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Human cell-based anti-inflammatory effects of rosiglitazone

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Abstract

Purpose

The C-X-C motif chemokine ligand 10 (CXCL10) participates in diabetes and diabetic cardiomyopathy development from the early stages. Rosiglitazone (RGZ) exhibits anti-inflammatory properties and can target cardiomyocytes secreting CXCL10, under interferon (IFN)γ and tumor necrosis factor (TNF)α challenge. Cardiomyocyte remodeling, CD4 + T cells and dendritic cells (DCs) significantly contribute to the inflammatory milieu underlying and promoting disease development. We aimed to study the effect of RGZ onto inflammation-induced secretion of CXCL10, IFNγ, TNFα, interleukin (IL)-6 and IL-8 by human CD4 + T and DCs, and onto IFNγ/TNFα-dependent signaling in human cardiomyocytes associated with chemokine release.

Methods

Cells maintained within an inflammatory-like microenvironment were exposed to RGZ at near therapy dose (5 µM). ELISA quantified cytokine secretion; qPCR measured mRNA expression; Western blot analyzed protein expression and activation; immunofluorescent analysis detected intracellular IFNγ/TNFα-dependent trafficking.

Results

In human CD4 + T cells and DCs, RGZ inhibited CXCL10 release likely with a transcriptional mechanism, and reduced TNFα only in CD4 + T cells. In human cardiomyocytes, RGZ impaired IFNγ/TNFα signal transduction, blocking the phosphorylation/nuclear translocation of signal transducer and activator of transcription 1 (Stat1) and nuclear factor-kB (NF-kB), in association with a significant decrease in CXCL10 expression, IL-6 and IL-8 release.

Conclusion

As the combination of Th1 biomarkers like CXCL10, IL-8, IL-6 with classical cardiovascular risk factors seems to improve the accuracy in predicting T2D and coronary events, future studies might be desirable to further investigate the anti-Th1 effect of RGZ.

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Data availability

The data are available from the corresponding author upon reasonable request.

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Acknowledgements

Thanks to Prof. Gabriella Barbara Vannelli for providing human fetal tissues. In memory of the beloved “Maestro” Prof. Mario Serio, ten years after his death.

Funding

PRIN 2015, PROGETTI DI RICERCA DI RILEVANTE INTERESSE NAZIONALE-Prot. 2015ZTT5KB (M.L.).

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Author notes

  1. M. Sottili and T. Filardi equally contributed to the work.

Authors and Affiliations

  1. Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Florence, Viale Pieraccini 6, 50139, Florence, Italy

    M. Sottili, G. Cantini & M. Luconi

  2. Department of Experimental Medicine, “Sapienza” University of Rome, Viale Regina Elena 324, 00161, Rome, Italy

    T. Filardi, S. Morano & A. Lenzi

  3. DENOTHE Center of Excellence for Research, Transfer and High Education, University of Florence, 50139, Florence, Italy

    G. Cantini & M. Luconi

  4. Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy

    L. Cosmi

  5. Istituto Nazionale Biostrutture E Biosistemi (INBB), viale delle Medaglie d’Oro 305, 00136, Rome, Italy

    M. Luconi

  6. Department of Movement, Human and Health Sciences, Section of Health Sciences, University of Rome “Foro Italico”, Piazza L. de Bosis 6, 00135, Rome, Italy

    C. Crescioli

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All procedures performed in this study involving human subjects and human fetal tissues were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards; human fetal tissue use was approved by the committee for investigation in humans of the Azienda Ospedaliero-Universitaria Careggi, Florence, Italy (protocol no. 6783–04).

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Sottili, M., Filardi, T., Cantini, G. et al. Human cell-based anti-inflammatory effects of rosiglitazone. J Endocrinol Invest 45, 105–114 (2022). https://doi.org/10.1007/s40618-021-01621-5

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