Hippo-Yap Pathway Orchestrates Neural Crest Ontogenesis

Zhao, Xiaolei; Le, Tram P.; Erhardt, Shannon; Findley, Tina O.; Wang, Jun

doi:10.3389/fcell.2021.706623

Cited by 15 publications

(10 citation statements)

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“…addition, NCC-derived eMSC osteogenesis in vivo is more complex than that of NCCs in vitro and is regulated by an intricate signaling network (52). We also cannot exclude the possibility that Yap and Taz only function in a certain group of NCC-derived eMSCs instead of all NCCs, which is worthy of further investigation in the future.…”

Section: Discussionmentioning

confidence: 91%

“…An important limitation of our in vivo model is that the mutant embryos retain a single functional copy of Yap , which may be sufficient to support some of the redundant roles of Yap and Taz in vivo or in a subset of skull structures. In addition, NCC-derived eMSC osteogenesis in vivo is more complex than that of NCCs in vitro and is regulated by an intricate signaling network ( 52 ). We also cannot exclude the possibility that Yap and Taz only function in a certain group of NCC-derived eMSCs instead of all NCCs, which is worthy of further investigation in the future.…”

Section: Discussionmentioning

confidence: 99%

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Yap and Taz promote osteogenesis and prevent chondrogenesis in neural crest cells in vitro and in vivo

Zhao

Tang

et al. 2022

Sci. Signal.

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Neural crest cells (NCCs) are multipotent stem cells that can differentiate into multiple cell types, including the osteoblasts and chondrocytes, and constitute most of the craniofacial skeleton. Here, we show through in vitro and in vivo studies that the transcriptional regulators Yap and Taz have redundant functions as key determinants of the specification and differentiation of NCCs into osteoblasts or chondrocytes. Primary and cultured NCCs deficient in Yap and Taz switched from osteogenesis to chondrogenesis, and NCC-specific deficiency for Yap and Taz resulted in bone loss and ectopic cartilage in mice. Yap bound to the regulatory elements of key genes that govern osteogenesis and chondrogenesis in NCCs and directly regulated the expression of these genes, some of which also contained binding sites for the TCF/LEF transcription factors that interact with the Wnt effector β-catenin. During differentiation of NCCs in vitro and NCC-derived osteogenesis in vivo, Yap and Taz promoted the expression of osteogenic genes such as Runx2 and Sp7 but repressed the expression of chondrogenic genes such as Sox9 and Col2a1 . Furthermore, Yap and Taz interacted with β-catenin in NCCs to coordinately promote osteoblast differentiation and repress chondrogenesis. Together, our data indicate that Yap and Taz promote osteogenesis in NCCs and prevent chondrogenesis, partly through interactions with the Wnt–β-catenin pathway.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Yap and Taz promote osteogenesis and prevent chondrogenesis in neural crest cells in vitro and in vivo

Zhao

Tang

et al. 2022

Sci. Signal.

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“…In addition, other pathways have been suggested to play a role in neural crest development, such as retinoic acid signaling [ 40 , 41 ] and the Hippo/YAP pathway. For example, recent findings suggest that Hippo/YAP promotes neural crest fate and migration, as well as fate specification of neural crest cells (reviewed by Zhao et al, 2021 [ 42 ]): YAP activation could benefit the EMT and migration of neural crest cells, and studies have suggested the crosstalk of YAP signaling with that of BMP and Wnt [ 43 ], retinoic acid [ 44 ], and Notch [ 45 ] during neural crest development.…”

Section: In Vivo Development Of Schwann Cellsmentioning

confidence: 99%

Development and In Vitro Differentiation of Schwann Cells

Hörner

Couturier

Gueiber

et al. 2022

Cells

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Schwann cells are glial cells of the peripheral nervous system. They exist in several subtypes and perform a variety of functions in nerves. Their derivation and culture in vitro are interesting for applications ranging from disease modeling to tissue engineering. Since primary human Schwann cells are challenging to obtain in large quantities, in vitro differentiation from other cell types presents an alternative. Here, we first review the current knowledge on the developmental signaling mechanisms that determine neural crest and Schwann cell differentiation in vivo. Next, an overview of studies on the in vitro differentiation of Schwann cells from multipotent stem cell sources is provided. The molecules frequently used in those protocols and their involvement in the relevant signaling pathways are put into context and discussed. Focusing on hiPSC- and hESC-based studies, different protocols are described and compared, regarding cell sources, differentiation methods, characterization of cells, and protocol efficiency. A brief insight into developments regarding the culture and differentiation of Schwann cells in 3D is given. In summary, this contribution provides an overview of the current resources and methods for the differentiation of Schwann cells, it supports the comparison and refinement of protocols and aids the choice of suitable methods for specific applications.

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“…One of the central regulators is the Hippo pathway, which plays a pivotal role in heart failure (Wang et al, 2018 ). The Hippo pathway targets not only mitochondria but also other organelles and pathways (Zhao et al, 2021 ). Mammalian sterile 20-like kinase 1 (MST1) is a crucial component in the Hippo pathway (Zhao et al, 2021 ).…”

mentioning

confidence: 99%

“…The Hippo pathway targets not only mitochondria but also other organelles and pathways (Zhao et al, 2021 ). Mammalian sterile 20-like kinase 1 (MST1) is a crucial component in the Hippo pathway (Zhao et al, 2021 ). Feng et al observed that knockout of Mst1 inhibited mitochondrial division and reduced left ventricular remodeling in diabetic cardiomyopathy, thereby highlighting the critical role of the Hippo pathway in the regulation of mitochondria and CVDs.…”

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confidence: 99%

Editorial: Metabolic Regulation in the Development of Cardiovascular Diseases

Bhuiyan

Kim

et al. 2021

Front. Cell Dev. Biol.

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Editorial on the Research Topic Metabolic Regulation in the Development of Cardiovascular DiseasesMetabolic syndromes increase the risk of cardiovascular diseases (CVDs) (North and Sinclair, 2012), and metabolic reprogramming can either reverse or rescue the molecular events that lead to CVDs (Chen et al., 2020a). However, the metabolic mechanisms underlying CVDs are not fully understood. We have prepared a special Research Topic. This Research Topic entitled "Metabolic Regulation in the Development of Cardiovascular Diseases" received 11 original articles, 7 review articles, and 2 opinion articles. This special issue highlights recent research findings to clarify the relationship between metabolism and CVD.Metabolic dysregulation and metabolic syndromes are independent risk factors for CVDs (Zhou et al., 2018). Genetic mutations in metabolic enzymes, as well as transcription factors, can cause CVDs (Austin et al., 2019). In this issue, Zhang et al. identify the occurrence of mutations in transcription factor EB (TFEB), which controls lysosomal biogenesis and metabolism (Settembre et al., 2013), as a potential risk factor for acute myocardial infarction. This study detected novel variants of the metabolic regulator, TFEB, that might contribute to the development of acute myocardial infarction. Furthermore, pregnancy-related CVDs, such as arterial dissection, are also affected by metabolic conditions (Wang et al., 2021). Deng et al. emphasized the importance of glycemic control in pregnant women, which could improve the understanding, prevention, and treatment of pregnancy-related arterial dissection.Genetic mutations, or dysregulation of metabolic enzymes and their regulators, directly alter cell metabolism, intracellular metabolites, and physiological functions of vascular cells such as endothelial cells (ECs) (Tang et al., 2014). Endothelial metabolic homeostasis and reprogramming can regulate endothelial functions, including angiogenesis, inflammation, and barrier maintenance (Tang et al., 2014;Subramanian et al., 2021). Peng et al. provided an overview of the metabolic pathways in ECs under normal and pathological conditions. Their review highlighted the metabolic reprogramming of endothelium as a potential therapeutic approach for controlling CVDs.Glucose metabolism in ECs is critical for cardiovascular homeostasis and diseases (Dumas et al., 2021). Glucose catabolism is regulated by enzymes such as 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), whose dysfunction drives endothelial injury and vascular inflammation (Bartrons et al., 2018). The role of PFKFB3 in non-EC vascular cells remains unclear. In this regard, Poels et al. show that PFKFB3 expression in monocytes is positively correlated with the occurrence of coronary arteries with unstable plaque phenotypes. Inhibition of PFKFB3 reduced the number of late plaques in vulnerable phenotypes Publisher's Note: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated orga...

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Hippo-Yap Pathway Orchestrates Neural Crest Ontogenesis

Cited by 15 publications

References 59 publications

Yap and Taz promote osteogenesis and prevent chondrogenesis in neural crest cells in vitro and in vivo

Yap and Taz promote osteogenesis and prevent chondrogenesis in neural crest cells in vitro and in vivo

Development and In Vitro Differentiation of Schwann Cells

Editorial: Metabolic Regulation in the Development of Cardiovascular Diseases

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