Molecular mechanisms of Sox transcription factors during the development of liver, bile duct, and pancreas

Yin, Chunyue

doi:10.1016/j.semcdb.2016.08.015

Cited by 38 publications

(23 citation statements)

References 106 publications

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“…Moreover, the implanted human cells successfully recruited tunica external and media cells from the mouse body to form a mature vasculature structure, as evidenced by IF staining for human CD31 (endothelial layer, internal), anti‐mouse α‐SMA (smooth muscle cells, middle), and anti‐mouse vimentin (connective tissue, external; Figure h). Besides, the transcriptional levels of both Lgr5+/PRMT and Sox9/GATA4, which are important genes during intestinal and hepatic epithelium generation, were up‐regulated as Caco2 and Hep G2 grew. Similarly, early neurogenic markers, such as Fgf5 for primitive ectoderm and Sox1 for neuroectoderm, were expressed along the cultivation of SH‐SY5Y in THAG.…”

Section: Resultsmentioning

confidence: 99%

Engineering a Tumor Microenvironment‐Mimetic Niche for Tissue Regeneration with Xenogeneic Cancer Cells

Wang

Abudukeremu

et al. 2018

Advanced Science

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The insufficient number of cells suitable for transplantation is a long‐standing problem to cell‐based therapies aimed at tissue regeneration. Xenogeneic cancer cells (XCC) may be an alternative source of therapeutic cells, but their transplantation risks both immune rejection and unwanted spreading. In this study, a strategy to facilitate XCC transplantation is reported and their spreading in vivo is confined by constructing an engineering matrix that mimics the characteristics of tumor microenvironment. The data show that this matrix, a tumor homogenate‐containing hydrogel (THAG), successfully creates an immunosuppressive enclave after transplantation into immunocompetent mice. XCC of different species and tissue origins seeded into THAG survive well, integrated with the host and developed the intrinsic morphology of the native tissue, without being eliminated or spreading out of the enclave. Most strikingly, immortalized human hepatocyte cells and rat β‐cells loaded into THAG exert the physiological functions of the human liver and rat pancreas islets, respectively, in the mouse body. This study demonstrates a novel and feasible approach to harness the unique features of tumor development for tissue transplantation and regenerative medicine.

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Section: Resultsmentioning

confidence: 99%

Engineering a Tumor Microenvironment‐Mimetic Niche for Tissue Regeneration with Xenogeneic Cancer Cells

Wang

Abudukeremu

et al. 2018

Advanced Science

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“…For instance, we observed PCB126-induced hypermethylation of sox9a and sox9b genes , which encode transcription factors critical for normal development. In mammals, SOX9 is responsible for maintaining homeostasis in the liver and the regenerative capacity is dependent on SOX9-positive hepatic progenitor cells [ 47 ]. Similarly, in the zebrafish regeneration model, ablation of hepatocytes causes transdifferentiation of biliary cells into hepatocytes and this process is blocked in sox9b mutants [ 48 ], suggesting an important role in liver regeneration.…”

Section: Discussionmentioning

confidence: 99%

Role of DNA methylation in altered gene expression patterns in adult zebrafish (Danio rerio) exposed to 3, 3’, 4, 4’, 5-pentachlorobiphenyl (PCB 126)

Aluru

Karchner

Krick

et al. 2018

Environmental Epigenetics

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There is growing evidence that environmental toxicants can affect various physiological processes by altering DNA methylation patterns. However, very little is known about the impact of toxicant-induced DNA methylation changes on gene expression patterns. The objective of this study was to determine the genome-wide changes in DNA methylation concomitant with altered gene expression patterns in response to 3, 3’, 4, 4’, 5-pentachlorobiphenyl (PCB126) exposure. We used PCB126 as a model environmental chemical because the mechanism of action is well-characterized, involving activation of aryl hydrocarbon receptor, a ligand-activated transcription factor. Adult zebrafish were exposed to 10 nM PCB126 for 24 h (water-borne exposure) and brain and liver tissues were sampled at 7 days post-exposure in order to capture both primary and secondary changes in DNA methylation and gene expression. We used enhanced Reduced Representation Bisulfite Sequencing and RNAseq to quantify DNA methylation and gene expression, respectively. Enhanced reduced representation bisulfite sequencing analysis revealed 573 and 481 differentially methylated regions in the liver and brain, respectively. Most of the differentially methylated regions are located more than 10 kilobases upstream of transcriptional start sites of the nearest neighboring genes. Gene Ontology analysis of these genes showed that they belong to diverse physiological pathways including development, metabolic processes and regeneration. RNAseq results revealed differential expression of genes related to xenobiotic metabolism, oxidative stress and energy metabolism in response to polychlorinated biphenyl exposure. There was very little correlation between differentially methylated regions and differentially expressed genes suggesting that the relationship between methylation and gene expression is dynamic and complex, involving multiple layers of regulation.

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“…SOX9 has been implicated in control of liver progenitor cells and organ development [236]. A recent study reported that leptin stimulates SOX9 expression, and SOX9 suppresses PPARγ expression by binding to its promoter region to stimulate HSC activation [237].…”

Section: Mechanisms Of Hsc Activationmentioning

confidence: 99%

Hepatic stellate cells as key target in liver fibrosis

Higashi

Friedman

Hoshida

2017

Advanced Drug Delivery Reviews

1,085

894

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Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or “activation”) of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation. Dysregulated intracellular signaling, epigenetic changes, and cellular stress response represent candidate targets to deactivate stellate cells by inducing reversion to inactivated state, cellular senescence, apoptosis, and/or clearance by immune cells. Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation will enable more effective and less toxic precision antifibrotic therapies.

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Molecular mechanisms of Sox transcription factors during the development of liver, bile duct, and pancreas

Cited by 38 publications

References 106 publications

Engineering a Tumor Microenvironment‐Mimetic Niche for Tissue Regeneration with Xenogeneic Cancer Cells

Engineering a Tumor Microenvironment‐Mimetic Niche for Tissue Regeneration with Xenogeneic Cancer Cells

Role of DNA methylation in altered gene expression patterns in adult zebrafish (Danio rerio) exposed to 3, 3’, 4, 4’, 5-pentachlorobiphenyl (PCB 126)

Hepatic stellate cells as key target in liver fibrosis

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