Evidence map›Paper›PMID 39671362›Full record

ArticlePloS one2024

Colon mucosal proteomics of ankylosing spondylitis versus gut inflammation.

Miao Cheng, Siqi Xiao, Shaer Kayi, Yujie Guan, Yingxin Liu, Jianmei Chen, Hua Chen, Lei Wang, Xiaojin He

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In one paragraph

Article in PloS one, 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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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Miao ChengThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Siqi XiaoThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Shaer KayiThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Yujie GuanSuzhou Hospital of Integrated Traditional Chinese and Western Medicine, Suzhou, China.
Yingxin LiuThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Jianmei ChenThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Hua ChenSchool of Nursing, Nanjing University of Chinese Medicine, Nanjing, China.
Lei WangThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.
Xiaojin HeThe Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.ORCID 0000-0002-2262-416X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAnkylosing spondylitis (AS) patients often present with microscopic signs of gut inflammation. We used proteomic techniques to identify the differentially expressed proteins (DEPs) in the colon tissues of patients with AS and patients with gut inflammation, and then used investigated the influence of NMRAL1 protein on inflammatory cytokines to explore its potential role in the pathogenesis of AS and gut inflammation.

methodsColonic mucosal tissues were collected from four different groups: healthy individuals (group A), patients with gut inflammation only (group B), patients with AS only (group C), and patients with AS combined with gut inflammation (group D). A total of 20 samples were processed for proteomic analysis, wherein proteins were extracted using SDT lysis, followed by separation via sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The proteins were digested using the filter-aided sample preparation (FASP) method and then analyzed using a timsTOF Pro mass spectrometer. The resulting peptide data were used to identify differentially expressed proteins (DEPs) across the different groups. To further explore the inflammation-related function of NMRAL1 protein, the murine monocyte/macrophage cell line RAW264.7 was used. NMRAL1 mRNA expression levels were assessed via RT-qPCR, and inflammatory cytokine levels (TNF-α, IL-1β, IL-17 and IL-23) were measured using ELISA following NMRAL1 siRNA transfection in LPS-treated macrophages.

resultsWe collected colonic mucosa specimens from 20 patients, including groups A,B, C and D with 5 patients in each group. We established a database of DEPs and identified 107 (63 upregulated and 44 downregulated) between group B and group A, 78 (16 upregulated and 62 downregulated) between group D and group C, 45 (8 upregulated and 37 downregulated) between group D and group B, and 57 (33 upregulated and 24 downregulated) between group C and group A. Further analysis revealed that the NmrA-like family domain containing 1 (NMRAL1) protein was identified as a DEP specifically associated with group D. The results of in vitro results showed a significant decrease in NMRAL1 mRNA expression in LPS-treated cells (P<0.001), which was further reduced in NMRAL1 siRNA-transfected cells (P<0.0001), confirming successful transfection. ELISA results revealed that the levels of key inflammatory cytokines (TNF-α, IL-1β, IL-17 and IL-23) were significantly elevated in the LPS-treated model group (P<0.0001, P<0.001), but these levels were significantly decreased after NMRAL1 siRNA transfection (P<0.0001, P<0.01, P<0.05).

conclusionNMRAL1 is identified as a key differentially expressed protein in AS patients with gut inflammation. Knockdown of NMRAL1 significantly reduced the levels of inflammatory cytokines, suggesting its potential role in the pathogenesis of AS and gut inflammation, and as a possible therapeutic target.

Indexed as

ColonCytokinesIntestinal MucosaProteomicsSpondylitis, AnkylosingAdultAnimalsFemaleHumansInflammationMaleMiceMiddle AgedRAW 264.7 CellsCytokines

Identifiers

PMID39671362
PMCPMC11642932

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