Wnt5a and its signaling pathway in angiogenesis

Shi, Yaning; Zhu, Neng; Liu, Chan; Wu, Hongtao; Gui, Yu; Liao, Duan‐Fang; Qin, Li

doi:10.1016/j.cca.2017.06.017

Cited by 50 publications

(40 citation statements)

References 82 publications

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“…In the non-canonical pathway, various receptors or co-receptors on the cell surface and extracellular matrix are involved in the pathway [30]. For non-canonical Wnt signaling, the majority of Wnt proteins bind to multiple Frizzled (Fzd) receptors, which belong to a family of G-protein-coupled transmembrane proteins [31].…”

Section: Canonical/non-canonical Wnt Signaling Pathwaymentioning

confidence: 99%

“…For non-canonical Wnt signaling, the majority of Wnt proteins bind to multiple Frizzled (Fzd) receptors, which belong to a family of G-proteincoupled transmembrane proteins [31]. Other Wnt proteins can bind to Ror1 or Ror2, RYK, and lowdensity lipoprotein receptor-related protein 5/6 (LRP5/6), which act as transmembrane co-receptors to form a complex with Fzd ( Figure 1) [30][31][32][33]. Non-canonical Wnt pathway: Wnt signaling activates another mechanism independent of β-catenin.…”

mentioning

confidence: 99%

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The Role of Carcinogenesis-Related Biomarkers in the Wnt Pathway and Their Effects on Epithelial–Mesenchymal Transition (EMT) in Oral Squamous Cell Carcinoma

Bai

Sha

Kanno

2020

Cancers

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As oral squamous cell carcinoma (OSCC) can develop from potentially malignant disorders (PMDs), it is critical to develop methods for early detection to improve the prognosis of patients. Epithelial–mesenchymal transition (EMT) plays an important role during tumor progression and metastasis. The Wnt signaling pathway is an intercellular pathway in animals that also plays a fundamental role in cell proliferation and regeneration, and in the function of many cell or tissue types. Specific components of master regulators such as epithelial cadherin (E-cadherin), Vimentin, adenomatous polyposis coli (APC), Snail, and neural cadherin (N-cadherin), which are known to control the EMT process, have also been implicated in the Wnt cascade. Here, we review recent findings on the Wnt signaling pathway and the expression mechanism. These regulators are known to play roles in EMT and tumor progression, especially in OSCC. Characterizing the mechanisms through which both EMT and the Wnt pathway play a role in these cellular pathways could increase our understanding of the tumor genesis process and may allow for the development of improved therapeutics for OSCC.

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Section: Canonical/non-canonical Wnt Signaling Pathwaymentioning

confidence: 99%

mentioning

confidence: 99%

The Role of Carcinogenesis-Related Biomarkers in the Wnt Pathway and Their Effects on Epithelial–Mesenchymal Transition (EMT) in Oral Squamous Cell Carcinoma

Bai

Sha

Kanno

2020

Cancers

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“…Wnts, a family of secreted glycoproteins, participate in an autocrine or paracrine manner in a variety of developmental processes during embryogenesis, such as cell proliferation, differentiation, polarity, migration, and angiogenesis (Logan & Nusse, 2004;Shi et al, 2017).…”

mentioning

confidence: 99%

Wnt5a suppresses osteoblastic differentiation of human periodontal ligament stem cell‐like cells via Ror2/JNK signaling

Hasegawa

Wada

Yoshida

et al. 2017

Journal Cellular Physiology

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Wnt5a, a non-canonical Wnt protein, is known to play important roles in several cell functions. However, little is known about the effects of Wnt5a on osteoblastic differentiation of periodontal ligament (PDL) cells. Here, we examined the effects of Wnt5a on osteoblastic differentiation and associated intracellular signaling in human PDL stem/progenitor cells (HPDLSCs). We found that Wnt5a suppressed expression of bone-related genes (ALP, BSP, and Osterix) and alizarin red-positive mineralized nodule formation in HPDLSCs under osteogenic conditions. Immunohistochemical analysis revealed that a Wnt5a-related receptor, receptor tyrosine kinase-like orphan receptor 2 (Ror2), was expressed in rat PDL tissue. Interestingly, knockdown of Ror2 by siRNA inhibited the Wnt5a-induced downregulation of bone-related gene expression in HPDLSCs. Moreover, Western blotting analysis showed that phosphorylation of the intracellular signaling molecule, c-Jun N-terminal kinase (JNK) was upregulated in HPDLSCs cultured in osteoblast induction medium with Wnt5a, but knockdown of Ror2 by siRNA downregulated the phosphorylation of JNK. We also examined the effects of JNK inhibition on Wnt5a-induced suppression of osteoblastic differentiation of HPDLSCs. The JNK inhibitor, SP600125 inhibited the Wnt5a-induced downregulation of bone-related gene expression in HPDLSCs. Additionally, SP600125 inhibited the Wnt5a-induced suppression of the alizarin red-positive reaction in HPDLSCs. These results suggest that Wnt5a suppressed osteoblastic differentiation of HPDLSCs through Ror2/JNK signaling. Non-canonical Wnt signaling, including Wnt5a/Ror2/JNK signaling, may function as a negative regulator of mineralization, preventing the development of non-physiological mineralization in PDL tissue.

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“…For instance, several stimuli with known pro-regenerative functions were detected in MSC CM and/or EV+ CM fraction. Wnt5a signals through both the canonical and non-canonical signaling pathways to activate proangiogenic pathways in vivo through endothelial cells 86 or through the M2-polarization of infiltrating monocytes 86,87 . Likewise, VEGF-A, ANGPT1 and POSTN have also demonstrated proregenerative function in previous studies [88][89][90] .…”

Section: Discussionmentioning

confidence: 99%

Ultrafiltration Segregates Tissue Regenerative Stimuli Harboured Within and Independent of Extracellular Vesicles

Cooper

Sherman

Dayarathna

et al. 2020

Preprint

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The release of extracellular vesicles (EV) from human multipotent stromal cells (MSC) has been proposed as a mechanism by which MSC mediate regenerative functions in vivo. Our recent work has characterized MSC derived from human pancreatic tissues (Panc-MSC) that generated a tissue regenerative secretome which could be used as an injectable biotherapeutic agent in vivo. Despite these advancements, it remains unknown whether tissue regenerative stimuli released by Panc-MSC are released independent or within extracellular vesicles (EVs).Herein, this study demonstrates ultrafiltration is a simple method to enrich for EVs which can be injected in murine models of blood vessel or pancreatic islet regeneration. The enrichment of EVs from Panc-MSC conditioned media (CM) was validated using nanoscale flow cytometry and atomic force microscopy; in addition to the exclusive detection of classical EV-markers CD9, CD81, CD63 using label-free mass spectrometry. Additionally, we identified several proregenerative stimuli, such as WNT5A or ANGPT1, exclusively detected in Panc-MSC EVenriched versus EV-depleted conditioned media. Human microvascular endothelial cell tubule formation was enhanced in response to both Panc-MSC CM fractions in vitro yet only intramuscular injection of EV-enriched CM demonstrated vascular regenerative functions in NOD/SCID mice with unilateral hind-limb ischemia (*

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Wnt5a and its signaling pathway in angiogenesis

Cited by 50 publications

References 82 publications

The Role of Carcinogenesis-Related Biomarkers in the Wnt Pathway and Their Effects on Epithelial–Mesenchymal Transition (EMT) in Oral Squamous Cell Carcinoma

The Role of Carcinogenesis-Related Biomarkers in the Wnt Pathway and Their Effects on Epithelial–Mesenchymal Transition (EMT) in Oral Squamous Cell Carcinoma

Wnt5a suppresses osteoblastic differentiation of human periodontal ligament stem cell‐like cells via Ror2/JNK signaling

Ultrafiltration Segregates Tissue Regenerative Stimuli Harboured Within and Independent of Extracellular Vesicles

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