Evidence map›Paper›PMID 40569521›Full record

ArticleMolecular biology reports2025

T16 modulated extracellular matrix remodeling in fibroblasts via paracrine activation of TGF-β1 through M2 macrophage polarization.

Shuang You, Xiaoming Hao, Chenxi Wang, Hu Li, Quan Wei, Lina Hu, Shuaibin Liu

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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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

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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Shuang YouDepartment of Gynecology and Obstetrics, The second affiliated hospital of Chongqing Medical University, Chongqing, 40010, China.
Xiaoming HaoDepartment of Gynecology and Obstetrics, The second affiliated hospital of Chongqing Medical University, Chongqing, 40010, China.
Chenxi WangFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University, 350117, Fuzhou, China.
Hu LiDepartment of Gynecology and Obstetrics, The second affiliated hospital of Chongqing Medical University, Chongqing, 40010, China.
Quan WeiDepartment of Gynecology and Obstetrics, The second affiliated hospital of Chongqing Medical University, Chongqing, 40010, China.
Lina HuDepartment of Gynecology and Obstetrics, The second affiliated hospital of Chongqing Medical University, Chongqing, 40010, China.
Shuaibin LiuDepartment of Gynecology and Obstetrics, The second affiliated hospital of Chongqing Medical University, Chongqing, 40010, China. 304395@hospital.cqmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundT16 has demonstrated significant potential for regulating extracellular matrix (ECM) remodeling by modulating immune and fibroblast functions. This study investigated how T16 influences fibroblast-mediated extracellular matrix (ECM) remodeling through macrophage polarization.

methodsUterosacral ligaments were collected from 15 patients with pelvic organ prolapse (POP) and 6 patients without pelvic organ prolapse (POP). Fibroblasts isolated from these tissues were cultured and co-cultured with THP-1-derived macrophages in the following experimental groups: control, T16 + fibroblasts, M1 macrophages + fibroblasts, and T16 + M1 macrophages + fibroblasts. Cell proliferation was assessed using the CCK-8 assay, while protein and mRNA expression levels were analyzed by western blotting and qRT-PCR, respectively.

resultsOur findings revealed that T16 promoted macrophage polarization toward the anti-inflammatory M2 phenotype, which, in turn, exerted paracrine effects on fibroblasts. Specifically, M2 macrophages induced by T16 significantly enhance the activation of transforming growth factor beta-1 (TGF-β1), a key regulator of extracellular matrix (ECM) synthesis and remodeling. This paracrine signaling pathway facilitates fibroblast-mediated ECM stabilization, characterized by increased collagen synthesis and extracellular matrix turnover.

conclusionThese results highlight the therapeutic potential of T16 in conditions involving extracellular matrix (ECM) dysfunction, such as pelvic organ prolapse (POP), by targeting the crosstalk between immune cells and fibroblasts. Further research is required to explore its applications in regenerative medicine and tissue engineering.

Indexed as

Extracellular MatrixFibroblastsMacrophagesTransforming Growth Factor beta1Cell ProliferationCells, CulturedCoculture TechniquesFemaleHumansLigamentsMacrophage ActivationMiddle AgedParacrine CommunicationPelvic Organ ProlapseTHP-1 CellsTGFB1 protein, humanTransforming Growth Factor beta1Extracellular matrix (ECM) remodelingFibroblastsImmune modulationM2 macrophagesMacrophage polarizationPelvic organ prolapse (POP)T16TGF-β1Uterosacral ligaments

Identifiers

PMID40569521

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