Evaluation of periostin and factors associated with new bone formation in ankylosing spondylitis: Periostin may be associated with the Wnt pathway

Solmaz, Dilek; Uslu, Sadettin; Kozacı, Didem; Karaca, Neslihan Edeer; Bülbül, Hale; Tarhan, Emine Figen; Özmen, Mustafa; Can, Gerçek; Akar, Servet

doi:10.1111/1756-185x.13186

Cited by 16 publications

(16 citation statements)

References 32 publications

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“…As an upstream regulator of GSK3β, canonical Wnt/β-catenin signaling plays a role in osteogenic differentiation (Kikuchi et al, 2007;Maupin et al, 2013). Similarity, in human ankylosing spondylitis, a chronic inflammatory disease, Periostin is downregulated and associated with the Wnt pathway (Solmaz et al, 2018). In CTLA4-modified MSCs, Periostin promoted osteogenic differentiation via the Wnt signaling pathway.…”

Section: Discussionmentioning

confidence: 93%

Periostin regulates osteogenesis of mesenchymal stem cells from ovariectomized rats through actions on the ILK/Akt/GSK-3β Axis

et al. 2021

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Osteoporosis is a condition of the skeleton that mainly results from estrogen deficiency. Periostin is a matricellular component in bone that is involved in osteoblast differentiation. However, how Periostin promotes osteogenesis remains largely unknown. Here, we isolated bone marrow skeletal stem cells (BMSCs) derived from an ovariectomy (OVX)-induced osteoporosis rat model and the effects of periostin on BMSCs derived from OVX rats (OVX-BMSCs) were assessed. Overexpression of periostin enhanced alkaline phosphatase (ALP) and alizarin red staining in OVX-BMSCs as well as the osteogenic genes OCN, BSP and Runx2. ILK is a downstream effector of signals from the extracellular matrix and participates in bone homeostasis. Overexpression of periostin also increased expression of protein levels for ILK, as well as the downstream targets pAkt and pGSK3β. Suppression of ILK or Akt partially suppressed the enhancement of osteogenic ability induced by periostin overexpression in OVX-BMSCs. Thus, periostin may promote the osteogenic ability of OVX-BMSCs through actions on the ILK/Akt/GSK3β axis.

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Section: Discussionmentioning

confidence: 93%

Periostin regulates osteogenesis of mesenchymal stem cells from ovariectomized rats through actions on the ILK/Akt/GSK-3β Axis

et al. 2021

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“…26 SOST exhibits a prominently lower serum level in patients with AS in contrast to heavy subjects, which is in consistency with our results. 16,27 The above findings were largely consistent with our results. Dual luciferase reporter assay and immunohistochemical staining procedures confirmed that miR-96 targeted SOST and negatively regulated its expression.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐96 promotes osteoblast differentiation and bone formation in ankylosing spondylitis mice through activating the Wnt signaling pathway by binding to SOST

Wang

et al. 2019

J of Cellular Biochemistry

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Ankylosing spondylitis (AS) refers to a type of arthritis manifested with chronic inflammation of spine joints. microRNAs (MiRNAs) have been identified as new therapeutic targets for inflammatory diseases. In this study, we evaluated the influence of microRNA‐96 (miR‐96) on osteoblast differentiation together with bone formation in a murine model of AS. The speculated relationship that miR‐96 could bind to sclerostin (SOST) was verified by dual luciferase reporter assay. After successful model establishment, the mice with AS and osteoblasts isolated from mice with AS were treated with mimics or inhibitors of miR‐96, or DKK‐1 (a Wnt signaling inhibitor). The effects of gain‐ or loss‐of‐function of miR‐96 on the inflammatory cytokine release (IL‐6, IL‐10, and TNF‐α), alkaline phosphatase (ALP) activity, calcium nodule formation, along with the viability of osteoblasts were determined. It was observed that miR‐96 might target and regulate SOST. Besides, miR‐96 was expressed at a high level in AS mice while SOST expressed at a low level. TOP/FOP‐Flash luciferase reporter assay confirmed that miR‐96 activated the Wnt signaling pathway. Moreover, AS mice overexpressing miR‐96 exhibited increased contents of IL‐6, IL‐10 and TNF‐α, ALP activity, calcium nodule numbers, and viability of osteoblasts. In contrast, inhibition of miR‐96 resulted in suppression of the osteoblast differentiation and bone formation. In conclusion, the study implicates that overexpressing miR‐96 could improve osteoblast differentiation and bone formation in AS mice via Wnt signaling pathway activation, highlighting a potential new target for AS treatment.

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“…Among 241 eligible studies meeting the inclusion criteria, 76 articles were excluded due to unextractable data, insufficient data on HCs, irrelevant VEGF sample type (urine/synovial fluid/tear fluid), or inappropriate disease control groups. Finally, 165 studies were included in the meta-analysis, with 28,29,40,13,8,12,16,23, and six studies on SLE (20,21,, RA (12, 22-24, 38, 43, 52-74), SSc (11,38,39,64,, BD (111)(112)(113)(114)(115)(116)(117)(118)(119)(120)(121)(122)(123), KD (18,(124)(125)(126)(127)(128)(129)(130), AS (55,73,(131)(132)(133)(134)(135)(136)(137)(138)(139)(140)…”

Section: Search Results and Population Characteristicsmentioning

confidence: 99%

Association of Circulating Vascular Endothelial Growth Factor Levels With Autoimmune Diseases: A Systematic Review and Meta-Analysis

Zhan

Liu

et al. 2021

Front. Immunol.

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BackgroundAutoimmune diseases (ADs) are characterized by immune-mediated tissue damage, in which angiogenesis is a prominent pathogenic mechanism. Vascular endothelial growth factor (VEGF), an angiogenesis modulator, is significantly elevated in several ADs including rheumatoid arthritis (RA), systemic sclerosis (SSc), and systemic lupus erythematosus (SLE). We determined whether circulating VEGF levels were associated with ADs based on pooled evidence.MethodsThe analyses included 165 studies from the PubMed, EMBASE, Cochrane Library, and Web of Science databases and fulfilled the study criteria. Comparisons of circulating VEGF levels between patients with ADs and healthy controls were performed by determining pooled standard mean differences (SMDs) with 95% confidence intervals (CIs) in a random-effect model using STATA 16.0. Subgroup, sensitivity, and meta-regression analyses were performed to determine heterogeneity and to test robustness.ResultsCompared with healthy subjects, circulating VEGF levels were significantly higher in patients with SLE (SMD 0.84, 95% CI 0.25–1.44, P = 0.0056), RA (SMD 1.48, 95% CI 0.82–2.15, P <0.0001), SSc (SMD 0.56, 95% CI 0.36–0.75, P <0.0001), Behcet’s disease (SMD 1.65, 95% CI 0.88–2.41, P <0.0001), Kawasaki disease (SMD 2.41, 95% CI 0.10–4.72, P = 0.0406), ankylosing spondylitis (SMD 0.78, 95% CI 0.23–1.33, P = 0.0052), inflammatory bowel disease (SMD 0.57, 95% CI 0.43–0.71, P <0.0001), psoriasis (SMD 0.98, 95% CI 0.62–1.34, P <0.0001), and Graves’ disease (SMD 0.69, 95% CI 0.20–1.19, P = 0.0056). Circulating VEGF levels correlated with disease activity and hematological parameters in ADs.ConclusionCirculating VEGF levels were associated with ADs and could predict disease manifestations, severity and activity in patients with ADs.Systematic Review RegistrationPROSPERO, identifier CRD42021227843.

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Evaluation of periostin and factors associated with new bone formation in ankylosing spondylitis: Periostin may be associated with the Wnt pathway

Abstract: Our results suggest that periostin is down-regulated in AS patients with highly active disease and may contribute to disease pathogenesis through an interaction with Wnt signaling.

Cited by 16 publications

References 32 publications

Periostin regulates osteogenesis of mesenchymal stem cells from ovariectomized rats through actions on the ILK/Akt/GSK-3β Axis

Periostin regulates osteogenesis of mesenchymal stem cells from ovariectomized rats through actions on the ILK/Akt/GSK-3β Axis

microRNA‐96 promotes osteoblast differentiation and bone formation in ankylosing spondylitis mice through activating the Wnt signaling pathway by binding to SOST

Association of Circulating Vascular Endothelial Growth Factor Levels With Autoimmune Diseases: A Systematic Review and Meta-Analysis

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