Dual functions for WNT5A during cartilage development and in disease

Hosseini-Farahabadi, Sara; Geetha-Loganathan, Poongodi; Fu, Katherine; Nimmagadda, Suresh; Yang, Hoe Joong; Richman, Joy M.

doi:10.1016/j.matbio.2013.02.005

Cited by 55 publications

(73 citation statements)

References 57 publications

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“…5A). This is different from our previous study where WNT5A was able to antagonize Wnt3a and LiCl in similar culture conditions (70). The antagonistic effects of WNT11 are therefore dependent on GSK3␤.…”

Section: Wnt11 Regulates a Subset Of Genes Involved In Clefting-contrasting

confidence: 99%

“…In particular, WNT5A and WNT5B are prominently expressed in the faces of mouse and chicken (35,81). We showed that RCAS::WNT5A injected into the mandibular prominence leads to beak deviations (70). These defects may be due to abnormal cell behavior, which is a question that will be investigated in a separate study.…”

Section: Discussionmentioning

confidence: 78%

“…To maintain the context, the reporters were transfected into high density micromass cultures of maxillary mesenchyme (52,70). We continued to use the same WNT11 retrovirus as in the in vivo experiments so as to mimic as closely as possible the conditions present in the whole embryo (Fig.…”

Section: Wnt11 Regulates a Subset Of Genes Involved In Clefting-mentioning

confidence: 99%

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Avian Facial Morphogenesis Is Regulated by c-Jun N-terminal Kinase/Planar Cell Polarity (JNK/PCP) Wingless-related (WNT) Signaling

Geetha-Loganathan

Nimmagadda

et al. 2014

Journal of Biological Chemistry

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Background:Numerous genes contribute to the increased risk of facial clefting, but the cellular mechanisms involved are not well understood. Results: JNK/PCP wingless-related signaling is demonstrated as a major regulator of face shape. Conclusion: WNT11 induces clefting via inhibiting proliferation, compressing facial prominences, and changing cell behavior. Significance: JNK/PCP WNT signaling is implicated in the pathophysiology underlying craniofacial abnormalities.

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Section: Wnt11 Regulates a Subset Of Genes Involved In Clefting-contrasting

confidence: 99%

Section: Discussionmentioning

confidence: 78%

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Avian Facial Morphogenesis Is Regulated by c-Jun N-terminal Kinase/Planar Cell Polarity (JNK/PCP) Wingless-related (WNT) Signaling

Geetha-Loganathan

Nimmagadda

et al. 2014

Journal of Biological Chemistry

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“…Maxillary prominences from stage 24 embryos were dissected in Hank's buffer and placed into micromass culture as described (Hosseini-Farahabadi et al, 2013). To assess canonical WNT activity the SuperTopflash reporter (Ishitani et al, 2003) was used as described (Hosseini-Farahabadi et al, 2013).…”

Section: Micromass Cultures and Luciferase Assaysmentioning

confidence: 99%

Identification and functional analysis of novel facial patterning genes in the duplicated beak chicken embryo

Nimmagadda

Buchtová

et al. 2015

Developmental Biology

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Cranial neural crest cells form the majority of the facial skeleton. However exactly when the pattering information and hence jaw identity is established is not clear. We know that premigratory neural crest cells contain a limited amount of information about the lower jaw but the upper jaw and facial midline are specified later by local tissue interactions. The environmental signals leading to frontonasal identity have been explored by our group in the past. Altering the levels of two signaling pathways (Bone Morphogenetic Protein) and retinoic acid (RA) in the chicken embryo creates a duplicated midline on the side of the upper beak complete with egg tooth in place of maxillary derivatives (Lee et al., 2001). Here we analyze the transcriptome 16 h after bead placement in order to identify potential mediators of the identity change in the maxillary prominence. The gene list included RA, BMP and WNT signaling pathway genes as well as transcription factors expressed in craniofacial development. There was also cross talk between Noggin and RA such that Noggin activated the RA pathway. We also observed expression changes in several poorly characterized genes including the upregulation of Peptidase Inhibitor-15 (PI15). We tested the functional effects of PI15 overexpression with a retroviral misexpression strategy. PI15 virus induced a cleft beak analogous to human cleft lip. We next asked whether PI15 effects were mediated by changes in expression of major clefting genes and genes in the retinoid signaling pathway. Expression of TP63, TBX22, BMP4 and FOXE1, all human clefting genes, were upregulated. In addition, ALDH1A2, ALDH1A3 and RA target, RARβ were increased while the degradation enzyme CYP26A1 was decreased. Together these changes were consistent with activation of the RA pathway. Furthermore, PI15 retrovirus injected into the face was able to replace RA and synergize with Noggin to induce beak transformations. We conclude that the microarrays have generated a rich dataset containing genes with important roles in facial morphogenesis. Moreover, one of these facial genes, PI15 is a putative clefting gene and is in a positive feedback loop with RA.

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“…This result appears to support the notion that Wnt signals are stage-specifically expressed during chondrogenesis. 37 For instance, Wnt5a has been previously implicated as an early promoter 38 and Wnt11, which has been shown to stimulate Col2 deposition, 39 is a late promoter of chondrogenesis. 40 Another study reported that Wnt3a-canonical and noncanonical Wnt pathways counteracted one another in MSC chondrogenesis.…”

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor Ligand Dependent Proliferation and Chondrogenic Differentiation of Synovium-Derived Stem Cells and Concomitant Adaptation of Wnt/Mitogen-Activated Protein Kinase Signals

Pizzute

Zhang

et al. 2016

Tissue Engineering Part A

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Dual functions for WNT5A during cartilage development and in disease

Cited by 55 publications

References 57 publications

Avian Facial Morphogenesis Is Regulated by c-Jun N-terminal Kinase/Planar Cell Polarity (JNK/PCP) Wingless-related (WNT) Signaling

Avian Facial Morphogenesis Is Regulated by c-Jun N-terminal Kinase/Planar Cell Polarity (JNK/PCP) Wingless-related (WNT) Signaling

Identification and functional analysis of novel facial patterning genes in the duplicated beak chicken embryo

Fibroblast Growth Factor Ligand Dependent Proliferation and Chondrogenic Differentiation of Synovium-Derived Stem Cells and Concomitant Adaptation of Wnt/Mitogen-Activated Protein Kinase Signals

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