Innovative Molecular and Cellular Therapeutics in Cleft Palate Tissue Engineering

Oliver, Jeremie D.; Jia, Shihai; Halpern, L.; Graham, Emily M.; Turner, Emma; Colombo, John S.; Grainger, David W.; D’Souza, Rena N.

doi:10.1089/ten.teb.2020.0181

Cited by 21 publications

(11 citation statements)

References 271 publications

(250 reference statements)

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“…Therefore, it is of significant clinical importance to explore the pathogenesis of cleft lip and palate. Since morphological events in mice closely resemble those seen in humans, mouse genetic models with palatal defects have been valuable for analyzing the genes that regulate palatogenesis and for determining the genetic causes of human cleft palate (Oliver et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

The involvement of hormone-sensitive lipase in all-trans retinoic acid induced cleft palate

Zheng¹,

Ye²

2022

Int. J. Dev. Biol.

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Abnormally high concentrations of all-trans retinoic acid (atRA) induce cleft palate, which is accompanied by abnormal migration and proliferation of mouse embryonic palatal mesenchyme (MEPM) cells. Hormone-sensitive lipase (HSL) is involved in many embryonic development processes. The current study was designed to elucidate the mechanism of HSL in cleft palate induced by atRA. To establish a cleft palate model in Kunming mice, pregnant mice were administered atRA (70 mg/kg) by gavage at embryonic Day 10.5 (E10.5). Embryonic palates were obtained through the dissection of pregnant mice at E15.5. Hematoxylin and eosin (H&E) staining was used to evaluate growth changes in the palatal shelves. The levels of HSL in MEPM cells were detected by immunohistochemistry, quantitative real-time reverse transcription-polymerase chain reaction (qRT‒PCR) and western blotting. RNAi was applied to construct vectors expressing HSL small interference RNAs (siRNAs). The vectors were transfected into MEPM cells. Cell proliferation and migration were evaluated by the cell counting kit-8 (CCK-8) assay and wound healing assay, respectively. The palatal shelves in the atRA group had separated at E15.5 without fusing. In MEPM cells, the expression of HSL was reversed after atRA treatment, which caused cleft palate in vivo. In the atRA group, the proliferation of HSL siRNA-transfected cells was remarkably promoted, and the migration rate significantly increased in the HSL siRNA-transfected MEPM cells. These results suggested that HSL may be involved in cleft palate induced by atRA and that atRA enhances HSL levels to inhibit embryonic palate growth.

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Section: Discussionmentioning

confidence: 99%

The involvement of hormone-sensitive lipase in all-trans retinoic acid induced cleft palate

Zheng¹,

Ye²

2022

Int. J. Dev. Biol.

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“…The RNA-seq results suggested the stimulating effect of wild-type VEGFA on osteoblast differentiation was higher than that of mutant type, indicating that the mutation has a negative influence on osteogenesis. Oliver et al [ 37 ] also revealed that the tissue engineering scaffold of osteogenic growth factor is involved in regulating the molecular signal network related to driving the occurrence of CL/P, providing a new way for the CL/P surgical correction operation site to stimulate bone formation.…”

Section: Discussionmentioning

confidence: 99%

Functional identification of a rare vascular endothelial growth factor a ( VEGFA ) variant associating with the nonsyndromic cleft lip with/without cleft palate

et al. 2021

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Vascular endothelial growth factor A (VEGFA) is a crucial growth factor, which participates in multiple processes of human growth and development, such as angiogenesis and osteogenesis and is also necessary for development of palate. The purpose of this study was to investigate the effect of a rare VEGFA mutation (NM_001025366.2 773 T > C p.Val258Ala) on the cell functions and osteogenesis. Here, we found that the VEGFA mutation has adverse effects on the function of human embryonic palatal plate mesenchymal (HEPM) cells, and may affect the development of palate. The VEGFA mutation has adverse effects on promoting cell proliferation and migration and inhibiting apoptosis in HEPM and HEK-293 cells. In addition, the mutant VEGFA allele has a negative influence on osteogenesis. Taken together, the rare variant of the VEGFA gene had an adverse effect on cell functions and osteogenesis, which may impact the development of the palate. And these findings suggested that VEGFA mutation (c.773 T > C) may lead to nonsyndromic cleft lip with or without cleft palate and also provide a new insight into the mechanism of VEGFA gene in osteogenesis and palatogenesis.

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“…ECMs can serve conceptually similar roles controlling tissue development and homeostasis, as well as organ-specific mechanisms. Many questions remain unanswered, providing rich opportunities for future research and therapy (e.g., see Oliver et al 2021).…”

Section: Discussionmentioning

confidence: 99%

Extracellular Matrix in Human Craniofacial Development

Walma

Yamada

2021

J Dent Res

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The extracellular matrix (ECM) is a highly dynamic amalgamation of structural and signaling molecules whose quantitative and qualitative modifications drive the distinct programmed morphologic changes required for tissues to mature into their functional forms. The craniofacial complex houses a diverse array of tissues, including sensory organs, glands, and components of the musculoskeletal, neural, and vascular systems, alongside several other highly specialized tissues to form the most complex part of the vertebrate body. Through cell-ECM interactions, the ECM coordinates the cell movements, shape changes, differentiation, gene expression changes, and other behaviors that sculpt developing organs. In this review, we focus on several common key roles of the ECM to shape developing craniofacial organs and tissues. We summarize recent advances in our understanding of the ability of the ECM to biochemically and biomechanically orchestrate major events of craniofacial development, and we discuss how dysregulated ECM dynamics contributes to disease and disorders. As we expand our understanding of organ-specific matrix functionality and composition, we will improve our ability to rationally modify matrices to promote regeneration and/or prevent degenerative outcomes in vitro and in vivo.

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Innovative Molecular and Cellular Therapeutics in Cleft Palate Tissue Engineering

Cited by 21 publications

References 271 publications

The involvement of hormone-sensitive lipase in all-trans retinoic acid induced cleft palate

The involvement of hormone-sensitive lipase in all-trans retinoic acid induced cleft palate

Functional identification of a rare vascular endothelial growth factor a ( VEGFA ) variant associating with the nonsyndromic cleft lip with/without cleft palate

Extracellular Matrix in Human Craniofacial Development

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