1, 25-Dihydroxyvitamin D3 activates Apelin/APJ system and inhibits the production of adhesion molecules and inflammatory mediators in LPS-activated RAW264.7 cells

Faridvand, Yousef; Bagherpour-Hassanlouei, Nazanin; Nozari, Samira; Nasiri, Nasrin; Rajabi, Hadi; Ghaffari, Samad; Nouri, Mohammad

doi:10.1016/j.pharep.2019.04.012

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…The expression of APLN and its receptor APJ comprises a system that acts as a critical regulator of various physiological functions, such as glycometabolism, liver disease, and macrophage activation [48][49][50]. A limitation of our study is that we did not examine APJ expression in synovial tissues.…”

Section: Discussionmentioning

confidence: 98%

Apelin Affects the Progression of Osteoarthritis by Regulating VEGF-Dependent Angiogenesis and miR-150-5p Expression in Human Synovial Fibroblasts

Wang

Kuo

Liu

et al. 2020

Cells

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Synovium-induced angiogenesis is central to osteoarthritis (OA) pathogenesis and thus a promising therapeutic target. The adipokine apelin (APLN) is involved in both OA pathogenesis and angiogenesis. We examined the role of APLN in synovium-induced angiogenesis by investigating the crosstalk between APLN and vascular endothelial growth factor (VEGF) expression in human OA synovial fibroblasts (OASFs). We found higher levels of APLN and VEGF expression in OA samples compared with normal samples. APLN-induced stimulation of VEGF expression and VEGF-dependent angiogenesis in OASFs was mitigated by FAK/Src/Akt signaling. APLN also inhibited levels of microRNA-150-5p (miR-150-5p), which represses VEGF production and angiogenesis. Analyses of an OA animal model showed that shAPLN transfection of OASFs rescued pathologic changes in OA cartilage and histology. Here, we found APLN enhances VEGF expression and angiogenesis via FAK/Src/Akt cascade and via downstream suppression of miR-150-5p expression. These findings help to clarify the pathogenesis of adipokine-induced angiogenesis in OA synovium.

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Section: Discussionmentioning

confidence: 98%

Apelin Affects the Progression of Osteoarthritis by Regulating VEGF-Dependent Angiogenesis and miR-150-5p Expression in Human Synovial Fibroblasts

Wang

Kuo

Liu

et al. 2020

Cells

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“…The APJ receptor is a major receptor of APLN. The APLN/APJ system is a critical regulator of various physiological functions, such as glycometabolism, liver disease and macrophage activation [27][28][29]. This study did not examine APJ expression in synovial tissues.…”

Section: Discussionmentioning

confidence: 98%

Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

Chang

Wang

Kuo

et al. 2020

Aging

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“…In this study, 0.1 μM and 0.01 μM of vitamin D increased cell viability compared with LPS-treated cells. Faridvand et al in found that the optimal doses of vitamin D ranged from 0.05 μM to 0.1 μM [ 19 ]. Moreover, Bischoff-Ferarri et al determined that the optimal concentrations of vitamin D3 ranged from 0.07 μM to 0.01 μM in serum [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Inhibits Lipopolysaccharide (LPS)-Induced Inflammation in A549 Cells by Downregulating Inflammatory Cytokines

Gatera

Lesmana

Musfiroh

et al. 2021

Med Sci Monit Basic Res

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Background Studies have shown that lung inflammation affects lung function, with life-threatening results. Vitamin D may play an important role in inhibiting inflammatory cytokines. Vitamin D deficiency is related to several lung problems, including respiratory distress syndrome, alveolar inflammation, epithelial damage, and hypoxia. Few studies have evaluated the benefits of vitamin D in preventing inflammation in alveolar cells. Material/Methods We developed a cell inflammation model induced by lipopolysaccharide (LPS) treatment. The effects of vitamin D on LPS-induced inflammation in A549 cells were examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the anti-inflammatory mechanism of vitamin D was evaluated using western blot analysis. Results Our results indicated that vitamin D promoted A549 cell survival following LPS-induced inflammation by downregulating nuclear factor nuclear factor kappa light chain enhancer of activated B cells, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-12. Conclusions Our results indicated that vitamin D has the potential to manage lung inflammation, although further studies are needed.

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1, 25-Dihydroxyvitamin D3 activates Apelin/APJ system and inhibits the production of adhesion molecules and inflammatory mediators in LPS-activated RAW264.7 cells

Cited by 18 publications

References 30 publications

Apelin Affects the Progression of Osteoarthritis by Regulating VEGF-Dependent Angiogenesis and miR-150-5p Expression in Human Synovial Fibroblasts

Apelin Affects the Progression of Osteoarthritis by Regulating VEGF-Dependent Angiogenesis and miR-150-5p Expression in Human Synovial Fibroblasts

Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

Vitamin D Inhibits Lipopolysaccharide (LPS)-Induced Inflammation in A549 Cells by Downregulating Inflammatory Cytokines

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