Roles of Non-Canonical Wnt Signalling Pathways in Bone Biology

Lojk, Jasna; Marc, Janja

doi:10.3390/ijms221910840

Cited by 50 publications

(32 citation statements)

References 213 publications

(237 reference statements)

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“…In addition, BMP2 interacts with the Wnt/β-catenin pathway results in promoting the osteogenic differentiation and maintenance of osteoblast progenitors and bone homeostasis [ 51 ]. Several factors related to Wnt signaling such as Wnt3a, 4, 5a, 7b, 10b, and 16 in collaboration with the mTOR/JNK/c-Jun axis can promote the expression of osteogenesis-related genes [ 52 ]. Considering the existence of crosstalk between TGF-β family with other signaling cascades, it was also mentioned that the incorporation of MNPs into scaffolds can induce the mitogen-activated protein kinase (MAPK) pathway-related effectors such as MEK1, 4, c-JUN and, JunD factors.…”

Section: Resultsmentioning

confidence: 99%

PCL/Col I-based magnetic nanocomposite scaffold provides an osteoinductive environment for ADSCs in osteogenic cues-free media conditions

et al. 2022

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Background The bone tissue engineering (BTE) approach has been introduced as an alternative to conventional treatments for large non-healing bone defects. Magnetism promotes stem cells' adherence to biocompatible scaffolds toward osteoblast differentiation. Furthermore, osteogenic differentiation media are expensive and any changes in its composition affect stem cells differentiation. Moreover, media growth factors possess a short half-life resulting in the rapid loss of their functions in vivo. With the above in mind, we fabricated a multilayered nanocomposite scaffold containing the wild type of Type I collagen (Col I) with endogenous magnetic property to promote osteogenesis in rat ADSCs with the minimum requirement of osteogenic differentiation medium. Methods Fe3O4 NPs were synthesized by co-precipitation method and characterized using SEM, VSM, and FTIR. Then, a PCL/Col I nanocomposite scaffold entrapping Fe3O4 NPs was fabricated by electrospinning and characterized using SEM, TEM, AFM, VSM, Contact Angle, tensile stretching, and FTIR. ADSCs were isolated from rat adipose tissue and identified by flow cytometry. ADSCs were loaded onto PCL/Col I and PCL/Col I/Fe3O4-scaffolds for 1–3 weeks with/without osteogenic media conditions. The cell viability, cell adhesion, and osteogenic differentiation were evaluated using MTT assay, SEM, DAPI staining, ALP/ARS staining, RT-PCR, and western blotting, respectively. Results SEM, VSM, and FTIR results indicated that Fe3O4 was synthesized in nano-sized (15–30 nm) particles with spherical-shaped morphology and superparamagnetic properties with approved chemical structure as FTIR revealed. According to SEM images, the fabricated magnetic scaffolds consisted of nanofiber (500–700 nm). TEM images have shown the Fe3O4 NPs entrapped in the scaffold's fiber without bead formation. FTIR spectra analysis confirmed the maintenance of the natural structure of Col I, PCL, and Fe3O4 upon electrospinning. AFM data have shown that MNPs incorporation introduced stripe-like topography to nanofibers, while the depth of the grooves has decreased from 800 to 500 nm. Flow cytometry confirmed the phenotype of ADSCs according to their surface markers (i.e., CD29 and CD105). Additionally, Fe3O4 NP improved nanocomposite scaffold strength, wettability, porosity, biocompatibility and also facilitates the ALP activity, calcium-mineralization. Finally, magnetic nanocomposite scaffolds upregulated osteogenic-related genes or proteins’ expression (e.g., Col I, Runx2, OCN, ON, BMP2) in seeded ADSCs with/without osteo-differentiation media conditions. Conclusions Together, these results indicate that Fe3O4 NPs within the natural structure of Col I increase osteogenic differentiation in osteogenic cues-free media conditions. This effect could be translated in vivo toward bone defects healing. These findings support the use of natural ECM materials alongside magnetic particles as composite scaffolds to achieve their full therapeutic potential in BTE treatments. Graphical Abstract

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Section: Resultsmentioning

confidence: 99%

PCL/Col I-based magnetic nanocomposite scaffold provides an osteoinductive environment for ADSCs in osteogenic cues-free media conditions

et al. 2022

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“…Wnt signaling plays crucial roles in postnatal bone formation. Wnt signaling can promote the commitment of mesenchymal stem cells (MSCs) to osteoblastic lineage and promotes differentiation and bone formation at the critical steps of osteoblast differentiation (56). T lymphocytes and B lymphocytes can result in the production of RANKL, which causes osteoclasts to induce obvious alveolar bone resorption, even tooth loss (57).…”

Section: T Lymphocytes (T Cells)mentioning

confidence: 99%

The Role of Immune Microenvironment in Maxillofacial Bone Homeostasis

et al. 2021

Front. Dent. Med

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Maxillofacial bone defects are common medical problems caused by congenital defects, necrosis, trauma, tumor, inflammation, and fractures non-union. Maxillofacial bone defects often need bone graft, which has many difficulties, such as limited autogenous bone supply and donor site morbidity. Bone tissue engineering is a promising strategy to overcome the above-mentioned problems. Osteoimmunology is the inter-discipline that focuses on the relationship between the skeletal and immune systems. The immune microenvironment plays a crucial role in bone healing, tissue repair and regeneration in maxillofacial region. Recent studies have revealed the vital role of immune microenvironment and bone homeostasis. In this study, we analyzed the complex interaction between immune microenvironment and bone regeneration process in oral and maxillofacial region, which will be important to improve the clinical outcome of the bone injury treatment.

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“…The intracellular responses that WNT ligands trigger can be classified into canonical (b-catenin-dependent) and non-canonical (b-cateninindependent) signaling (2,3). WNT is a family of nineteen hydrophobic cysteine-rich secreted glycoproteins which serve as ligands for ten members of the Frizzled (Fz) family of 7transmembrane receptors, the co-receptors low-density lipoprotein receptor-related proteins 5/6 (LRP 5/6), and non-classical WNT receptors like RYK and ROR (4)(5)(6)(7)(8). Abnormal WNT/b-catenin signaling is involved in many diseases including Alzheimer's disease, heart disease, osteoarthritis, and cancer (9,10).…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation-Dependent Regulation of WNT/Beta-Catenin Signaling

Shah

Kazi

2022

Front. Oncol.

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WNT/β-catenin signaling is a highly complex pathway that plays diverse roles in various cellular processes. While WNT ligands usually signal through their dedicated Frizzled receptors, the decision to signal in a β-catenin-dependent or -independent manner rests upon the type of co-receptors used. Canonical WNT signaling is β-catenin-dependent, whereas non-canonical WNT signaling is β-catenin-independent according to the classical definition. This still holds true, albeit with some added complexity, as both the pathways seem to cross-talk with intertwined networks that involve the use of different ligands, receptors, and co-receptors. β-catenin can be directly phosphorylated by various kinases governing its participation in either canonical or non-canonical pathways. Moreover, the co-activators that associate with β-catenin determine the output of the pathway in terms of induction of genes promoting proliferation or differentiation. In this review, we provide an overview of how protein phosphorylation controls WNT/β-catenin signaling, particularly in human cancer.

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Roles of Non-Canonical Wnt Signalling Pathways in Bone Biology

Cited by 50 publications

References 213 publications

PCL/Col I-based magnetic nanocomposite scaffold provides an osteoinductive environment for ADSCs in osteogenic cues-free media conditions

PCL/Col I-based magnetic nanocomposite scaffold provides an osteoinductive environment for ADSCs in osteogenic cues-free media conditions

The Role of Immune Microenvironment in Maxillofacial Bone Homeostasis

Phosphorylation-Dependent Regulation of WNT/Beta-Catenin Signaling

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