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Journal articles on the topic 'Cell differentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2024

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1

J, Otsuka. "A Theoretical Study on the Cell Differentiation Forming Stem Cells in Higher Animals." Physical Science & Biophysics Journal 5, no. 2 (2021): 1–10. http://dx.doi.org/10.23880/psbj-16000191.

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The recent genome sequencing of multicellular diploid eukaryotes reveals an enlarged repertoire of protein genes for signal transmission but it is still difficult to elucidate the network of signal transmission to drive the life cycle of such an eukaryote only from biochemical and genetic studies. In the present paper, a theoretical study is carried out for the cell differentiation, the formation of stem cells and the growth from a child to the adult in the higher animal. With the intercellular and intracellular signal transmission in mind, the cell differentiation is theoretically derived from the process by the transition of proliferated cells from proliferation mode to differentiation mode and by both the long-range interaction between distinctive types of cells and the short-range interaction between the same types of cells. As the hierarchy of cell differentiation is advanced, the original types of self-reproducible cells are replaced by the self-reproducible cells returned from the cells differentiated already. The latter type of self-reproducible cells are marked with the signal specific to the preceding differentiation and become the stem cells for the next stage of cell differentiation. This situation is realized under the condition that the differentiation of cells occurs immediately after their proliferation in the development. The presence of stem cells in the respective lineages of differentiated cells strongly suggests another signal transmission for the growth of a child to a definite size of adult that the proliferation of stem cells in one lineage is activated by the signal from the differentiated cells in the other lineage(s) and is suppressed by the signal from the differentiated cells in its own lineage. This style of signal transmission also explains the metamorphosis and maturation of germ cells in higher animals.

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2

Zhang, Yu, Patrick Babczyk, Andreas Pansky, Matthias Ulrich Kassack, and Edda Tobiasch. "P2 Receptors Influence hMSCs Differentiation towards Endothelial Cell and Smooth Muscle Cell Lineages." International Journal of Molecular Sciences 21, no. 17 (August 27, 2020): 6210. http://dx.doi.org/10.3390/ijms21176210.

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Background: Human mesenchymal stem cells (hMSCs) have shown their multipotential including differentiating towards endothelial and smooth muscle cell lineages, which triggers a new interest for using hMSCs as a putative source for cardiovascular regenerative medicine. Our recent publication has shown for the first time that purinergic 2 receptors are key players during hMSC differentiation towards adipocytes and osteoblasts. Purinergic 2 receptors play an important role in cardiovascular function when they bind to extracellular nucleotides. In this study, the possible functional role of purinergic 2 receptors during MSC endothelial and smooth muscle differentiation was investigated. Methods and Results: Human MSCs were isolated from liposuction materials. Then, endothelial and smooth muscle-like cells were differentiated and characterized by specific markers via Reverse Transcriptase-PCR (RT-PCR), Western blot and immunochemical stainings. Interestingly, some purinergic 2 receptor subtypes were found to be differently regulated during these specific lineage commitments: P2Y4 and P2Y14 were involved in the early stage commitment while P2Y1 was the key player in controlling MSC differentiation towards either endothelial or smooth muscle cells. The administration of natural and artificial purinergic 2 receptor agonists and antagonists had a direct influence on these differentiations. Moreover, a feedback loop via exogenous extracellular nucleotides on these particular differentiations was shown by apyrase digest. Conclusions: Purinergic 2 receptors play a crucial role during the differentiation towards endothelial and smooth muscle cell lineages. Some highly selective and potent artificial purinergic 2 ligands can control hMSC differentiation, which might improve the use of adult stem cells in cardiovascular tissue engineering in the future.

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3

Fuchs, Elaine, and Eric Olson. "Cell differentiation." Current Opinion in Cell Biology 8, no. 6 (December 1996): 823–25. http://dx.doi.org/10.1016/s0955-0674(96)80083-4.

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4

Fuchs, Elaine, and Fiona M. Watt. "Cell differentiation." Current Opinion in Cell Biology 15, no. 6 (December 2003): 738–39. http://dx.doi.org/10.1016/j.ceb.2003.10.018.

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5

Goldstein, Lawrence, and Sean Morrison. "Cell differentiation." Current Opinion in Cell Biology 16, no. 6 (December 2004): 679–80. http://dx.doi.org/10.1016/j.ceb.2004.10.001.

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6

Brand, Andrea H., and Frederick J. Livesey. "Cell differentiation." Current Opinion in Cell Biology 17, no. 6 (December 2005): 637–38. http://dx.doi.org/10.1016/j.ceb.2005.10.007.

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7

Bronner-Fraser, Marianne. "Cell differentiation." Current Opinion in Cell Biology 18, no. 6 (December 2006): 690–91. http://dx.doi.org/10.1016/j.ceb.2006.10.011.

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8

Farmer, Stephen R., and Bruce M. Spiegelman. "Cell differentiation." Current Opinion in Cell Biology 19, no. 6 (December 2007): 603–4. http://dx.doi.org/10.1016/j.ceb.2007.11.002.

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9

Derynck, Rik, and ErwinF Wagner. "Cell differentiation." Current Opinion in Cell Biology 7, no. 6 (January 1995): 843–44. http://dx.doi.org/10.1016/0955-0674(95)80068-9.

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10

Steel, Michael. "CELL DIFFERENTIATION." Lancet 341, no. 8854 (May 1993): 1187–88. http://dx.doi.org/10.1016/0140-6736(93)91010-j.

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11

Lindholm, Dan, and Urmas Arumäe. "Cell differentiation." Journal of Cell Biology 167, no. 2 (October 25, 2004): 193–95. http://dx.doi.org/10.1083/jcb.200409171.

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The molecular mechanisms by which differentiated cells combat cell death and injury have remained unclear. In the current issue, it has been shown in neurons that cell differentiation is accompanied by a decrease in Apaf-1 and the activity of the apoptosome with an increased ability of the inhibitor of apoptosis proteins (IAPs) to sustain survival (Wright et al., 2004). These results, together with earlier ones, deepen our understanding of how cell death and the apoptosome are regulated during differentiation and in tumor cells.

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12

Bennett, Vann. "Cell differentiation." Current Opinion in Cell Biology 20, no. 6 (December 2008): 607–8. http://dx.doi.org/10.1016/j.ceb.2008.10.006.

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13

Ogushi, Fumiko, and Hiroshi Kori. "3P277 Dependence of cell differentiation ratio on cell-cell interaction and noise(24. Mathematical biology,Poster)." Seibutsu Butsuri 53, supplement1-2 (2013): S257. http://dx.doi.org/10.2142/biophys.53.s257_6.

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14

Park, Hyo Eun, Donghee Kim, Hyun Sook Koh, Sungbo Cho, Jung-Suk Sung, and Jae Young Kim. "Real-Time Monitoring of Neural Differentiation of Human Mesenchymal Stem Cells by Electric Cell-Substrate Impedance Sensing." Journal of Biomedicine and Biotechnology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/485173.

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Stem cells are useful for cell replacement therapy. Stem cell differentiation must be monitored thoroughly and precisely prior to transplantation. In this study we evaluated the usefulness of electric cell-substrate impedance sensing (ECIS) forin vitroreal-time monitoring of neural differentiation of human mesenchymal stem cells (hMSCs). We cultured hMSCs in neural differentiation media (NDM) for 6 days and examined the time-course of impedance changes with an ECIS array. We also monitored the expression of markers for neural differentiation, total cell count, and cell cycle profiles. Cellular expression of neuron and oligodendrocyte markers increased. The resistance value of cells cultured in NDM was automatically measured in real-time and found to increase much more slowly over time compared to cells cultured in non-differentiation media. The relatively slow resistance changes observed in differentiating MSCs were determined to be due to their lower growth capacity achieved by induction of cell cycle arrest in G0/G1. Overall results suggest that the relatively slow change in resistance values measured by ECIS method can be used as a parameter for slowly growing neural-differentiating cells. However, to enhance the competence of ECIS forin vitroreal-time monitoring of neural differentiation of MSCs, more elaborate studies are needed.

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15

Pines, Jonathon, and Frank Lafont. "Cell differentiation and Cell multiplication." Current Opinion in Cell Biology 13, no. 6 (December 2001): 657–58. http://dx.doi.org/10.1016/s0955-0674(00)00266-0.

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16

Curti, Antonio, Elisa Ferri, Simona Pandolfi, Alessandro Isidori, and Roberto M. Lemoli. "Dendritic Cell Differentiation." Journal of Immunology 172, no. 1 (December 19, 2003): 3–4. http://dx.doi.org/10.4049/jimmunol.172.1.3.

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17

Salim, Ali, Amato J. Giaccia, and Michael T. Longaker. "Stem cell differentiation." Nature Biotechnology 22, no. 7 (July 1, 2004): 804–5. http://dx.doi.org/10.1038/nbt0704-804.

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18

James, SharonY, MarcA Williams, AdrianC Newland, and KayW Colston. "Leukemia Cell Differentiation." General Pharmacology: The Vascular System 32, no. 1 (January 1999): 143–54. http://dx.doi.org/10.1016/s0306-3623(98)00098-6.

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19

Rosenthal, N. "Muscle cell differentiation." Current Opinion in Cell Biology 1, no. 6 (December 1989): 1094–101. http://dx.doi.org/10.1016/s0955-0674(89)80056-0.

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20

Zorick, Todd S., and Greg Lemke. "Schwann cell differentiation." Current Opinion in Cell Biology 8, no. 6 (December 1996): 870–76. http://dx.doi.org/10.1016/s0955-0674(96)80090-1.

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21

Sinkovics, Joseph G. "Chondrosarcoma cell differentiation." Pathology & Oncology Research 10, no. 3 (September 2004): 174–87. http://dx.doi.org/10.1007/bf03033749.

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22

Gusterson, B. "Tumor Cell Differentiation." Journal of Clinical Pathology 41, no. 4 (April 1, 1988): 480. http://dx.doi.org/10.1136/jcp.41.4.480-c.

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23

MacDonald, H. R. "T-cell differentiation." Research in Immunology 140, no. 5-6 (January 1989): 635–36. http://dx.doi.org/10.1016/0923-2494(89)90126-0.

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24

Reth, M. "B-cell differentiation." Research in Immunology 140, no. 5-6 (January 1989): 636–38. http://dx.doi.org/10.1016/0923-2494(89)90127-2.

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25

Lin, Mong-Shang, and Yung-Wu Chen. "B Cell Differentiation." Cellular Immunology 150, no. 2 (September 1993): 343–52. http://dx.doi.org/10.1006/cimm.1993.1202.

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26

Miller, R. G. "T cell differentiation." International Journal of Cell Cloning 4, S1 (1986): 26–38. http://dx.doi.org/10.1002/stem.5530040708.

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27

Dorshkind, Kenneth. "B-cell differentiation." Immunology Today 7, no. 11 (November 1986): 322–23. http://dx.doi.org/10.1016/0167-5699(86)90131-3.

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28

Pera, Renee, Carlos Simón, and Jose Medrano. "Germ Cell Differentiation from Pluripotent Cells." Seminars in Reproductive Medicine 31, no. 01 (January 17, 2013): 014–23. http://dx.doi.org/10.1055/s-0032-1331793.

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29

Braun, Robert E. "Stem Cells and Germ Cell Differentiation." Biology of Reproduction 83, Suppl_1 (November 1, 2010): 44. http://dx.doi.org/10.1093/biolreprod/83.s1.44.

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30

Xu, Wei, Chirag H. Patel, Jesse Alt, Liang Zhao, Im-Hong Sun, Min-Hee Oh, Im-Meng Sun, et al. "GOT1 constrains TH17 cell differentiation, while promoting iTreg cell differentiation." Nature 614, no. 7946 (February 1, 2023): E1—E11. http://dx.doi.org/10.1038/s41586-022-05602-3.

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31

Vaidya, Milind M., and Deepak Kanojia. "Keratins: Markers of cell differentiation or regulators of cell differentiation?" Journal of Biosciences 32, no. 4 (June 2007): 629–34. http://dx.doi.org/10.1007/s12038-007-0062-8.

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32

Gendreizig, Sarah, Laura Martinez-Ruiz, Javier Florido, Alba López-Rodríguez, Harkiren Pabla, Frank Brasch, Germaine Escames, et al. "Abstract 5818: Differentiation of human papillomavirus-positive head and neck squamous cell carcinoma cells." Cancer Research 84, no. 6_Supplement (March 22, 2024): 5818. http://dx.doi.org/10.1158/1538-7445.am2024-5818.

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Abstract Head and neck squamous cell carcinoma (HNSCC) represents a highly malignant disease and death rates remain at approximately 50% for decades. Thus, new tumor-targeting treatment strategies are desperately needed. In a previous study, we dissected human papillomavirus (HPV)-negative HNSCC cell differentiation via cornification and detected an epigenetically determined loss of cell malignancy. Analyzing the mechanisms underlying the differentiation of HNSCC cells may identify targets for anti-tumor therapy. Using patient-derived tumor cells, we created an HNSCC differentiation model in HPV+ tumor cells. Similar to HPV- cells, we observed a loss of malignant characteristics in HPV+ cell cultures in differentiating cell culture conditions including irregular enlarged cell morphology, cell cycle arrest with downregulation of Ki67, and reduced cell viability. Even though cornification was detected in HPV+ tumor cell cultures and HPV+ FFPE tumor tissue sections, cornification was not induced during HPV+ cell differentiation. Instead, RNA-seq and subsequent Gene Ontology analysis showed myocyte-like differentiation with upregulation of markers of myofibril assembly including TPM1, TAGLN, and ACTA1. Immunofluorescence staining of differentiated and undifferentiated primary HPV+ HNSCC cells confirmed an upregulation of these markers and the formation of parallel actin fibers, reminiscent of myoblast-lineage cells. Moreover, multi-marker immunofluorescence analysis of HPV+ tumor tissue sections revealed areas of cells co-expressing the identified markers of myofibril assembly, HPV surrogate marker p16, and stress-associated basal keratinocyte marker KRT17, indicating that the observed myocyte-like differentiation observed in vitro also occurred in human tissue. Normal tissue displayed a co-expression of TPM1, TAGLN, and ACTA1 in differentiating keratinocytes between the basal cell layer and the fully differentiated corneocytes. This shows that the expression of myocyte-lineage markers is reflected in differentiating non-malignant mucosal tissue. Our study suggests that the targeted differentiation of tumor cells might be therapeutically valuable in HPV+ HNSCCs as well. Citation Format: Sarah Gendreizig, Laura Martinez-Ruiz, Javier Florido, Alba López-Rodríguez, Harkiren Pabla, Frank Brasch, Germaine Escames, Tobias Busche, Holger Sudhoff, Lars U. Scholtz, Ingo Todt, Felix Oppel. Differentiation of human papillomavirus-positive head and neck squamous cell carcinoma cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5818.

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33

Thoma, Eva C., Katja Maurus, Toni U. Wagner, and Manfred Schartl. "Parallel Differentiation of Embryonic Stem Cells into Different Cell Types by a Single Gene-Based Differentiation System." Cellular Reprogramming 14, no. 2 (April 2012): 106–11. http://dx.doi.org/10.1089/cell.2011.0067.

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34

Rosenbloom, Alyssa B., Marcin Tarczyński, Nora Lam, Ravi S. Kane, Lukasz J. Bugaj, and David V. Schaffer. "β-Catenin signaling dynamics regulate cell fate in differentiating neural stem cells." Proceedings of the National Academy of Sciences 117, no. 46 (November 2, 2020): 28828–37. http://dx.doi.org/10.1073/pnas.2008509117.

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Stem cells undergo differentiation in complex and dynamic environments wherein instructive signals fluctuate on various timescales. Thus, cells must be equipped to properly respond to the timing of signals, for example, to distinguish sustained signaling from transient noise. However, how stem cells respond to dynamic variations in differentiation cues is not well characterized. Here, we use optogenetic activation of β-catenin signaling to probe the dynamic responses of differentiating adult neural stem cells (NSCs). We discover that, while elevated, sustained β-catenin activation sequentially promotes proliferation and differentiation, transient β-catenin induces apoptosis. Genetic perturbations revealed that the neurogenic/apoptotic fate switch was mediated through cell-cycle regulation by Growth Arrest and DNA Damage 45 gamma (Gadd45γ). Our results thus reveal a role for β-catenin dynamics in NSC fate decisions and may suggest a role for signal timing to minimize cell-fate errors, analogous to kinetic proofreading of stem-cell differentiation.

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35

Clark, Allison J., Kathryn M. Doyle, and Patrick O. Humbert. "Cell-intrinsic requirement for pRb in erythropoiesis." Blood 104, no. 5 (September 1, 2004): 1324–26. http://dx.doi.org/10.1182/blood-2004-02-0618.

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Abstract Retinoblastoma (Rb) and family members have been implicated as key regulators of cell proliferation and differentiation. In particular, accumulated data have suggested that the Rb gene product pRb is an important controller of erythroid differentiation. However, current published data are conflicting as to whether the role of pRb in erythroid cells is cell intrinsic or non–cell intrinsic. Here, we have made use of an in vitro erythroid differentiation culture system to determine the cell-intrinsic requirement for pRb in erythroid differentiation. We demonstrate that the loss of pRb function in primary differentiating erythroid cells results in impaired cell cycle exit and terminal differentiation. Furthermore, we have used coculture experiments to establish that this requirement is cell intrinsic. Together, these data unequivocally demonstrate that pRb is required in a cell-intrinsic manner for erythroid differentiation and provide clarification as to its role in erythropoiesis.

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36

Nagayama, Masafumi, Tsutomu Uchida, Toshio Taira, Kyoko Shimizu, Masato Sakai, and Kazutoshi Gohara. "1P460 Cell division of primary stromal-vascular cells during adipose differentiation(21. Development and differentiation,Poster Session,Abstract,Meeting Program of EABS &BSJ 2006)." Seibutsu Butsuri 46, supplement2 (2006): S261. http://dx.doi.org/10.2142/biophys.46.s261_4.

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37

Valtieri, M., G. Boccoli, U. Testa, C. Barletta, and C. Peschle. "Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF." Blood 77, no. 8 (April 15, 1991): 1804–12. http://dx.doi.org/10.1182/blood.v77.8.1804.1804.

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Abstract The human AML-193 cell line requires exogenous granulocyte-monocyte colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) for growth in liquid or semisolid medium. However, these CSFs do not stimulate the differentiation of the cell line. We show that addition of all-trans retinoic acid (RA) or 1,25 dihydroxyvitamin D3 (D3) induces AML-193 cells to differentiate into the granulocytic or monocytic lineage, respectively. On the other hand, addition of either G- or M-CSF alone exerts virtually no differentiative effect. Terminal granulocytic or monocytic differentiation was observed when AML-193 cells were treated with RA and G-CSF, or D3 and M-CSF, respectively, as evaluated by cell morphology, analysis of surface antigens, and phagocytic functions. These positive interactions indicate that the differentiating activity of G- and M-CSF on leukemic cells may be unmasked by preliminary treatment with RA and D3, respectively, ie, the physiologic inducers override the leukemic differentiation blockade and CFSs exert their differentiative activity on the unblocked leukemic cells. These preliminary observations on a single cell line may pave the way for the designing of clinical protocols combining physiologic inducer(s) and hematopoietic growth factor(s) in the treatment of acute leukemia.

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38

Valtieri, M., G. Boccoli, U. Testa, C. Barletta, and C. Peschle. "Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF." Blood 77, no. 8 (April 15, 1991): 1804–12. http://dx.doi.org/10.1182/blood.v77.8.1804.bloodjournal7781804.

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The human AML-193 cell line requires exogenous granulocyte-monocyte colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) for growth in liquid or semisolid medium. However, these CSFs do not stimulate the differentiation of the cell line. We show that addition of all-trans retinoic acid (RA) or 1,25 dihydroxyvitamin D3 (D3) induces AML-193 cells to differentiate into the granulocytic or monocytic lineage, respectively. On the other hand, addition of either G- or M-CSF alone exerts virtually no differentiative effect. Terminal granulocytic or monocytic differentiation was observed when AML-193 cells were treated with RA and G-CSF, or D3 and M-CSF, respectively, as evaluated by cell morphology, analysis of surface antigens, and phagocytic functions. These positive interactions indicate that the differentiating activity of G- and M-CSF on leukemic cells may be unmasked by preliminary treatment with RA and D3, respectively, ie, the physiologic inducers override the leukemic differentiation blockade and CFSs exert their differentiative activity on the unblocked leukemic cells. These preliminary observations on a single cell line may pave the way for the designing of clinical protocols combining physiologic inducer(s) and hematopoietic growth factor(s) in the treatment of acute leukemia.

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39

Filvaroff, E., D. F. Stern, and G. P. Dotto. "Tyrosine phosphorylation is an early and specific event involved in primary keratinocyte differentiation." Molecular and Cellular Biology 10, no. 3 (March 1990): 1164–73. http://dx.doi.org/10.1128/mcb.10.3.1164-1173.1990.

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Very little is known about early molecular events triggering epithelial cell differentiation. We have examined the possible role of tyrosine phosphorylation in this process, as observed in cultures of primary mouse keratinocytes after exposure to calcium or 12-O-tetradecanoylphorbol-13-acetate (TPA). Immunoblotting with phosphotyrosine-specific antibodies as well as direct phosphoamino acid analysis revealed that induction of tyrosine phosphorylation occurs as a very early and specific event in keratinocyte differentiation. Very little or no induction of tyrosine phosphorylation was observed in a keratinocyte cell line resistant to the differentiating effects of calcium. Treatment of cells with tyrosine kinase inhibitors prevented induction of tyrosine phosphorylation by calcium and TPA and interfered with the differentiative effects of these agents. These results suggest that specific activation of tyrosine kinase(s) may play an important regulatory role in keratinocyte differentiation.

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40

Filvaroff, E., D. F. Stern, and G. P. Dotto. "Tyrosine phosphorylation is an early and specific event involved in primary keratinocyte differentiation." Molecular and Cellular Biology 10, no. 3 (March 1990): 1164–73. http://dx.doi.org/10.1128/mcb.10.3.1164.

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Very little is known about early molecular events triggering epithelial cell differentiation. We have examined the possible role of tyrosine phosphorylation in this process, as observed in cultures of primary mouse keratinocytes after exposure to calcium or 12-O-tetradecanoylphorbol-13-acetate (TPA). Immunoblotting with phosphotyrosine-specific antibodies as well as direct phosphoamino acid analysis revealed that induction of tyrosine phosphorylation occurs as a very early and specific event in keratinocyte differentiation. Very little or no induction of tyrosine phosphorylation was observed in a keratinocyte cell line resistant to the differentiating effects of calcium. Treatment of cells with tyrosine kinase inhibitors prevented induction of tyrosine phosphorylation by calcium and TPA and interfered with the differentiative effects of these agents. These results suggest that specific activation of tyrosine kinase(s) may play an important regulatory role in keratinocyte differentiation.

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41

Turksen, Kursad, and Tammy-Claire Troy. "Epidermal cell lineage." Biochemistry and Cell Biology 76, no. 6 (December 1, 1998): 889–98. http://dx.doi.org/10.1139/o98-088.

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The epidermis is a stratified squamous epithelium, which is under a constant state of proliferation, commitment, differentiation, and elimination so that the functional integrity of the tissue is maintained. The intact epidermis has the ability to respond to diverse environmental stimuli by continuous turnover to maintain its normal homeostasis throughout an organism's life. This is achieved by a tightly regulated balance between stem cell self-renewal and the generation of a population of cells that undergo a limited number of more rapid (amplifying) transit divisions before giving rise to nonproliferative, terminally differentiating cells. This process makes it an excellent model system to study lineage, commitment, and differentiation, although neither the identity of epidermal stem cells nor the precise steps and regulators that lead to mature epidermal cells have yet been determined. Furthermore, the identities of genes that initiate epidermal progenitor commitment to the epidermal lineage, from putative epidermal stem cells, are unknown. This is mainly due to the lack of an in vitro model system, as well as the lack of specific reagents, to study the early events in epidermal lineage. Our recent development of a differentiating embryonic stem cell model for epidermal lineage now offers the opportunity to analyze the factors that regulate epidermal lineage. These studies will provide new insight into epidermal lineage and lead to a better understanding of various hyperproliferative skin diseases such as psoriasis and cancer.Key words: epidermis, lineage differentiation, embryonic stem cells.

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42

Pines, Jonathon, Luca Toldo, and Frank Lafont. "Web alert Cell multiplication Cell differentiation." Current Opinion in Cell Biology 9, no. 6 (December 1997): 755–56. http://dx.doi.org/10.1016/s0955-0674(97)80073-7.

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43

Cohen, Stephen, and Kai Simons. "Cell differentiation Cell asymmetry in development." Current Opinion in Cell Biology 9, no. 6 (December 1997): 831–32. http://dx.doi.org/10.1016/s0955-0674(97)80084-1.

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44

Pines, Jonathon, Luca Toldo, and Frank Lafont. "Cell differentiation Cell multiplication Web alert." Current Opinion in Cell Biology 10, no. 6 (December 1998): 683–84. http://dx.doi.org/10.1016/s0955-0674(98)80106-3.

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45

Weber, MC, and ML Tykocinski. "Bone marrow stromal cell blockade of human leukemic cell differentiation." Blood 83, no. 8 (April 15, 1994): 2221–29. http://dx.doi.org/10.1182/blood.v83.8.2221.bloodjournal8382221.

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Bone marrow (BM) stromal cell inhibition of leukemic cell differentiation was studied in cellular coculture experiments. In coculture, a significant percentage of cells from the human myeloid leukemic cell lines HL-60, PLB-985, and K562 adhere to fibroblastic KM- 102 BM stromal cells. A sensitive two-color immunofluorescence assay was developed to monitor stromal cellular effects upon leukemic cell differentiation. After chemical induction with 1 alpha,25- dihydroxyvitamin D3, strongly adherent HL-60 and PLB-985 cells were inhibited from differentiating into more mature monocytic cells, as measured by the monocytic surface marker CD14. In contrast, loosely adherent and nonadherent HL-60 and PLB-985 leukemic cells in the same cocultures, as well as both adherent and nonadherent K562 cells induced with phorbol ester, were not blocked in their capacity to differentiate. Scanning electron microscopy and intercellular dye transfer experiments correlated intimate stromal cell/leukemic cell interaction and intercellular communication with the blockade of leukemic cell differentiation. These studies indicate that there is significant variability among leukemic lines with respect to the nature of their adhesion to stromal cells. Moreover, the data implicate gap- junction formation as a potentially significant event in stromal cell- mediated leukemic cell regulation.

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46

Shah, Syed Mohmad, Neha Saini, Syma Ashraf, Manoj Kumar Singh, Radhey Sham Manik, Suresh Kumar Singla, Prabhat Palta, and Manmohan Singh Chauhan. "Cumulus cell-conditioned medium supports embryonic stem cell differentiation to germ cell-like cells." Reproduction, Fertility and Development 29, no. 4 (2017): 679. http://dx.doi.org/10.1071/rd15159.

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Cumulus cells provide cellular interactions and growth factors required for oogenesis. In vitro studies of oogenesis are limited primarily because of the paucity of their source, first trimester fetal gonads, and the small number of germ lineage precursor cells present within these tissues. In order to understand this obscure but vitally important process, the present study was designed to direct differentiation of embryonic stem (ES) cells into germ lineage cells. For this purpose, buffalo ES cells were differentiated, as embryoid bodies (EBs) and monolayer adherent cultures, in the presence of different concentrations of cumulus-conditioned medium (CCM; 10%, 20% and 40%) for different periods of culture (4, 8 and 14 days) to identify the optimum differentiation-inducing concentration and time. Quantitative polymerase chain reaction analysis revealed that 20%–40% CCM induced the highest expression of primordial germ cell-specific (deleted in Azoospermia- like (Dazl), dead (Asp-Glu-Ala-Asp) box polypeptide 4 (Vasa also known as DDX4) and promyelocytic leukemia zinc finger protein (Plzf)); meiotic (synaptonemal complex protein 3 (Sycp3), mutl homolog I (Mlh1), transition protein 1/2 (Tnp1/2) and protamine 2 (Prm2); spermatocyte-specific boule-like RNA binding protein (Boule) and tektin 1 (Tekt1)) and oocyte-specific growth differentiation factor 9 (Gdf9) and zona pellucida 2 /3 (Zp2/3)) genes over 8–14 days in culture. Immunocytochemical analysis revealed expression of primordial germ cell (c-KIT, DAZL and VASA), meiotic (SYCP3, MLH1 and PROTAMINE 1), spermatocyte (ACROSIN and HAPRIN) and oocyte (GDF9 and ZP4) markers in both EBs and monolayer differentiation cultures. Western blotting revealed germ lineage-specific protein expression in Day 14 EBs. The significantly lower (P < 0.05) concentration of 5-methyl-2-deoxycytidine in differentiated EBs compared to undifferentiated EBs suggests that methylation erasure may have occurred. Oocyte-like structures obtained in monolayer differentiation stained positive for ZONA PELLUCIDA protein 4 and progressed through various embryo-like developmental stages in extended cultures.

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Gobbi, Giuliana, Prisco Mirandola, Cecilia Carubbi, Cristina Micheloni, Chiara Malinverno, Paolo Lunghi, Antonio Bonati, and Marco Vitale. "Phorbol ester–induced PKCϵ down-modulation sensitizes AML cells to TRAIL-induced apoptosis and cell differentiation." Blood 113, no. 13 (March 26, 2009): 3080–87. http://dx.doi.org/10.1182/blood-2008-03-143784.

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AbstractDespite the relevant therapeutic progresses made in these last 2 decades, the prognosis of acute myeloid leukemia (AML) remains poor. Phorbol esters are used at very low concentrations as differentiating agents in the therapy of myeloid leukemias. Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), in turn, is a death ligand that spares normal cells and is therefore currently under clinical trials for cancer therapy. Emerging evidence, however, suggests that TRAIL is also involved in nonapoptotic functions, like cell differentiation. PKCϵ is differentially modulated along normal hematopoiesis, and its levels modulate the response of hematopoietic precursors to TRAIL. Here, we investigated the effects of the combination of phorbol esters (phorbol ester 4-β-phorbol-12,13-dibutyrate [PDBu]) and TRAIL in the survival/differentiation of AML cells. We demonstrate here that PDBu sensitizes primary AML cells to both the apoptogenic and the differentiative effects of TRAIL via PKCϵ down-modulation, without affecting TRAIL receptor surface expression. We believe that the use of TRAIL in combination with phorbol esters (or possibly more specific PKCϵ down-modulators) might represent a significative improvement of our therapeutic arsenal against AML.

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Filippi, Marie-Dominique, Françoise Porteu, Françoise Le Pesteur, Philippe Rameau, Maria Manuela Nogueira, Najet Debili, William Vainchenker, Frederic J. de Sauvage, Anne Dubart Kupperschmitt, and Françoise Sainteny. "Embryonic stem cell differentiation to hematopoietic cells." Experimental Hematology 28, no. 12 (December 2000): 1363–72. http://dx.doi.org/10.1016/s0301-472x(00)00549-x.

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Chakraborty, Damayanti, M. A. Karim Rumi, and Michael Soares. "NK cells, hypoxia and trophoblast cell differentiation." Cell Cycle 11, no. 13 (July 2012): 2427–30. http://dx.doi.org/10.4161/cc.20542.

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Abdullah, Leena, Francesco Emiliani, Chinmay Vaidya, Aaron McKenna, and Yina H. Huang. "Dynamic single cell lineage recording of endogenous viral specific CD8 T cells reveals multiple potential cell fate pathways." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 239.04. http://dx.doi.org/10.4049/jimmunol.210.supp.239.04.

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Abstract In response to viral infection, antigen specific naïve CD8 T cells expand to give rise to a heterogenous pool of effector cells consisting of short-lived effector cells (SLECs) and memory precursor effector cells (MPECs). While these effector populations are phenotypically and functionally well characterized, we still don’t fully understand how they arise from antigen responsive naïve CD8 T cells. We have combined progressive lineage recording with single-cell RNA sequencing and T cell receptor sequencing to delineate the early differentiation of OVA-specific endogenous CD8 T cells in response to acute VSV infection. Transcriptional profiling of CD8 T cells captured at the peak of T cell response confirmed 8 distinct T cell states including a unique interferon responsive cluster. RNA Velocity trajectory analysis supported an asymmetric model of CD8 T cell differentiation where early effector cells gave rise to SLECs while MPECs differentiated into further memory precursors. Moreover, our CRISPR/Cas9-based lineage recorder uncovered T cell clones of various sizes and allowed us to follow up to 5 generations of differentiating CD8 T cells. We observed that expanded clones comprised of memory and effector CD8 T cells while medium size clones preferred memory or effector fate, suggesting that different clones follow different differentiation models. Thus, using RNA-seq based trajectory analyses and a dynamic lineage recorder we uncovered potential differentiation pathways taken by early viral specific CD8 T cells. Our single cell full length TCR-seq will further add to our current models and highlight TCR sequences with better memory potential in response to infection. Supported by grants from NIH (R01 AI089805, R01 CA254042) and a training fellowship from the Burroughs Wellcome Fund.

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