Evidence map›Paper›PMID 39690756›Full record

ArticleBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences2024

[Mechanism of melatonin regulating the expression level of rhythm genes to alleviate interstitial pulmonary fibrosis].

Bingle Li, Lingyan Zhu, Yongfu Wang, Li Bai

Abstract readEnglish Abstract
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Article in Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Bingle LiBaotou Medical College, Inner Mongolia University of Science and Technology, Baotou 014010, Inner Mongolia, China.
Lingyan ZhuDepartment of Rheumatology and Immunology, the First Affiliated Hospital of Baotou Medical College, Baotou 014010, Inner Mongolia, China.
Yongfu WangDepartment of Rheumatology and Immunology, the First Affiliated Hospital of Baotou Medical College, Baotou 014010, Inner Mongolia, China.
Li BaiThe Central Lab, the First Affiliated Hospital of Baotou Medical College, Baotou 014010, Inner Mongolia, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the intervention of melatonin (MT) in the expression of circadian genes in patients with pulmonary fibrosis and to analyze the mechanism by which it alleviates the progression of pulmonary fibrosis.

methodsBy utilizing the Gene Expression Omnibus (GEO) database, we identified differentially expressed circadian genes between patients with pulmonary fibrosis and controls. We analyzed the correlation between circadian genes and pulmonary function as well as genes related to pulmonary fibrosis. A bleomycin-induced mouse model of pulmonary fibrosis (BLM group) was constructed to observe the expression differences of PER2 and CRY2 by sequencing and immunohistochemical staining in the BLM group and after MT intervention (BLM+MT group). Hematoxylin and eosin (HE) staining and Masson staining were used to observe the effects of MT on fibrosis. We used Western blot to detect the expression of P-smad2/3 in lung epithelial cells induced by transforming growth factor β (TGF-β). Reverse transcription quantitative real-time PCR technology was employed to investigate the rhythmic expression changes of circadian genes in the control group, TGF-β group, and TGF-β+MT group. Finally, luzindole, a MT receptor antagonist, was used to intervene in TGF-β+MT group, and Western blot was used to explore the receptor dependence of MT in alleviating TGF-β-induced epithelial-mesenchymal transition.

results(1) Analysis of the GEO dataset (GSE) revealed a negative correlation between circadian genes

conclusionMT, by binding to its receptors, can restore the periodic expression of the circadian genes

Indexed as

BleomycinMelatoninPulmonary FibrosisAnimalsCryptochromesDisease Models, AnimalEpithelial CellsHumansLungMiceMice, Inbred C57BLPeriod Circadian ProteinsSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaBleomycinCryptochromesMelatoninPER2 protein, humanPeriod Circadian ProteinsSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaMelatoninPulmonary fibrosisRhythm genes

Identifiers

PMID39690756
PMCPMC11652973

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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.