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Journal articles on the topic 'Cell differentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 June 2025

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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

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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15

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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16

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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17

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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18

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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19

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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20

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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21

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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22

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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23

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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24

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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25

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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26

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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27

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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28

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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29

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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30

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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31

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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32

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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33

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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34

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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35

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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36

Matthews, K. R., and K. Gull. "Evidence for an interplay between cell cycle progression and the initiation of differentiation between life cycle forms of African trypanosomes." Journal of Cell Biology 125, no. 5 (June 1, 1994): 1147–56. http://dx.doi.org/10.1083/jcb.125.5.1147.

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Successful transmission of the African trypanosome between the mammalian host blood-stream and the tsetse fly vector involves dramatic alterations in the parasite's morphology and biochemistry. This differentiation through to the tsetse midgut procyclic form is accompanied by re-entry into a proliferative cell cycle. Using a synchronous differentiation model and a variety of markers diagnostic for progress through both differentiation and the cell cycle, we have investigated the interplay between these two processes. Our results implicate a relationship between the trypanosome cell cycle position and the perception of the differentiation signal and demonstrate that irreversible commitment to the differentiation occurs rapidly after induction. Furthermore, we show that re-entry into the cell cycle in the differentiating population is synchronous, and that once initiated, progress through the differentiation pathway can be uncoupled from progress through the cell cycle.

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37

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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38

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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39

Qiu, Zhijuan, Camille Khairallah, Jessica Nancy Imperato, Timothy H. Chu, Daqi Xu, Galina Romanov, Lynn Puddington, and Brian S. Sheridan. "Lymph Node Priming Licenses Intestinal CD103+ CD8 Tissue-Resident Memory T Cell Development." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 232.8. http://dx.doi.org/10.4049/jimmunol.204.supp.232.8.

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Abstract CD8 tissue-resident memory T (TRM) cells provide front-line protective immunity at barrier tissues. Understanding TRM cell development will provide significant insights for vaccine design targeting infections and cancers at barrier tissues. Here, we demonstrate that pathogen-induced inflammation and pathogen-derived cognate antigen had minimal impact on intestinal CD103+ TRM cell differentiation. Instead, T cell priming in the mesenteric lymph nodes (MLN) was the principal determinant of CD103+ TRM cell differentiation in the intestine. In contrast, T cells primed in the spleen were incapable of differentiating into intestinal CD103+ TRM cells. Foodborne rechallenge of spleen-primed memory T cells was unable to induce intestinal CD103+ TRM cell differentiation, suggesting initial priming promoted a lasting fate. Moreover, both CD103− and CD103+ naïve T cells were highly efficient in differentiating into CD103+ TRM cells in the intestine after priming in the MLN, suggesting preconditioning of naïve T cells by TGF-b during homeostasis had little impact on intestinal CD103+ TRM cell differentiation. We further demonstrate that MLN priming initiated a CD103+ TRM cell program before effector T cell migration to the intestine and promoted CD103+ TRM cell differentiation in situ in part by promoting CCR9 expression and the ability to respond to TGF-b in a cell-extrinsic manner. Thus, mesenteric lymph node priming is specialized to license intestinal CD103+ CD8 TRM cell development.

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40

Santos, Mark, Wenying Zhang, Jason Whalley, and Matthew Hsu. "Rapid assessment of CD4 + T cell differentiation towards more specialized cell types using impedance based technology (P6325)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 184.24. http://dx.doi.org/10.4049/jimmunol.190.supp.184.24.

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Abstract Cellular differentiation is a fundamental process in developmental biology. Progenitor cells must have the ability to differentiate into more specialized cell types for the body to respond to infections during autoimmunity. In an immunological response to infections, CD4+ T cells can give rise to a variety of T helper cells depending on the nature of the immune response, and subsequently release a distinct subset of signature cytokines. Similarly, when monocytes are exposed to established lineage specific conditions in vitro, human monocytes differentiate toward mature dendritic cells. In all cases, a characteristic inherent in cell differentiation is that during this process cells undergo a dramatic change in cell size, metabolic activity, and responsiveness to signals. Current methods such as flow cytometry or phase contrast morphology for determining cell differentiation are informative; however, drawbacks to these methods are that either it is too subjective or labor intensive. Here we utilized the coulter principle of impedance based particle detection as an alternative method for rapidly assessing cell differentiation. This study outlines a method for implementing the coulter principle to rapidly analyze CD4+ T cell differentiation towards various Th cell lineages, as well as monocyte differentiaton towards DCs. We have employed impedance based technology for determining cell volume to investigate the relationship between cell differentiation and cell size changes.

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41

Ulmschneider, Bryne, Bree K. Grillo-Hill, Marimar Benitez, Dinara R. Azimova, Diane L. Barber, and Todd G. Nystul. "Increased intracellular pH is necessary for adult epithelial and embryonic stem cell differentiation." Journal of Cell Biology 215, no. 3 (November 7, 2016): 345–55. http://dx.doi.org/10.1083/jcb.201606042.

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Despite extensive knowledge about the transcriptional regulation of stem cell differentiation, less is known about the role of dynamic cytosolic cues. We report that an increase in intracellular pH (pHi) is necessary for the efficient differentiation of Drosophila adult follicle stem cells (FSCs) and mouse embryonic stem cells (mESCs). We show that pHi increases with differentiation from FSCs to prefollicle cells (pFCs) and follicle cells. Loss of the Drosophila Na+–H+ exchanger DNhe2 lowers pHi in differentiating cells, impairs pFC differentiation, disrupts germarium morphology, and decreases fecundity. In contrast, increasing pHi promotes excess pFC cell differentiation toward a polar/stalk cell fate through suppressing Hedgehog pathway activity. Increased pHi also occurs with mESC differentiation and, when prevented, attenuates spontaneous differentiation of naive cells, as determined by expression of microRNA clusters and stage-specific markers. Our findings reveal a previously unrecognized role of pHi dynamics for the differentiation of two distinct types of stem cell lineages, which opens new directions for understanding conserved regulatory mechanisms.

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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

Andrés, V., and K. Walsh. "Myogenin expression, cell cycle withdrawal, and phenotypic differentiation are temporally separable events that precede cell fusion upon myogenesis." Journal of Cell Biology 132, no. 4 (February 15, 1996): 657–66. http://dx.doi.org/10.1083/jcb.132.4.657.

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During terminal differentiation of skeletal myoblasts, cells fuse to form postmitotic multinucleated myotubes that cannot reinitiate DNA synthesis. Here we investigated the temporal relationships among these events during in vitro differentiation of C2C12 myoblasts. Cells expressing myogenin, a marker for the entry of myoblasts into the differentiation pathway, were detected first during myogenesis, followed by the appearance of mononucleated cells expressing both myogenin and the cell cycle inhibitor p21. Although expression of both proteins was sustained in mitogen-restimulated myocytes, 5-bromodeoxyuridine incorporation experiments in serum-starved cultures revealed that myogenin-positive cells remained capable of replicating DNA. In contrast, subsequent expression of p21 in differentiating myoblasts correlated with the establishment of the postmitotic state. Later during myogenesis, postmitotic (p21-positive) mononucleated myoblasts activated the expression of the muscle structural protein myosin heavy chain, and then fused to form multinucleated myotubes. Thus, despite the asynchrony in the commitment to differentiation, skeletal myogenesis is a highly ordered process of temporally separable events that begins with myogenin expression, followed by p21 induction and cell cycle arrest, then phenotypic differentiation, and finally, cell fusion.

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Polonsky, Michal, Jacob Rimer, Amos Kern-Perets, Irina Zaretsky, Stav Miller, Chamutal Bornstein, Eyal David, et al. "Induction of CD4 T cell memory by local cellular collectivity." Science 360, no. 6394 (June 14, 2018): eaaj1853. http://dx.doi.org/10.1126/science.aaj1853.

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Cell differentiation is directed by signals driving progenitors into specialized cell types. This process can involve collective decision-making, when differentiating cells determine their lineage choice by interacting with each other. We used live-cell imaging in microwell arrays to study collective processes affecting differentiation of naïve CD4+ T cells into memory precursors. We found that differentiation of precursor memory T cells sharply increases above a threshold number of locally interacting cells. These homotypic interactions involve the cytokines interleukin-2 (IL-2) and IL-6, which affect memory differentiation orthogonal to their effect on proliferation and survival. Mathematical modeling suggests that the differentiation rate is continuously modulated by the instantaneous number of locally interacting cells. This cellular collectivity can prioritize allocation of immune memory to stronger responses.

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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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Qiu, Zhijuan, Camille Khairallah, Timothy H. Chu, Jessica N. Imperato, Galina Romanov, Lynn Puddington, and Brian S. Sheridan. "Mesenteric lymph node priming licenses intestinal CD103+ CD8 tissue-resident memory T cell development." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 55.02. http://dx.doi.org/10.4049/jimmunol.206.supp.55.02.

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Abstract CD8 tissue-resident memory T (TRM) cells provide front-line protective immunity at barrier tissues; however, mechanisms regulating their development are not completely understood. Priming dictates the migration of effector CD8 T cells to the tissue, while factors in the tissue induce in situ TRM cell differentiation. Whether priming also regulates in situ differentiation of CD8 TRM cells has not been addressed. Here, we demonstrate that T cell priming in the mesenteric lymph nodes (MLN) was the principal determinant of CD103+ CD8 TRM cell differentiation in the intestine. In contrast, CD8 T cells primed in the spleen were inefficient at differentiating into intestinal CD103+ TRM cells. Moreover, both CD103− and CD103+ naïve T cells were highly efficient in differentiating into CD103+ TRM cells in the intestine after priming in the MLN, suggesting preconditioning of naïve T cells by TGF-b during homeostasis had little impact on intestinal CD103+ TRM cell differentiation. We further demonstrate that MLN priming initiated CD103+ CD8 TRM cell signature gene expression and licensed rapid CD103+ CD8 TRM precursor cell differentiation in response to factors in the tissue by providing retinoic acid signaling to CD8 T cells. Thus, MLN priming is specialized to license intestinal CD103+ CD8 TRM cell development.

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Lees, Simon J., Christopher R. Rathbone, and Frank W. Booth. "Age-associated decrease in muscle precursor cell differentiation." American Journal of Physiology-Cell Physiology 290, no. 2 (February 2006): C609—C615. http://dx.doi.org/10.1152/ajpcell.00408.2005.

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Muscle precursor cells (MPCs) are required for the regrowth, regeneration, and/or hypertrophy of skeletal muscle, which are deficient in sarcopenia. In the present investigation, we have addressed the issue of age-associated changes in MPC differentiation. MPCs, including satellite cells, were isolated from both young and old rat skeletal muscle with a high degree of myogenic purity (>90% MyoD and desmin positive). MPCs isolated from skeletal muscle of 32-mo-old rats exhibited decreased differentiation into myotubes and demonstrated decreased myosin heavy chain (MHC) and muscle creatine kinase (CK-M) expression compared with MPCs isolated from 3-mo-old rats. p27Kip1is a cyclin-dependent kinase inhibitor that has been shown to enhance muscle differentiation in culture. Herein we describe our finding that p27Kip1protein was lower in differentiating MPCs from skeletal muscle of 32-mo-old rats than in 3-mo-old rat skeletal muscle. Although MHC and CK-M expression were ∼50% lower in differentiating MPCs isolated from 32-mo-old rats, MyoD protein content was not different and myogenin protein concentration was twofold higher. These data suggest that there are inherent differences in cell signaling during the transition from cell cycle arrest to the formation of myotubes in MPCs isolated from sarcopenic muscle. Furthermore, there is an age-associated decrease in muscle-specific protein expression in differentiating MPCs despite normal MyoD and elevated myogenin levels.

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Messina, Graziella, Cristiana Blasi, Severina Anna La Rocca, Monica Pompili, Attilio Calconi, and Milena Grossi. "p27Kip1 Acts Downstream of N-Cadherin-mediated Cell Adhesion to Promote Myogenesis beyond Cell Cycle Regulation." Molecular Biology of the Cell 16, no. 3 (March 2005): 1469–80. http://dx.doi.org/10.1091/mbc.e04-07-0612.

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It is widely acknowledged that cultured myoblasts can not differentiate at very low density. Here we analyzed the mechanism through which cell density influences myogenic differentiation in vitro. By comparing the behavior of C2C12 myoblasts at opposite cell densities, we found that, when cells are sparse, failure to undergo terminal differentiation is independent from cell cycle control and reflects the lack of p27Kip1 and MyoD in proliferating myoblasts. We show that inhibition of p27Kip1 expression impairs C2C12 cell differentiation at high density, while exogenous p27Kip1 allows low-density cultured C2C12 cells to enter the differentiative program by regulating MyoD levels in undifferentiated myoblasts. We also demonstrate that the early induction of p27Kip1 is a critical step of the N-cadherin-dependent signaling involved in myogenesis. Overall, our data support an active role of p27Kip1 in the decision of myoblasts to commit to terminal differentiation, distinct from the regulation of cell proliferation, and identify a pathway that, reasonably, operates in vivo during myogenesis and might be part of the phenomenon known as “community effect”.

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