Glucocorticoid receptor-dependent induction of cripto-1 (one-eyed pinhead) inhibits zebrafish caudal fin regeneration

Garland, Michael A.; Sengupta, Sumitra; Mathew, Lijoy K.; Truong, Lisa; Jong, Esther de; Piersma, Aldert H.; Du, Jane La; Tanguay, Robert L.

doi:10.1016/j.toxrep.2019.05.013

Cited by 9 publications

(7 citation statements)

References 52 publications

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“…It plays an important role in the early embryonic development and the regeneration and differentiation of stem cells (Chambers et al, 2007;Bianco et al, 2009). There were few studies on Tgdf1 gene in fish, especially those related to pluripotency (Garland et al, 2019;Hoover et al, 2019). Our data showed that Oct4, Nanog, and Tgdf1 were characteristic genes to identify the pluripotency status of fish iPS-like cells.…”

Section: Discussionmentioning

confidence: 65%

Defining the Pluripotent Marker Genes for Identification of Teleost Fish Cell Pluripotency During Reprogramming

Xiang

et al. 2022

Front. Genet.

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Pluripotency is a transient state in early embryos, which is regulated by an interconnected network of pluripotency-related genes. The pluripotent state itself seems to be highly dynamic, which leads to significant differences in the description of induced pluripotent stem cells from different species at the molecular level. With the application of cell reprogramming technology in fish, the establishment of a set of molecular standards for defining pluripotency will be important for the research and potential application of induced pluripotent stem cells in fish. In this study, by BLAST search and expression pattern analysis, we screen out four pluripotent genes (Oct4, Nanog, Tdgf1, and Gdf3) in zebrafish (Danio rerio) and crucian carp (Carassius). These genes were highly expressed in the short period of early embryonic development, but significantly down-regulated after differentiation. Moreover, three genes (Oct4, Nanog and Tdgf1) have been verified that are suitable for identifying the pluripotency of induced pluripotent stem cells in zebrafish and crucian carp. Our study expands the understanding of the pluripotent markers of induced pluripotent stem cells in fish.

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Section: Discussionmentioning

confidence: 65%

Defining the Pluripotent Marker Genes for Identification of Teleost Fish Cell Pluripotency During Reprogramming

Xiang

et al. 2022

Front. Genet.

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“…There is mounting evidence indicating that part of CRIPTO’s elusiveness involves its relegation to allostatic processes during injury and regeneration that can call it out from ‘hiding’. In zebrafish fin regeneration studies, CRIPTO was found to be induced by glucocorticoids, in a manner that is conserved in mammals, while retinoic acid (RA) inhibited CRIPTO induction in this setting [ 77 ]. In a mouse model of acute injury, secreted CRIPTO promotes myogenic commitment and differentiation, enhances early regeneration and reduces necrotic fibrotic areas [ 37 , 78 ].…”

Section: Rise and Fall Of Criptomentioning

confidence: 99%

“…Recombinant human NODAL triggered downstream SMAD2 phosphorylation in DU145 and LNCaP cells and attenuated AR signaling, suggesting that CRIPTO might mechanistically support the acquisition of a castration resistant phenotypes [ 151 ]. Paradoxically, in the zebrafish injury model, glucocorticoid receptor (GR) signaling induces CRIPTO expression but inhibits fin regeneration [ 77 ]. In cancer GR agonists are often tumor suppressive, likely because of downregulation of hormone signaling.…”

Section: Classical and Emerging Mechanisms Of Signalingmentioning

confidence: 99%

Whence CRIPTO: The Reemergence of an Oncofetal Factor in ‘Wounds’ That Fail to Heal

Freeman

Sousa

Karkampouna

et al. 2021

IJMS

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There exists a set of factors termed oncofetal proteins that play key roles in ontogeny before they decline or disappear as the organism’s tissues achieve homeostasis, only to then re-emerge in cancer. Although the unique therapeutic potential presented by such factors has been recognized for more than a century, their clinical utility has yet to be fully realized1. This review highlights the small signaling protein CRIPTO encoded by the tumor derived growth factor 1 (TDGF1/Tdgf1) gene, an oft cited oncofetal protein whose presence in the cancer literature as a tumor promoter, diagnostic marker and viable therapeutic target continues to grow. We touch lightly on features well established and well-reviewed since its discovery more than 30 years ago, including CRIPTO’s early developmental roles and modulation of SMAD2/3 activation by a selected set of transforming growth factor β (TGF-β) family ligands. We predominantly focus instead on more recent and less well understood additions to the CRIPTO signaling repertoire, on its potential upstream regulators and on new conceptual ground for understanding its mode of action in the multicellular and often stressful contexts of neoplastic transformation and progression. We ask whence it re-emerges in cancer and where it ‘hides’ between the time of its fetal activity and its oncogenic reemergence. In this regard, we examine CRIPTO’s restriction to rare cells in the adult, its potential for paracrine crosstalk, and its emerging role in inflammation and tissue regeneration—roles it may reprise in tumorigenesis, acting on subsets of tumor cells to foster cancer initiation and progression. We also consider critical gaps in knowledge and resources that stand between the recent, exciting momentum in the CRIPTO field and highly actionable CRIPTO manipulation for cancer therapy and beyond.

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“…There is also evidence for vertebrate‐conserved SAR in GR signaling, which guides the development of novel GCs with the goal of preventing unwanted side effects (I. H. Song, Gold, Straub, Burmester, & Buttgereit, 2005). For example, some GCs like beclomethasone dipropionate increase expression of the feto‐oncogene Cripto‐1 / Tdgf1 in embryonic mouse cells, which could perturb several developmental pathways relevant to orofacial development (Garland et al, 2019). The development of GCs with lower risk for teratogenicity would be beneficial for pregnant women, especially for those who may unexpectedly require immunosuppression in emergency situations.…”

Section: Environmental Signaling Pathways In Orofacial Cleftsmentioning

confidence: 99%

Environmental mechanisms of orofacial clefts

Garland

Reynolds

Zhou

2020

Birth Defects Research

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Orofacial clefts (OFCs) are among the most common birth defects and impart a significant burden on afflicted individuals and their families. It is increasingly understood that many nonsyndromic OFCs are a consequence of extrinsic factors, genetic susceptibilities, and interactions of the two. Therefore, understanding the environmental mechanisms of OFCs is important in the prevention of future cases. This review examines the molecular mechanisms associated with environmental factors that either protect against or increase the risk of OFCs. We focus on essential metabolic pathways, environmental signaling mechanisms, detoxification pathways, behavioral risk factors, and biological hazards that may disrupt orofacial development.

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Glucocorticoid receptor-dependent induction of cripto-1 (one-eyed pinhead) inhibits zebrafish caudal fin regeneration

Abstract: Graphical abstract

Cited by 9 publications

References 52 publications

Defining the Pluripotent Marker Genes for Identification of Teleost Fish Cell Pluripotency During Reprogramming

Defining the Pluripotent Marker Genes for Identification of Teleost Fish Cell Pluripotency During Reprogramming

Whence CRIPTO: The Reemergence of an Oncofetal Factor in ‘Wounds’ That Fail to Heal

Environmental mechanisms of orofacial clefts

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