Evidence map›Paper›PMID 38689229›Full record

ArticleBMC oral health2024

Ropinirole suppresses LPS-induced periodontal inflammation by inhibiting the NAT10 in an ac4C-dependent manner.

Haiqing Liao, Huabing Ma, Hongying Meng, Na Kang, Lufei Wang

Abstract read
In one paragraph

Article in BMC oral health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. 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

5 authors.

Haiqing Liao *Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction & Guangxi Health Commission Key Laboratory of Prevention and Treatment for Oral Infectious Diseases & College and Hospital of Stomatology, Guangxi Medical University, No.10, Shuangyong Road, Nanning, 530021, Guangxi, China.
Huabing Ma *Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction & Guangxi Health Commission Key Laboratory of Prevention and Treatment for Oral Infectious Diseases & College and Hospital of Stomatology, Guangxi Medical University, No.10, Shuangyong Road, Nanning, 530021, Guangxi, China.
Hongying MengGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction & Guangxi Health Commission Key Laboratory of Prevention and Treatment for Oral Infectious Diseases & College and Hospital of Stomatology, Guangxi Medical University, No.10, Shuangyong Road, Nanning, 530021, Guangxi, China.
Na KangGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction & Guangxi Health Commission Key Laboratory of Prevention and Treatment for Oral Infectious Diseases & College and Hospital of Stomatology, Guangxi Medical University, No.10, Shuangyong Road, Nanning, 530021, Guangxi, China. kangna05@163.com.
Lufei WangGuangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction & Guangxi Health Commission Key Laboratory of Prevention and Treatment for Oral Infectious Diseases & College and Hospital of Stomatology, Guangxi Medical University, No.10, Shuangyong Road, Nanning, 530021, Guangxi, China. wlfdentist@outlook.com.

Funding

Guangxi Science and Technology Base and Talent Special Project GuikeAD21220008Joint Project on Regional High-Incidence Diseases Research of Guangxi Natural Science Foundation 2023GXNSFBA026125National Natural Science Foundation of China 82101016National Natural Science Foundation of China 82360191
6 · The paper itself

Abstract

backgroundPeriodontitis is a chronic osteolytic inflammatory disease, where anti-inflammatory intervention is critical for restricting periodontal damage and regenerating alveolar bone. Ropinirole, a dopamine D2 receptor agonist, has previously shown therapeutic potential for periodontitis but the underlying mechanism is still unclear.

methodsHuman gingival fibroblasts (HGFs) treated with LPS were considered to mimic periodontitis in vitro. The dosage of Ropinirole was selected through the cell viability of HGFs evaluation. The protective effects of Ropinirole on HGFs were evaluated by detecting cell viability, cell apoptosis, and pro-inflammatory factor levels. The molecular docking between NAT10 and Ropinirole was performed. The interaction relationship between NAT10 and KLF6 was verified by ac4C Acetylated RNA Immunoprecipitation followed by qPCR (acRIP-qPCR) and dual-luciferase reporter assay.

resultsRopinirole alleviates LPS-induced damage of HGFs by promoting cell viability, inhibiting cell apoptosis and the levels of IL-1β, IL-18, and TNF-α. Overexpression of NAT10 weakens the effects of Ropinirole on protecting HGFs. Meanwhile, NAT10-mediated ac4C RNA acetylation promotes KLF6 mRNA stability. Upregulation of KLF6 reversed the effects of NAT10 inhibition on HGFs.

conclusionsTaken together, Ropinirole protected HGFs through inhibiting the NAT10 ac4C RNA acetylation to decrease the KLF6 mRNA stability from LPS injury. The discovery of this pharmacological and molecular mechanism of Ropinirole further strengthens its therapeutic potential for periodontitis.

Indexed as

FibroblastsIndolesKruppel-Like Factor 6N-Terminal AcetyltransferasesPeriodontitisAcetylationApoptosisCells, CulturedCell SurvivalGingivaHumansLipopolysaccharidesMolecular Docking SimulationIndolesKLF6 protein, humanKruppel-Like Factor 6LipopolysaccharidesNAT10 protein, humanN-Terminal Acetyltransferasesropiniroleac4CHuman gingival fibroblastsKLF6NAT10Periodontitis

Identifiers

PMID38689229
PMCPMC11059654

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.