Promoting ER stress in a plasmacytoid dendritic cell line drives fibroblast activation DOI Creative Commons
Beatriz H. Ferreira, Inês S. Silva, Andreia Mendes

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 7, 2025

Abstract Background Fibrosis remains a major complication in several chronic diseases, including systemic sclerosis (SSc). Plasmacytoid dendritic cells (pDCs) are innate immune that play key role the development of fibrosis SSc patients, through still poorly defined mechanisms. Interestingly, endoplasmic reticulum (ER) stress signaling pathways dysregulated pDCs from patients with SSc, but their contribution to unclear. Thus, this study aimed unravel mechanisms behind involvement and ER fibrosis. Methods To address question, we established an vitro model designed interactions between fibroblasts. More specifically, IMR-90 fibroblasts were co-cultured CAL-1, pDC cell line. was then induced by bacterial toxin SubAB. Extracellular matrix (ECM) production assessed using immunoblotting, qPCR confocal microscopy. The importance cell-to-cell contact investigated conditioned media (CM) transwell assays. Results Direct CAL-1 under conditions led increased expression fibronectin alpha-smooth muscle actin (α-SMA). This effect required sensor protein kinase R-like (PERK) observed only upon direct both types. Conclusions Overall, our data suggest induction promotes fibroblast activation, which may contribute SSc.

Language: Английский

Promoting ER stress in a plasmacytoid dendritic cell line drives fibroblast activation DOI Creative Commons
Beatriz H. Ferreira, Inês S. Silva, Andreia Mendes

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 7, 2025

Abstract Background Fibrosis remains a major complication in several chronic diseases, including systemic sclerosis (SSc). Plasmacytoid dendritic cells (pDCs) are innate immune that play key role the development of fibrosis SSc patients, through still poorly defined mechanisms. Interestingly, endoplasmic reticulum (ER) stress signaling pathways dysregulated pDCs from patients with SSc, but their contribution to unclear. Thus, this study aimed unravel mechanisms behind involvement and ER fibrosis. Methods To address question, we established an vitro model designed interactions between fibroblasts. More specifically, IMR-90 fibroblasts were co-cultured CAL-1, pDC cell line. was then induced by bacterial toxin SubAB. Extracellular matrix (ECM) production assessed using immunoblotting, qPCR confocal microscopy. The importance cell-to-cell contact investigated conditioned media (CM) transwell assays. Results Direct CAL-1 under conditions led increased expression fibronectin alpha-smooth muscle actin (α-SMA). This effect required sensor protein kinase R-like (PERK) observed only upon direct both types. Conclusions Overall, our data suggest induction promotes fibroblast activation, which may contribute SSc.

Language: Английский

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