1,25-hydroxyvitamin D3 decreases endoplasmic reticulum stress-induced inflammatory response in mammary epithelial cells

Wen, Gaiping; Eder, Klaus; Ringseis, Robert

doi:10.1371/journal.pone.0228945

Cited by 14 publications

(13 citation statements)

References 61 publications

(51 reference statements)

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“…Increasing studies have reported VD-mediated inhibition of ER stress play key roles in various diseases. VD3 treatment decreased ER stress-induced inflammatory response in mammary epithelial cells (Wen et al, 2020). Moreover, VD treatment promoted proliferation, inhibited apoptosis, reduced the levels of endogenous markers of ER stress in human umbilical vein endothelial cells, and improved the impaired wound healing in diabetic mice by suppressing ER stress (Yuan et al, 2018).…”

Section: Discussionmentioning

confidence: 93%

Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice

Shen

Liu

et al. 2022

Food Sci. Technol

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Vitamin D (VD) was reported to play protective roles in skeletal muscle. This study aimed to explore whether endoplasmic reticulum (ER) stress inhibition is associated with the protective effects of VD/VD receptor (VDR) signaling on skeletal muscle functions. C2C12 skeletal muscle cells were treated with palmitic acid (PA) and then incubated with different concentrations of 1,25-(OH)2-vitamin D3 (VD3), and we found that VD3 improved the impaired cell viability induced by PA and increased VDR expression in a dose-dependent manner. Then 100 nM VD3 treatment and VDR overexpression both ameliorated PA-induced ER stress, apoptosis, inflammation and glucose uptake inhibition in C2C12 myocytes. Furthermore, VDR knockdown reversed the protective effects of VD3 on C2C12 cell functions. Additionally, PA-treated C2C12 cells were treated with VD3 alone or together with AMPK signaling inhibitor Compound C. VD3 promoted phosphorylation of AMPK and SIRT1 expression, while Compound C reversed these effects and abolished the protective effects of VD3 in C2C12 cells. High-fat diet (HFD)-fed mice were treated with VD3, and VD3 alleviated skeletal muscle loss and insulin resistance in mice. In conclusion, VD inhibited AMPK/SIRT1-mediated ER stress by increasing VDR expression, and further ameliorated skeletal muscle loss and insulin resistance in mice.

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Section: Discussionmentioning

confidence: 93%

Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice

Shen

Liu

et al. 2022

Food Sci. Technol

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“…Although fibroblasts are the major contributors to airway remodeling in asthma and COPD, other cell types within the lung, including smooth muscle cells are also involved. On the other hand, vitamin D3 through its active metabolite 1,25D3, is known to possess anti-inflammatory and anti-fibrotic mechanisms (26)(27)(28), and have shown to improve immune responses (29,30). Therefore, we investigated the role of 1,25D3 in polyI:C-induced pro-inflammatory and pro-fibrotic responses in primary BSMCs isolated from subjects with asthma and COPD.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D3 Attenuates Viral-Induced Inflammation and Fibrotic Responses in Bronchial Smooth Muscle Cells

et al. 2021

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Toll-like receptor 3 (TLR3) activation by viral infections plays a key role in promoting inflammatory immune responses that contribute to pulmonary fibrosis in chronic inflammatory respiratory diseases. Vitamin D3 has been shown to be beneficial to patients with asthma and chronic obstructive pulmonary disease (COPD) through its anti-inflammatory and anti-fibrotic properties. Smooth muscle cells are one of the major contributors to airway remodeling in asthma and COPD. We therefore aimed to investigate the effect of vitamin D3 treatment on viral-induced TLR3 responses in Bronchial Smooth Muscle Cells (BSMCs) as a mechanism contributing to pulmonary fibrosis in asthma and COPD. Primary BSMCs from patients with asthma (n=4), COPD (n=4), and healthy control subjects (n=6) were treated with polyinosinic: polycytidylic acid (polyI:C), TLR3 agonist in the presence or absence of vitamin D3 (1,25D3). Here we report the mRNA expression and protein levels of pro-inflammatory and pro-fibrotic markers (IL-6, IFN-β1, CCL2/MCP-1, fibronectin 1 and type I collagen) among BSMCs groups: asthma, COPD, and healthy controls. We show that at the baseline, prior to polyI:C stimulation, asthma and COPD BSMCs presented increased pro-inflammatory and pro-fibrotic state compared to healthy control subjects, as measured by quantitative PCR and immunoassays (ELISA/Flow Cytometry. Ligation of TLR3 by polyI:C in BSMCs was associated with increased TLR3 mRNA expression, and 1,25D3 treatment significantly reduced its expression. In addition, 1,25D3 decreased the expression of IL-6, IFN-β1, CCL2, FN1 and COL1A1 induced by polyI:C in BSMCs. The regulatory effect of 1,25D3 treatment on polyI:C-stimulated BSMCs was further confirmed at protein levels. Our findings suggest that vitamin D3 attenuates TLR3 agonist-induced inflammatory and fibrotic responses in BSMCs and support the clinical relevance of vitamin D3 supplementation in patients with viral infections having chronic respiratory diseases, such as asthma and COPD.

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“…After reaching confluence, cells were treated with either 10 µM RSV, 0.1 µg/mL TM or 10 µM RSV combined with 0.1 µg/mL TM or 0.1% DMSO as vehicle control in 6H medium for 6 or 48 h. Following treatment, total RNA was extracted from cells using Trizol reagent (Invitrogen, Karlsruhe, Germany) according to the manufacturer’s protocol. The synthesis of cDNA and qPCR analysis were performed as described recently in detail [ 52 , 53 , 54 ]. Characteristics of gene-specific primers synthesized by Eurofins MWG Operon (Ebersberg, Germany) are listed in Table 1 .…”

Section: Methodsmentioning

confidence: 99%

Resveratrol Alleviates the Inhibitory Effect of Tunicamycin-Induced Endoplasmic Reticulum Stress on Expression of Genes Involved in Thyroid Hormone Synthesis in FRTL-5 Thyrocytes

Wen

Eder

Ringseis

2021

IJMS

Self Cite

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Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. The present study tested the hypothesis that resveratrol (RSV) alleviates this effect of TM in FRTL-5 cells. While treatment of FRTL-5 cells with TM alone (0.1 µg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 µg/mL) and RSV (10 µM) for 48 h attenuated this effect of TM. In conclusion, RSV alleviates TM-induced ER stress and attenuates the strong impairment of expression of genes involved in thyroid hormone synthesis and their regulators in FRTL-5 thyrocytes exposed to TM-induced ER stress. Thus, RSV may be useful for the treatment of specific thyroid disorders, provided that strategies with improved oral bioavailability of RSV are applied.

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1,25-hydroxyvitamin D3 decreases endoplasmic reticulum stress-induced inflammatory response in mammary epithelial cells

Cited by 14 publications

References 61 publications

Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice

Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice

Vitamin D3 Attenuates Viral-Induced Inflammation and Fibrotic Responses in Bronchial Smooth Muscle Cells

Resveratrol Alleviates the Inhibitory Effect of Tunicamycin-Induced Endoplasmic Reticulum Stress on Expression of Genes Involved in Thyroid Hormone Synthesis in FRTL-5 Thyrocytes

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