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Journal articles on the topic 'Cell transdifferentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

OKADA, T. S. "Transdifferentiation in Animal Cells: Fact or Artifact?. (cell commitment/transdifferentiation/cell type conversion)." Development, Growth and Differentiation 28, no. 3 (May 1986): 213–21. http://dx.doi.org/10.1111/j.1440-169x.1986.00213.x.

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2

Zhao, Zhiliang, Mengyao Xu, Meng Wu, Xiaocheng Tian, Cuiping Zhang, and Xiaobing Fu. "Transdifferentiation of Fibroblasts by Defined Factors." Cellular Reprogramming 17, no. 3 (June 2015): 151–59. http://dx.doi.org/10.1089/cell.2014.0089.

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3

Maclean, Norman. "Transdifferentiation: Flexibility in cell differentiation." Trends in Biochemical Sciences 17, no. 8 (August 1992): 322. http://dx.doi.org/10.1016/0968-0004(92)90447-h.

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4

Mitashov, V. I. "Genetic Mechanisms of Cell Transdifferentiation." Russian Journal of Developmental Biology 36, no. 4 (July 2005): 240–46. http://dx.doi.org/10.1007/s11174-005-0039-1.

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5

Lee, Tsong-Hai, Pei-Shan Liu, Su-Jane Wang, Ming-Ming Tsai, Velayuthaprabhu Shanmugam, and Hsi-Lung Hsieh. "Bradykinin, as a Reprogramming Factor, Induces Transdifferentiation of Brain Astrocytes into Neuron-like Cells." Biomedicines 9, no. 8 (July 30, 2021): 923. http://dx.doi.org/10.3390/biomedicines9080923.

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Kinins are endogenous, biologically active peptides released into the plasma and tissues via the kallikrein-kinin system in several pathophysiological events. Among kinins, bradykinin (BK) is widely distributed in the periphery and brain. Several studies on the neuro-modulatory actions of BK by the B2BK receptor (B2BKR) indicate that this neuropeptide also functions during neural fate determination. Previously, BK has been shown to induce differentiation of nerve-related stem cells into neuron cells, but the response in mature brain astrocytes is unknown. Herein, we used rat brain astrocyte (RBA) to investigate the effect of BK on cell transdifferentiation into a neuron-like cell morphology. Moreover, the signaling mechanisms were explored by zymographic, RT-PCR, Western blot, and immunofluorescence staining analyses. We first observed that BK induced RBA transdifferentiation into neuron-like cells. Subsequently, we demonstrated that BK-induced RBA transdifferentiation is mediated through B2BKR, PKC-δ, ERK1/2, and MMP-9. Finally, we found that BK downregulated the astrocytic marker glial fibrillary acidic protein (GFAP) and upregulated the neuronal marker neuron-specific enolase (NSE) via the B2BKR/PKC-δ/ERK pathway in the event. Therefore, BK may be a reprogramming factor promoting brain astrocytic transdifferentiation into a neuron-like cell, including downregulation of GFAP and upregulation of NSE and MMP-9 via the B2BKR/PKC-δ/ERK cascade. Here, we also confirmed the transdifferentiative event by observing the upregulated neuronal nuclear protein (NeuN). However, the electrophysiological properties of the cells after BK treatment should be investigated in the future to confirm their phenotype.

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6

English, Denis. "Transdifferentiation Wars." Stem Cells and Development 14, no. 6 (December 2005): 605–7. http://dx.doi.org/10.1089/scd.2005.14.605.

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Eisenberg, Leonard M., and Carol A. Eisenberg. "Stem cell plasticity, cell fusion, and transdifferentiation." Birth Defects Research Part C: Embryo Today: Reviews 69, no. 3 (August 2003): 209–18. http://dx.doi.org/10.1002/bdrc.10017.

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8

Luo, Liang, Da-Hai Hu, James Q. Yin, and Ru-Xiang Xu. "Molecular Mechanisms of Transdifferentiation of Adipose-Derived Stem Cells into Neural Cells: Current Status and Perspectives." Stem Cells International 2018 (September 13, 2018): 1–14. http://dx.doi.org/10.1155/2018/5630802.

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Neurological diseases can severely compromise both physical and psychological health. Recently, adult mesenchymal stem cell- (MSC-) based cell transplantation has become a potential therapeutic strategy. However, most studies related to the transdifferentiation of MSCs into neural cells have had disappointing outcomes. Better understanding of the mechanisms underlying MSC transdifferentiation is necessary to make adult stem cells more applicable to treating neurological diseases. Several studies have focused on adipose-derived stromal/stem cell (ADSC) transdifferentiation. The purpose of this review is to outline the molecular characterization of ADSCs, to describe the methods for inducing ADSC transdifferentiation, and to examine factors influencing transdifferentiation, including transcription factors, epigenetics, and signaling pathways. Exploring and understanding the mechanisms are a precondition for developing and applying novel cell therapies.

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Huang, Shian, Xiulong Zhu, Wenjun Huang, Yuan He, Lingpin Pang, Xiaozhong Lan, Xiaorong Shui, Yanfang Chen, Can Chen, and Wei Lei. "Quercetin Inhibits Pulmonary Arterial Endothelial Cell Transdifferentiation Possibly by Akt and Erk1/2 Pathways." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/6147294.

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This study aimed to investigate the effects and mechanisms of quercetin on pulmonary arterial endothelial cell (PAEC) transdifferentiation into smooth muscle-like cells. TGF-β1-induced PAEC transdifferentiation models were applied to evaluate the pharmacological actions of quercetin. PAEC proliferation was detected with CCK8 method and BurdU immunocytochemistry. Meanwhile, the identification and transdifferentiation of PAECs were determined by FVIII immunofluorescence staining andα-SMA protein expression. The related mechanism was elucidated based on the levels of Akt and Erk1/2 signal pathways. As a result, quercetin effectively inhibited the TGF-β1-induced proliferation and transdifferentiation of the PAECs and activation of Akt/Erk1/2 cascade in the cells. In conclusion, quercetin is demonstrated to be effective for pulmonary arterial hypertension (PAH) probably by inhibiting endothelial transdifferentiation possibly via modulating Akt and Erk1/2 expressions.

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Corbett, James L., and David Tosh. "Conversion of one cell type into another: implications for understanding organ development, pathogenesis of cancer and generating cells for therapy." Biochemical Society Transactions 42, no. 3 (May 22, 2014): 609–16. http://dx.doi.org/10.1042/bst20140058.

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Metaplasia is the irreversible conversion of one differentiated cell or tissue type into another. Metaplasia usually occurs in tissues that undergo regeneration, and may, in a pathological context, predispose to an increased risk of disease. Studying the conditions leading to the development of metaplasia is therefore of significant clinical interest. In contrast, transdifferentiation (or cellular reprogramming) is a subset of metaplasia that describes the permanent conversion of one differentiated cell type into another, and generally occurs between cells that arise from neighbouring regions of the same germ layer. Transdifferentiation, although rare, has been shown to occur in Nature. New insights into the signalling pathways involved in normal tissue development may be obtained by investigating the cellular and molecular mechanisms in metaplasia and transdifferentiation, and additional identification of key molecular regulators in transdifferentiation and metaplasia could provide new targets for therapeutic treatment of diseases such as cancer, as well as generating cells for transplantation into patients with degenerative disorders. In the present review, we focus on the transdifferentiation of pancreatic cells into hepatocyte-like cells, the development of Barrett's metaplasia in the oesophagus, and the cellular and molecular mechanisms underlying both processes.

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11

Rogers, Ian. "Transdifferentiation of endogenous cells: Cell therapy without the cells." Cell Cycle 8, no. 24 (December 15, 2009): 4023–28. http://dx.doi.org/10.4161/cc.8.24.10512.

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12

Moimas, Silvia, Francesco Salton, Beata Kosmider, Nadja Ring, Maria C. Volpe, Karim Bahmed, Luca Braga, et al. "miR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation." ERJ Open Research 5, no. 4 (October 2019): 00138–2019. http://dx.doi.org/10.1183/23120541.00138-2019.

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RationaleAlveolar type II (ATII) cells act as adult stem cells contributing to alveolar type I (ATI) cell renewal and play a major role in idiopathic pulmonary fibrosis (IPF), as supported by familial cases harbouring mutations in genes specifically expressed by these cells. During IPF, ATII cells lose their regenerative potential and aberrantly express pathways contributing to epithelial–mesenchymal transition (EMT). The microRNA miR-200 family is downregulated in IPF, but its effect on human IPF ATII cells remains unproven. We wanted to 1) evaluate the characteristics and transdifferentiating ability of IPF ATII cells, and 2) test whether miR-200 family members can rescue the regenerative potential of fibrotic ATII cells.MethodsATII cells were isolated from control or IPF lungs and cultured in conditions promoting their transdifferentiation into ATI cells. Cells were either phenotypically monitored over time or transfected with miR-200 family members to evaluate the microRNA effect on the expression of transdifferentiation, senescence and EMT markers.ResultsIPF ATII cells show a senescent phenotype (p16 and p21), overexpression of EMT (ZEB1/2) and impaired expression of ATI cell markers (AQP5 and HOPX) after 6 days of culture in differentiating medium. Transfection with certain miR-200 family members (particularly miR-200b-3p and miR-200c-3p) reduced senescence marker expression and restored the ability to transdifferentiate into ATI cells.ConclusionsWe demonstrated that ATII cells from IPF patients express senescence and EMT markers, and display a reduced ability to transdifferentiate into ATI cells. Transfection with certain miR-200 family members rescues this phenotype, reducing senescence and restoring transdifferentiation marker expression.

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13

Wells, William A. "Is transdifferentiation in trouble?" Journal of Cell Biology 157, no. 1 (March 26, 2002): 15–18. http://dx.doi.org/10.1083/jcb.200203037.

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Spectacular examples of transdifferentiation—such as brain cells turning to blood and blood to brain—have given way to sneaking suspicions about artifacts in culture, fusion, and clonality. Could cell fates be relatively fixed after all?

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14

Slack, Jonathan M. W., and David Tosh. "Transdifferentiation and metaplasia — switching cell types." Current Opinion in Genetics & Development 11, no. 5 (October 2001): 581–86. http://dx.doi.org/10.1016/s0959-437x(00)00236-7.

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15

Lipton, Bruce H., Klaus G. Bensch, and Marvin A. Karasek. "Microvessel endothelial cell transdifferentiation: phenotypic characterization." Differentiation 46, no. 2 (March 1991): 117–33. http://dx.doi.org/10.1111/j.1432-0436.1991.tb00872.x.

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16

Purnell, B. A. "Epigenetics Direct Transdifferentiation." Science Signaling 7, no. 339 (August 19, 2014): ec222-ec222. http://dx.doi.org/10.1126/scisignal.2005804.

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17

Cordeiro-Rudnisky, Fernanda, Yue Sun, and Rayan Saade. "Prostate Carcinoma With Overlapping Features of Small Cell and Acinar Adenocarcinoma: A Case Report." American Journal of Clinical Pathology 152, Supplement_1 (September 11, 2019): S66—S67. http://dx.doi.org/10.1093/ajcp/aqz113.072.

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Abstract Introduction Prostate neuroendocrine (NE) cells can stimulate prostate adenocarcinoma (PA) cell growth, but occasionally adenocarcinoma cells themselves acquire NE characteristics, a phenomenon known as NE transdifferentiation of prostate adenocarcinoma. During this process, tumor cells acquire small cell-like morphology and become positive for neuroendocrine markers. NE transdifferentiation is associated with decreased androgen receptor (AR) signaling, a mechanism of resistance to AR-targeted treatments. Case A 74-year-old male with a history of cirrhosis, splenomegaly, and thrombocytopenia presented with hematuria and urinary obstruction. PSA was 0.31 ng/mL. CT scan demonstrated bladder wall thickening. Surgery showed a bladder tumor, clinically diagnosed as urothelial tumor. Pathology revealed a poorly differentiated carcinoma, with small cell-like morphology. The tumor cells had high nuclear to cytoplasmic ratio, focal nuclear molding, and high mitotic rate, like small cell carcinoma. But the nucleoli were intermediate between small cell carcinoma and usual adenocarcinoma of the prostate. Immunostains showed that the tumor cells were positive for NKX3.1 and focally positive for NE markers, including chromogranin, synaptophysin, INSM1, and FOXA2. The tumor cells were negative for PSA and GATA3. The morphology and immunoprofile are consistent with Gleason pattern 5 PA in transdifferentiation to small cell carcinoma. Discussion The incidence of neuroendocrine phenotype is 1% in primary PA and 25% in metastatic castrate-resistant PA. Typically, NE transdifferentiation occurs in response to androgen deprivation therapy/AR inhibitors. Pretreatment NE transdifferentiation is relatively uncommon. PA depends on androgens for its progression, which is the basis for antiandrogen therapy. Decreased AR expression associated with NE transdifferentiation is a mechanism of resistance to AR-targeted therapy. These tumors are often more aggressive with worse prognosis. Conclusion Our patient has Gleason pattern 5 PA with NE transdifferentiation invading the bladder, which is a high-grade, aggressive tumor.

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Xie, Chao, William Donelan, Shun Lu, and Li Jun Yang. "Developing a Sensitive Reporter System for Monitoring of Pancreatic and Duodenal Homeobox Gene 1 (Pdx1) and Neurogenin 3 (Ngn3) – Mediated Transdifferentiation from Human Hepatic Cells into Insulin-Producing Beta-Like Cells." Advanced Materials Research 989-994 (July 2014): 1003–6. http://dx.doi.org/10.4028/www.scientific.net/amr.989-994.1003.

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It is well known that cellular differentiation is not a terminal process. Transdifferentiation is the conversion of one differentiated cell type to another. There are many examples of induced transdifferentiation between cell types by expression of ectopic transcription factors. Here we show that combined lentiviral expression of Pdx1 or Pdx1-VP16 fusion protein and Ngn3 can direct the transdifferentiation of hepatic cells into insulin producing cells. We showed that the Pdx1 or Pdx1-VP16 fusion protein and Ngn3 together synergistically increased transactivation for the insulin gene. This provides a useful model to study the transdifferentiation process.

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19

Chua, Shawn J., Robert F. Casper, and Ian M. Rogers. "Toward Transgene-Free Induced Pluripotent Stem Cells: Lessons from Transdifferentiation Studies." Cellular Reprogramming 13, no. 4 (August 2011): 273–80. http://dx.doi.org/10.1089/cell.2010.0108.

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20

Kaur, Keerat, Jinpu Yang, Carol A. Eisenberg, and Leonard M. Eisenberg. "5-Azacytidine Promotes the Transdifferentiation of Cardiac Cells to Skeletal Myocytes." Cellular Reprogramming 16, no. 5 (October 2014): 324–30. http://dx.doi.org/10.1089/cell.2014.0021.

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21

Yuan, Zhao-Di, Wei-Ning Zhu, Ke-Zhi Liu, Zhan-Peng Huang, and Yan-Chuang Han. "Small Molecule Epigenetic Modulators in Pure Chemical Cell Fate Conversion." Stem Cells International 2020 (October 20, 2020): 1–12. http://dx.doi.org/10.1155/2020/8890917.

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Although innovative technologies for somatic cell reprogramming and transdifferentiation provide new strategies for the research of translational medicine, including disease modeling, drug screening, artificial organ development, and cell therapy, recipient safety remains a concern due to the use of exogenous transcription factors during induction. To resolve this problem, new induction approaches containing clinically applicable small molecules have been explored. Small molecule epigenetic modulators such as DNA methylation writer inhibitors, histone methylation writer inhibitors, histone acylation reader inhibitors, and histone acetylation eraser inhibitors could overcome epigenetic barriers during cell fate conversion. In the past few years, significant progress has been made in reprogramming and transdifferentiation of somatic cells with small molecule approaches. In the present review, we systematically discuss recent achievements of pure chemical reprogramming and transdifferentiation.

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22

Perán, Macarena, Juan Antonio Marchal, Fernando Rodríguez‑Serrano, Pablo Álvarez, and Antonia Aránega. "Transdifferentiation: why and how?" Cell Biology International 35, no. 4 (March 2, 2011): 373–79. http://dx.doi.org/10.1042/cbi20100445.

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23

Miettinen, P. J., R. Ebner, A. R. Lopez, and R. Derynck. "TGF-beta induced transdifferentiation of mammary epithelial cells to mesenchymal cells: involvement of type I receptors." Journal of Cell Biology 127, no. 6 (December 15, 1994): 2021–36. http://dx.doi.org/10.1083/jcb.127.6.2021.

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The secreted polypeptide transforming growth factor-beta (TGF-beta) exerts its multiple activities through type I and II cell surface receptors. In epithelial cells, activation of the TGF-beta signal transduction pathways leads to inhibition of cell proliferation and an increase in extracellular matrix production. TGF-beta is widely expressed during development and its biological activity has been implicated in epithelial-mesenchymal interactions, e.g., in branching morphogenesis of the lung, kidney, and mammary gland, and in inductive events between mammary epithelium and stroma. In the present study, we investigated the effects of TGF-beta on mouse mammary epithelial cells in vitro. TGF-beta reversibly induced an alteration in the differentiation of normal mammary epithelial NMuMG cells from epithelial to fibroblastic phenotype. The change in cell morphology correlated with (a) decreased expression of the epithelial markers E-cadherin, ZO-1, and desmoplakin I and II; (b) increased expression of mesenchymal markers, such as fibronectin; and (c) a fibroblast-like reorganization of actin fibers. This phenotypic differentiation displays the hallmarks of an epithelial to mesenchymal transdifferentiation event. Since NMuMG cells make high levels of the type I TGF-beta receptor Tsk7L, yet lack expression of the ALK-5/R4 type I receptor which has been reported to mediate TGF-beta responsiveness, we evaluated the role of the Tsk7L receptor in TGF-beta-mediated transdifferentiation. We generated NMuMG cells that stably overexpress a truncated Tsk7L type I receptor that lacks most of the cytoplasmic kinase domain, thus function as a dominant negative mutant. These transfected cells no longer underwent epithelial to mesenchymal morphological change upon exposure to TGF-beta, yet still displayed some TGF-beta-mediated responses. We conclude that TGF-beta has the ability to modulate E-cadherin expression and induce a reversible epithelial to mesenchymal transdifferentiation in epithelial cells. Unlike other transdifferentiating growth factors, such as bFGF and HGF, these changes are accompanied by growth inhibition. Our results also implicate the Tsk7L type I receptor as mediating the TGF-beta-induced epithelial to mesenchymal transition.

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Ha, Seon-Ah, Hyun K. Kim, JinAh Yoo, SangHee Kim, Seung M. Shin, Youn S. Lee, Soo Y. Hur, et al. "Transdifferentiation-inducing HCCR-1 oncogene." BMC Cell Biology 11, no. 1 (2010): 49. http://dx.doi.org/10.1186/1471-2121-11-49.

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25

Di Tullio, Alessandro, and Thomas Graf. "C/EBPαbypasses cell cycle-dependency during immune cell transdifferentiation." Cell Cycle 11, no. 14 (January 15, 2012): 2739–46. http://dx.doi.org/10.4161/cc.21119.

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26

Grove, Lisa M., Maradumane L. Mohan, Susamma Abraham, Rachel G. Scheraga, Brian D. Southern, James F. Crish, Sathyamangla V. Naga Prasad, and Mitchell A. Olman. "Translocation of TRPV4-PI3Kγ complexes to the plasma membrane drives myofibroblast transdifferentiation." Science Signaling 12, no. 607 (November 12, 2019): eaau1533. http://dx.doi.org/10.1126/scisignal.aau1533.

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Myofibroblasts are key contributors to pathological fibrotic conditions of several major organs. The transdifferentiation of fibroblasts into myofibroblasts requires both a mechanical signal and transforming growth factor–β (TGF-β) signaling. The cation channel transient receptor potential vanilloid 4 (TRPV4) is a critical mediator of myofibroblast transdifferentiation and in vivo fibrosis through its mechanosensitivity to extracellular matrix stiffness. Here, we showed that TRPV4 promoted the transdifferentiation of human and mouse lung fibroblasts through its interaction with phosphoinositide 3-kinase γ (PI3Kγ), forming nanomolar-affinity, intracellular TRPV4-PI3Kγ complexes. TGF-β induced the recruitment of TRPV4-PI3Kγ complexes to the plasma membrane and increased the activities of both TRPV4 and PI3Kγ. Using gain- and loss-of-function approaches, we showed that both TRPV4 and PI3Kγ were required for myofibroblast transdifferentiation as assessed by the increased production of α-smooth muscle actin and its incorporation into stress fibers, cytoskeletal changes, collagen-1 production, and contractile force. Expression of various mutant forms of the PI3Kγ catalytic subunit (p110γ) in cells lacking PI3Kγ revealed that only the noncatalytic, amino-terminal domain of p110γ was necessary and sufficient for TGF-β–induced TRPV4 plasma membrane recruitment and myofibroblast transdifferentiation. These data suggest that TGF-β stimulates a noncanonical scaffolding action of PI3Kγ, which recruits TRPV4-PI3Kγ complexes to the plasma membrane, thereby increasing myofibroblast transdifferentiation. Given that both TRPV4 and PI3Kγ have pleiotropic actions, targeting the interaction between them could provide a specific therapeutic approach for inhibiting myofibroblast transdifferentiation.

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Krishnamurthy, Akilan, A. Jimmy Ytterberg, Meng Sun, Koji Sakuraba, Johanna Steen, Vijay Joshua, Nataliya K. Tarasova, et al. "Citrullination Controls Dendritic Cell Transdifferentiation into Osteoclasts." Journal of Immunology 202, no. 11 (April 24, 2019): 3143–50. http://dx.doi.org/10.4049/jimmunol.1800534.

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28

Beresford, William A. "Transdifferentiation: Flexibility in Cell Differentiation.T. S. Okada." Quarterly Review of Biology 68, no. 1 (March 1993): 110–11. http://dx.doi.org/10.1086/417954.

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29

Xie, Xin, Chenwen Huang, Yanbin Fu, Long Yuan, and Quan Wang. "Chemical-Mediated Somatic Cell Reprogramming and Transdifferentiation." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): OR19–1. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_or19-1.

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30

Cantaluppi, Vincenzo, Stefania Bruno, and Giovanni Camussi. "Pancreatic ductal transdifferentiation for β-cell neogenesis." Expert Opinion on Therapeutic Patents 18, no. 8 (August 2008): 963–67. http://dx.doi.org/10.1517/13543776.18.8.963.

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31

Yi, Fei, Guang-Hui Liu, and Juan Carlos Izpisua Belmonte. "Rejuvenating liver and pancreas through cell transdifferentiation." Cell Research 22, no. 4 (February 28, 2012): 616–19. http://dx.doi.org/10.1038/cr.2012.33.

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32

Sisakhtnezhad, Sajjad, and Maryam M. Matin. "Transdifferentiation: a cell and molecular reprogramming process." Cell and Tissue Research 348, no. 3 (April 25, 2012): 379–96. http://dx.doi.org/10.1007/s00441-012-1403-y.

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Yan, Jiawei, Ruoning Wang, and Tiffany Horng. "mTOR Is Key to T Cell Transdifferentiation." Cell Metabolism 29, no. 2 (February 2019): 241–42. http://dx.doi.org/10.1016/j.cmet.2019.01.008.

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34

Kalra, Rajkumar Singh, Jaspreet Kaur Dhanjal, Mriganko Das, Birbal Singh, and Rajesh Naithani. "Cell Transdifferentiation and Reprogramming in Disease Modeling: Insights into the Neuronal and Cardiac Disease Models and Current Translational Strategies." Cells 10, no. 10 (September 27, 2021): 2558. http://dx.doi.org/10.3390/cells10102558.

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Cell transdifferentiation and reprogramming approaches in recent times have enabled the manipulation of cell fate by enrolling exogenous/artificial controls. The chemical/small molecule and regulatory components of transcription machinery serve as potential tools to execute cell transdifferentiation and have thereby uncovered new avenues for disease modeling and drug discovery. At the advanced stage, one can believe these methods can pave the way to develop efficient and sensitive gene therapy and regenerative medicine approaches. As we are beginning to learn about the utility of cell transdifferentiation and reprogramming, speculations about its applications in translational therapeutics are being largely anticipated. Although clinicians and researchers are endeavoring to scale these processes, we lack a comprehensive understanding of their mechanism(s), and the promises these offer for targeted and personalized therapeutics are scarce. In the present report, we endeavored to provide a detailed review of the original concept, methods and modalities enrolled in the field of cellular transdifferentiation and reprogramming. A special focus is given to the neuronal and cardiac systems/diseases towards scaling their utility in disease modeling and drug discovery.

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O'Neill, Kathy E., Shifaan Thowfeequ, Wan-Chun Li, Daniel Eberhard, James R. Dutton, David Tosh, and Jonathan M. W. Slack. "Hepatocyte-Ductal Transdifferentiation Is Mediated by Reciprocal Repression of SOX9 and C/EBPα." Cellular Reprogramming 16, no. 5 (October 2014): 314–23. http://dx.doi.org/10.1089/cell.2014.0032.

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36

Feng, Jian. "Kinetic barriers in transdifferentiation." Cell Cycle 15, no. 8 (February 22, 2016): 1019–20. http://dx.doi.org/10.1080/15384101.2016.1151730.

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37

Keilhoff, Gerburg, Alexander Goihl, Kristina Langnäse, Hisham Fansa, and Gerald Wolf. "Transdifferentiation of mesenchymal stem cells into Schwann cell-like myelinating cells." European Journal of Cell Biology 85, no. 1 (January 2006): 11–24. http://dx.doi.org/10.1016/j.ejcb.2005.09.021.

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38

Li, Wan-Chun, Wei-Yuan Yu, Jonathan M. Quinlan, Zoë D. Burke, and David Tosh. "The molecular basis of transdifferentiation." Journal of Cellular and Molecular Medicine 9, no. 3 (July 2005): 569–82. http://dx.doi.org/10.1111/j.1582-4934.2005.tb00489.x.

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Fu, Lina, Xiping Zhu, Fei Yi, Guang-Hui Liu, and Juan Carlos Izpisua Belmonte. "Regenerative medicine: Transdifferentiation in vivo." Cell Research 24, no. 2 (December 17, 2013): 141–42. http://dx.doi.org/10.1038/cr.2013.165.

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40

Zhang, Jingxue, Shen Wu, Zi-Bing Jin, and Ningli Wang. "Stem Cell-Based Regeneration and Restoration for Retinal Ganglion Cell: Recent Advancements and Current Challenges." Biomolecules 11, no. 7 (July 5, 2021): 987. http://dx.doi.org/10.3390/biom11070987.

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Glaucoma is a group of irreversible blinding eye diseases characterized by the progressive loss of retinal ganglion cells (RGCs) and their axons. Currently, there is no effective method to fundamentally resolve the issue of RGC degeneration. Recent advances have revealed that visual function recovery could be achieved with stem cell-based therapy by replacing damaged RGCs with cell transplantation, providing nutritional factors for damaged RGCs, and supplying healthy mitochondria and other cellular components to exert neuroprotective effects and mediate transdifferentiation of autologous retinal stem cells to accomplish endogenous regeneration of RGC. This article reviews the recent research progress in the above-mentioned fields, including the breakthroughs in the fields of in vivo transdifferentiation of retinal endogenous stem cells and reversal of the RGC aging phenotype, and discusses the obstacles in the clinical translation of the stem cell therapy.

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Zhao, Lan, Min Yee, and Michael A. O'Reilly. "Transdifferentiation of alveolar epithelial type II to type I cells is controlled by opposing TGF-β and BMP signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 6 (September 15, 2013): L409—L418. http://dx.doi.org/10.1152/ajplung.00032.2013.

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Alveolar epithelial type II (ATII) cells are essential for maintaining normal lung homeostasis because they produce surfactant, express innate immune proteins, and can function as progenitors for alveolar epithelial type I (ATI) cells. Although autocrine production of transforming growth factor (TGF)-β1 has been shown to promote the transdifferentiation of primary rat ATII to ATI cells in vitro, mechanisms controlling this process still remain poorly defined. Here, evidence is provided that Tgf-β1, - 2, - 3 mRNA and phosphorylated SMAD2 and SMAD3 significantly increase as primary cultures of mouse ATII cells transdifferentiate to ATI cells. Concomitantly, bone morphogenetic protein ( Bmp)-2 and -4 mRNA, and phosphorylated SMAD1/5/8 expression decrease. Exogenously supplied recombinant human TGF-β1 inhibited BMP signaling and enhanced transdifferentiation by promoting the loss of ATII cell-specific gene expression and weakly stimulating ATI cell-specific gene expression. On the other hand, exogenously supplied recombinant human BMP-4 inhibited TGF-β signaling and delayed transdifferentiation by inhibiting the gain in ATI cell-specific gene expression and weakly delaying the loss of ATII cell-specific gene expression. In mouse lung epithelial (MLE15) cells, small-interfering RNA (siRNA) knockdown of TGF-β receptor type-1 enhanced basal expression of ATII genes while siRNA RNA knockdown of BMP receptors type-1a and -1b enhanced basal expression of ATI genes. Together, these results suggest that the rate of ATII cell transdifferentiation is controlled by the opposing actions of BMP and TGF-β signaling that switch during the process of transdifferentiation.

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Huang, Gui-Lin, Ni-Ni Zhang, Jun-Sheng Wang, Li Yao, Yu-Jie Zhao, and Yu-Ying Wang. "Transdifferentiation of Human Amniotic Epithelial Cells into Acinar Cells Using a Double-Chamber System." Cellular Reprogramming 14, no. 4 (August 2012): 377–83. http://dx.doi.org/10.1089/cell.2011.0096.

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Zhang, Nian, Liru Hu, Jiyuan Liu, Wenbin Yang, Ye Li, and Jian Pan. "Wnt Signaling Regulates the Lymphatic Endothelial Transdifferentiation of Adipose-Derived Stromal Cells In Vitro." Cellular Reprogramming 23, no. 2 (April 1, 2021): 117–26. http://dx.doi.org/10.1089/cell.2020.0058.

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Kim, Seung Hyun L., Seunghun S. Lee, Inseon Kim, Janet Kwon, Song Kwon, Taegeun Bae, Junho Hur, Hwajin Lee, and Nathaniel S. Hwang. "Ectopic transient overexpression of OCT-4 facilitates BMP4-induced osteogenic transdifferentiation of human umbilical vein endothelial cells." Journal of Tissue Engineering 11 (January 2020): 204173142090920. http://dx.doi.org/10.1177/2041731420909208.

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Limitation in cell sources for autologous cell therapy has been a recent focus in stem cell therapy and tissue engineering. Among various research advances, direct conversion, or transdifferentiation, is a notable and feasible strategy for the generation and acquirement of wanted cell source. So far, utilizing cell transdifferentiation technology in tissue engineering was mainly restricted at achieving single wanted cell type from diverse cell types with high efficiency. However, regeneration of a complete tissue always requires multiple cell types which poses an intrinsic complexity. In this study, enhanced osteogenic differentiation was achieved by transient ectopic expression of octamer-binding transcription factor 4 ( OCT-4) gene followed by bone morphogenetic protein 4 treatment on human umbilical vein endothelial cells. OCT-4 transfection and bone morphogenetic protein 4 treatment resulted in enhanced expression of osteogenic markers such as core-binding factor alpha 1, alkaline phosphatase, and collagen 1 compared with bone morphogenetic protein 4 treatment alone. Furthermore, we employed gelatin-heparin cryogel in cranial defect model for in vivo bone formation. Micro-computed tomography and histological analysis of in vivo samples showed that OCT-4 transfection followed by bone morphogenetic protein 4 treatment resulted in efficient transdifferentiation of endothelial cells to osteogenic cells. These results suggest that the combination of OCT-4 and bone morphogenetic protein 4 on endothelial cells would be a reliable multicellular transdifferentiation model which could be applied for bone tissue engineering.

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Wild, Sebastian L., and David Tosh. "Molecular mechanisms of transcription factor mediated cell reprogramming: conversion of liver to pancreas." Biochemical Society Transactions 49, no. 2 (March 5, 2021): 579–90. http://dx.doi.org/10.1042/bst20200219.

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Transdifferentiation is a type of cellular reprogramming involving the conversion of one differentiated cell type to another. This remarkable phenomenon holds enormous promise for the field of regenerative medicine. Over the last 20 years techniques used to reprogram cells to alternative identities have advanced dramatically. Cellular identity is determined by the transcriptional profile which comprises the subset of mRNAs, and therefore proteins, being expressed by a cell at a given point in time. A better understanding of the levers governing transcription factor activity benefits our ability to generate therapeutic cell types at will. One well-established example of transdifferentiation is the conversion of hepatocytes to pancreatic β-cells. This cell type conversion potentially represents a novel therapy in T1D treatment. The identification of key master regulator transcription factors (which distinguish one body part from another) during embryonic development has been central in developing transdifferentiation protocols. Pdx1 is one such example of a master regulator. Ectopic expression of vector-delivered transcription factors (particularly the triumvirate of Pdx1, Ngn3 and MafA) induces reprogramming through broad transcriptional remodelling. Increasingly, complimentary cell culture techniques, which recapitulate the developmental microenvironment, are employed to coax cells to adopt new identities by indirectly regulating transcription factor activity via intracellular signalling pathways. Both transcription factor-based reprogramming and directed differentiation approaches ultimately exploit transcription factors to influence cellular identity. Here, we explore the evolution of reprogramming and directed differentiation approaches within the context of hepatocyte to β-cell transdifferentiation focussing on how the introduction of new techniques has improved our ability to generate β-cells.

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Minami, Kohtaro. "Pancreatic acinar-to-beta cell transdifferentiation in vitro." Frontiers in Bioscience Volume, no. 13 (2008): 5824. http://dx.doi.org/10.2741/3119.

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Sharma, Anup D., Jayme Wiederin, Metin Uz, Pawel Ciborowski, Surya K. Mallapragada, Howard E. Gendelman, and Donald S. Sakaguchi. "Proteomic analysis of mesenchymal to Schwann cell transdifferentiation." Journal of Proteomics 165 (August 2017): 93–101. http://dx.doi.org/10.1016/j.jprot.2017.06.011.

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SHE, H., S. HAZRA, S. XIONG, J. WANG, C. SUNG, and H. TSUKAMOTO. "211 Adipogenic regulation of hepatic stellate cell transdifferentiation." Hepatology 38 (2003): 258. http://dx.doi.org/10.1016/s0270-9139(03)80254-9.

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Ibrahim, Michael, and Pavan Atluri. "Transdifferentiation: A new frontier in cardiovascular cell therapy." Journal of Thoracic and Cardiovascular Surgery 153, no. 1 (January 2017): 130–31. http://dx.doi.org/10.1016/j.jtcvs.2016.09.007.

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Mann, D. A., and J. Mann. "479 EPIGENETIC REGULATION OF HEPATIC STELLATE CELL TRANSDIFFERENTIATION." Journal of Hepatology 48 (January 2008): S182. http://dx.doi.org/10.1016/s0168-8278(08)60481-x.

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