory sequences are formed within ECs. We have also shown that these complexes may activate cathelicidin promoter and are required for its inducible expression in ECs. This is underscored by the fact that silencing of CREB and AP-1 results in failure of ECs to up-regulate cathelicidin, and hepatitis B virus X protein may use CREB to induce cathelicidin. On the other hand, inducible cAMP early repressor competes with CREB and AP-1 for binding to the cathelicidin promoter and represses transcription, thus functioning as a counter-regulatory mechanism. Finally, both CREB and AP-1 were shown to play major roles in the regulation of cathelicidin in sodium butyrate-differentiated HT-29 cells. This is the first report of a detailed mechanistic study of inducible cathelicidin expression in the mucosal ECs. At the same time, it describes a novel immunomodulatory function of cAMP.

Indexed as

Gene Expression RegulationAntimicrobial Cationic PeptidesCaco-2 CellsCathelicidinsCell Line, TumorCyclic AMPCyclic AMP Response Element-Binding ProteinCyclic AMP Response Element ModulatorEpithelial CellsHumansModels, GeneticMucous MembranePromoter Regions, GeneticProtein Structure, TertiarySignal TransductionTranscription Factor AP-1Antimicrobial Cationic PeptidesCathelicidinsCREM protein, humanCyclic AMPCyclic AMP Response Element-Binding ProteinCyclic AMP Response Element ModulatorTranscription Factor AP-1

Identifiers

PMID19531482
PMCPMC2755907
OpenAlexW2041396033

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.