Table 1.
Author/Year | Study Design | Country | Cell Type | Intervention | Outcomes |
---|---|---|---|---|---|
Bossé Y et al. (2007) [31] | In vitro experimental study | Canada | BSMC | Stimulation with 1α,25-dihydroxy-vitamin D3 at dose of 100 nM | Autocrine, contractility, and remodeling processes. |
Song Y et al. (2007) [27] | In vitro experimental study | China | HASMCs | Treatment with 1,25-(OH)2D3 (a vitamin D analog) at dose of 10 nM | Changes in cell proliferation, intracellular calcium levels, and cytokine production in response to treatment with 1,25-(OH)2D3. |
Damera G. (2009) [30] | In vitro experimental study | USA | HASMCs | Treatment with vitamin D (1,25-dihydroxyvitamin D3) at dose of 1 µM | Vitamin D has been found to hinder the growth of human airway smooth muscle cells by promoting the phosphorylation of retinoblastoma protein and checkpoint kinase 1. This effect occurs in response to growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and insulin-like growth factor-1 (IGF-1). |
Song Y et al. (2013) [26] | In vitro experimental study | China | HASMCs | Treatment with 1,25-dihydroxyvitamin D3 at dose of 10−7 m | Expression and phosphorylation of inhibitor IκBα, expression of NF-κB p65 subunit, mRNA stability, and NF-κB DNA binding activity. |
Britt RD Jr et al. (2016) [28] | In vitro experimental study | USA | HASMCs | Treatment with vitamin D at dose of 100 nM | In asthmatic patients, Vitamin D was observed to decrease the inflammation-induced contractility and remodeling of airway smooth muscle (ASM) cells. |
Kim, Sung-Ho et al. (2017) [25] | In vitro experimental study | China | HASMCs | Treatment with vitamin D. Various doses of 1,25(OH)2D3 used varied from 0 to 100 nM | The study used human airway smooth muscle cells (HASMCs) in vitro and evaluated the effect of active vitamin D3 on VEGF-induced ADAM33 expression and proliferation of these cells, which are associated with airway remodeling in asthma. |
Plesa M et al. (2020) [32] | In vitro experimental study | Canada | human asthmatic bronchial fibroblasts | Treatment with 1,25-dihydroxyvitamin D3 with two different doses, 50 nM or 100 nM | 1,25(OH)(2)D(3) was able to reduce the expression of extracellular matrix proteins and inhibit fibroblast proliferation and migration in asthmatic bronchial fibroblasts, potentially highlighting a role for vitamin D in the prevention of airway remodeling in asthma. |
Schrumpf JA. (2020) [29] | In vitro experimental study | USA | human asthmatic bronchial fibroblasts | Treatment with 1,25-dihydroxyvitamin D3 at dose of 100 nM | TGF-β1 impairs the ability of vitamin D to induce and maintain airway epithelial host defense mechanisms. Specifically, TGF-β1 inhibited vitamin D-induced expression of the antimicrobial peptide cathelicidin and reduced vitamin D receptor (VDR) expression. |
Jin A et al. (2021) [24] | In vitro experimental study | China | HBFs | Treatment with calcitriol and dose used at 10 nM | TSLP-induced collagen type-I synthesis through STAT3 and PRMT1. |
Abbreviations: Bronchial smooth muscle cells (BSMC); human airway smooth muscle cells (HASMCs); human asthmatic bronchial fibroblasts (HABFs); human bronchial fibroblasts (HBFs); thymic stromal lymphopoietin (TSLP); vitamin D receptor (VDR); insulin-like growth factor 1 (IGF1); and epidermal growth factor (EGF).