Suppression of Lens Stalk Cell Apoptosis by Hyaluronic Acid Leads to Faulty Separation of the Lens Vesicle

Ozeki, Hironori; Ogura, Yuichiro; Hirabayashi, Yoshifumi; Shimada, Shoichi

doi:10.1006/exer.2000.0923

Cited by 21 publications

(18 citation statements)

References 28 publications

(25 reference statements)

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“…This result is in line with the analysis of the CD44 null mutant mice, which, surprisingly, do not reveal major developmental defects (Protin et al, 1999). Although previous studies have demonstrated that in in vitro cellular systems hyaluronan provides cells with apoptotic protection via the interaction with hyaluronan receptor CD44 (Kaneko et al, 2000;Ozeki et al, 2001;Ohwada et al, 2008), our findings seem to point out that in a more complex in vivo system, other hyaluronan receptors might compensate for CD44 depletion (Nedvetzki et al, 2004). In this respect, it is important to note that RHAMM, another hyaluronan receptor, is expressed in cranial NCC during Xenopus development (Casini et al, 2010).…”

Section: Discussionmentioning

confidence: 49%

Hyaluronan is required for cranial neural crest cells migration and craniofacial development

Casini

Nardi

Ori

2011

Developmental Dynamics

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Background: Hyaluronan is a crucial glycosaminoglycan of the vertebrate embryonic extracellular matrix able to influence cell behaviour, both by assembling the pericellular matrices and by activating signal transducing receptors such as CD44. Results: We showed that the hyaluronan synthases, Has1 and Has2, and CD44 display a dynamic expression pattern during cranial neural crest cells (NCC) development. By knocking down Has1 and Has2 gene functions, we revealed that hyaluronan synthesized by Has1 and Has2 is necessary for the proper development of the visceral skeleton. Conclusions: The data suggest that hyaluronan helps to maintain the active migratory behaviour of cranial NCC, and that its presence around pre-chondrogenic NCC is crucial for their survival. CD44 knock down also suggests that the role of hyaluronan in cranial NCC migration could be mediated, at least in part, by the activation of CD44. These findings contribute to the unveiling of the functional relation between NCC and their extracellular environment during craniofacial development. Developmental Dynamics 241:294-302, 2012. V C 2011 Wiley Periodicals, Inc.Key words: hyaluronan; neural crest cell; craniofacial development; Has1; Has2; CD44; extracellular matrix; Xenopus Key findings:Cranial NCC migrate throughout a hyaluronan rich extracellular matrix Hyaluronan synthases 1 and 2 activity is necessary to maintain the migratory behaviour of cranial NCC After NCC migration, the presence of Hyaluronan in the extracellular matrix is necessary for the survival of pre-chondrogenic cranial NCC. CD44, a Hyaluronan receptor, is required for cranial NCC migration but not for their survival. In Xenopus, the craniofacial skeleton formation is deeply influenced by the composition of the extracellular matrix during cranial NCC migration and differentiation.

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Section: Discussionmentioning

confidence: 49%

Hyaluronan is required for cranial neural crest cells migration and craniofacial development

Casini

Nardi

Ori

2011

Developmental Dynamics

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“…49 FoxE3 is involved in this process and is expressed in the early lens placode around E9 until it is turned off in differentiating primary lens fibers at E12.5. 48 In FoxE3 –/– mice, the lens vesicle does not close and the lens remains irregular in shape and size with a persisting lens stalk.…”

Section: Discussionmentioning

confidence: 99%

Lens-specific deletion of theMsx2gene increased apoptosis by enhancing the caspase-3/caspase-8 signaling pathway

Zhou

Liu

et al. 2018

J Int Med Res

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ObjectiveTo investigate the influence of Msx2 conditional gene knockout during lens development in mice.MethodsLens-specific Msx2 knockout mice were generated using the Cre-loxP system. The eyes of Msx2 conditional knockout (Msx2CKO) and wild-type (Msx2WT) mice were examined during embryonic and early postnatal periods using histological, immunofluorescence, in situ hybridization, cell proliferation, apoptosis, and mRNA microarray analyses.ResultsMsx2CKO mice exhibited small lens formation and microphthalmia after birth, while Msx2CKO embryos exhibited a persistent lens stalk, small lens formation, and microphthalmia. Conditional deletion of Msx2 also led to an increased apoptosis rate, a significant reduction in FoxE3 expression, and an upregulation of Prox1 expression in the lens vesicle during the early embryonic period. Microarray comparison of Msx2CKO and Msx2WT lens transcriptomes identified a large number of differentially expressed genes. Real-time PCR showed that Casp8 and Casp3 expression was upregulated in Msx2CKO mice at post-natal day 1.ConclusionThe activation of apoptosis through the caspase-8/caspase-3 signaling pathway, together with the downregulation of FoxE3 expression, appeared to account for the smaller lens formation in Msx2CKO mice.

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“…This might be due to unidentified function(s) mediated by Shroom3 that are distinct from those involving p120-catenin. Several mouse mutants that display a similar lens stalk phenotype have disruptions in additional morphogenetic processes, such as proliferation, adhesion, differentiation and apoptosis, leaving open the possibility that Shroom3 might also function in these processes (Dimanlig et al, 2001;Ozeki et al, 2001;Medina-Martinez et al, 2005;Yoshimoto et al, 2005;Chen et al, 2008;Pontoriero et al, 2008Pontoriero et al, , 2009Kuracha et al, 2011;Cavalheiro et al, 2014).…”

Section: P120-catenin and Shroom3 Are Required For Normal Lens Morphomentioning

confidence: 99%

p120-catenin-dependent junctional recruitment of Shroom3 is required for apical constriction during lens pit morphogenesis

et al. 2014

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Apical constriction (AC) is a widely utilized mechanism of cell shape change whereby epithelial cells transform from a cylindrical to conical shape, which can facilitate morphogenetic movements during embryonic development. Invertebrate epithelial cells undergoing AC depend on the contraction of apical cortex-spanning actomyosin filaments that generate force on the apical junctions and pull them toward the middle of the cell, effectively reducing the apical circumference. A current challenge is to determine whether these mechanisms are conserved in vertebrates and to identify the molecules responsible for linking apical junctions with the AC machinery. Utilizing the developing mouse eye as a model, we have uncovered evidence that lens placode AC may be partially dependent on apically positioned myosin-containing filaments associated with the zonula adherens. In addition we found that, among several junctional components, p120-catenin genetically interacts with Shroom3, a protein required for AC during embryonic morphogenesis. Further analysis revealed that, similar to Shroom3, p120-catenin is required for AC of lens cells. Finally, we determined that p120-catenin functions by recruiting Shroom3 to adherens junctions. Together, these data identify a novel role for p120-catenin during AC and further define the mechanisms required for vertebrate AC.

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Suppression of Lens Stalk Cell Apoptosis by Hyaluronic Acid Leads to Faulty Separation of the Lens Vesicle

Cited by 21 publications

References 28 publications

Hyaluronan is required for cranial neural crest cells migration and craniofacial development

Hyaluronan is required for cranial neural crest cells migration and craniofacial development

Lens-specific deletion of theMsx2gene increased apoptosis by enhancing the caspase-3/caspase-8 signaling pathway

p120-catenin-dependent junctional recruitment of Shroom3 is required for apical constriction during lens pit morphogenesis

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