Spatial and temporal aspects of Wnt signaling and planar cell polarity during vertebrate embryonic development

Sokol, Sergei Y.

doi:10.1016/j.semcdb.2015.05.002

Cited by 86 publications

(57 citation statements)

References 159 publications

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“…In vertebrates, the Fz-PCP pathway has also been shown to control coordinated cellular behaviours within mesenchymal tissues. Examples include cell intercalation during gastrulation, cell orientation in the developing limb bud, and cell-to-cell interactions within migratory neural crest streams (Goodrich and Strutt, 2011;Gao and Yang, 2013;Mayor and Theveneau, 2014;Sokol, 2015). As there are vertebral defects in both Fz-PCP and the Fat4 and Dchs1 mutants, we considered the possibility that Fat4-Dchs1 might regulate polarised cell behaviours and rearrangements during sclerotomal morphogenesis.…”

Section: Discussionmentioning

confidence: 99%

Fat4-Dchs1 signalling controls cell proliferation in developing vertebrae

et al. 2016

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The protocadherins Fat4 and Dchs1 act as a receptor-ligand pair to regulate many developmental processes in mice and humans, including development of the vertebrae. Based on conservation of function between Drosophila and mammals, Fat4-Dchs1 signalling has been proposed to regulate planar cell polarity (PCP) and activity of the Hippo effectors Yap and Taz, which regulate cell proliferation, survival and differentiation. There is strong evidence for Fat regulation of PCP in mammals but the link with the Hippo pathway is unclear. In Fat4 −/− and Dchs1 −/− mice, many vertebrae are split along the midline and fused across the anterior-posterior axis, suggesting that these defects might arise due to altered cell polarity and/or changes in cell proliferation/differentiation. We show that the somite and sclerotome are specified appropriately, the transcriptional network that drives early chondrogenesis is intact, and that cell polarity within the sclerotome is unperturbed. We find that the key defect in Fat4 and Dchs1 mutant mice is decreased proliferation in the early sclerotome. This results in fewer chondrogenic cells within the developing vertebral body, which fail to condense appropriately along the midline. Analysis of Fat4;Yap and Fat4;Taz double mutants, and expression of their transcriptional target Ctgf, indicates that Fat4-Dchs1 regulates vertebral development independently of Yap and Taz. Thus, we have identified a new pathway crucial for the development of the vertebrae and our data indicate that novel mechanisms of Fat4-Dchs1 signalling have evolved to control cell proliferation within the developing vertebrae.

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Section: Discussionmentioning

confidence: 99%

Fat4-Dchs1 signalling controls cell proliferation in developing vertebrae

et al. 2016

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“…The two best characterised ones are the so-called canonical pathway, which regulates target gene expression, and the non-canonical planar cell polarity pathway (Sokol, 2015). Here we focus on canonical signalling, which is initiated by the binding of Wnt to a member of the Frizzled family of serpentine receptors and the coreceptor LRP5/6 (MacDonald and He, 2012).…”

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confidence: 99%

Making, Exporting, and Modulating Wnts

Langton

Kakugawa²,

Vincent

2016

Trends in Cell Biology

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“…We compared different concentrations of gelatin and found that 0.5% gelatin in DMEM significantly increased the proliferation of Ad-MSCs, possibly via activation of the canonical pathway for wnt signaling. The activation of wnt/catenin pathways leads to increased cell proliferation during embryonic development (Sokol, 2015). This also regulates cell proliferation in certain mammalian tissues, which are in a state of constant regeneration (Clevers et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Gelatin positively regulates the immunosuppressive capabilitiesof adipose-derived mesenchymal stem cells

et al. 2017

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IntroductionAdipose-derived mesenchymal stem cells (Ad-MSCs) are highly multipotent cells with a high potential for differentiation into multiple cell types (Vieira et al., 2010;Park et al., 2012;Mellor et al., 2015). Ad-MSCs produce various growth factors that contribute to injury healing and tissue regeneration (Salgado et al., 2010). The antiinflammatory, immunomodulatory, and antioxidant properties of mesenchymal stem cells (MSCs) make them desirable candidates for cell-based therapies (Soleymaninejadian et al., 2012).The usefulness of MSCs has been selectively enhanced by either manipulating the culture media composition (Langenbach and Handschel, 2013) or by gene transduction (Liu et al., 2015). Pretreatment with proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interferon-γ (INF-γ), and interleukin-6 (IL-6), enhances the immunosuppressive capacity of MSCs by upregulating the expression of indoleamine-2,3-dioxygenase (IDO), which inhibits the proliferation of lymphocytes (Hoogduijn et al., 2010). Gelatin sponges incorporating high amounts of β-tricalcium phosphate (β TCP) have been used to stimulate rat bone marrow MSC proliferation and osteogenic differentiation by stimulating higher alkaline phosphatase (AP) activity and osteocalcin expression (Takahashi et al., 2005). Similarly, a scaffold prepared by mixing chitosan with gelatin, β TCP, and hydroxyapatite (HA) has also been used to induce MSC adhesion, differentiation, and proliferation (Zhao et al., 2006).MSCs cultured in a hyperoxic environment have enhanced viability and paracrine therapeutic capabilities (Song et al., 2010), as well as increased expression of the naturally occurring antioxidant stanniocalcin-1 (SC-1), which prevents oxygen-induced bronchopulmonary dysplasia in rats (Waszak et al., 2012). HO-1, a potent antioxidant enzyme, can be induced in undifferentiated MSCs treated with hemin, which renders the MSCs more resistant to oxidative injury (Barbagallo et al., 2008). Osteogenic growth peptide (OGP) induces HO-1 expression in human bone marrow MSCs, which induces osteogenic differentiation as evidenced by elevated levels of bone morphogenic protein-2 (BMP-2) and osteonectin (Vanella et al., 2010(Vanella et al., , 2013. We have previously reported that gelatin-induced osteogenic cell sheets had active cell proliferation with abundant extracellular matrix and upregulation of osteogenic markers (Kim et al., 2016). In the present study, we evaluated the effects of gelatin on

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Spatial and temporal aspects of Wnt signaling and planar cell polarity during vertebrate embryonic development

Cited by 86 publications

References 159 publications

Fat4-Dchs1 signalling controls cell proliferation in developing vertebrae

Fat4-Dchs1 signalling controls cell proliferation in developing vertebrae

Making, Exporting, and Modulating Wnts

Gelatin positively regulates the immunosuppressive capabilitiesof adipose-derived mesenchymal stem cells

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