[P190]: Spatial organization of pax6‐protein‐containing cells, proliferating cells and differentiated cells in the embryonic shark forebrain

2006 ◽  
Vol 24 (8) ◽  
pp. 577-578
Author(s):  
I. Carrera ◽  
S. Ferreiro‐Galve ◽  
E. Candal ◽  
R. Anadon ◽  
I. Rodriguez‐Moldes
Keyword(s):  
Spatial Organization ◽  
Proliferating Cells ◽  
Differentiated Cells ◽  
Pax6 Protein

scholarly journals Distinct p63 and p73 Protein Interactions Predict Specific Functions in mRNA Splicing and Polyploidy Control in Epithelia

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 25
Author(s):  
Julian M. Rozenberg ◽  
Olga S. Rogovaya ◽  
Gerry Melino ◽  
Nickolai A. Barlev ◽  
Alexander Kagansky
Keyword(s):  
Protein Interactions ◽  
Transcriptional Repression ◽  
Genome Stability ◽  
Spindle Assembly Checkpoint ◽  
Genotoxic Stress ◽  
Protein Protein Interactions ◽  
Proliferating Cells ◽  
P53 Family ◽  
Differentiated Cells ◽  
Specific Localization

Epithelial organs are the first barrier against microorganisms and genotoxic stress, in which the p53 family members p63 and p73 have both overlapping and distinct functions. Intriguingly, p73 displays a very specific localization to basal epithelial cells in human tissues, while p63 is expressed in both basal and differentiated cells. Here, we analyse systematically the literature describing p63 and p73 protein–protein interactions to reveal distinct functions underlying the aforementioned distribution. We have found that p73 and p63 cooperate in the genome stability surveillance in proliferating cells; p73 specific interactors contribute to the transcriptional repression, anaphase promoting complex and spindle assembly checkpoint, whereas p63 specific interactors play roles in the regulation of mRNA processing and splicing in both proliferating and differentiated cells. Our analysis reveals the diversification of the RNA and DNA specific functions within the p53 family.

Nuclear expression of IL-33 in epidermal keratinocyte is up-regulated in differentiated cells, while suppressed in proliferating cells

2016 ◽  
Vol 84 (1) ◽  
pp. e43 ◽  
Author(s):  
Mayumi Komine ◽  
Atsuko Sato ◽  
Akimasa Adachi ◽  
Jitlada Meephansan ◽  
Hidetoshi Tsuda ◽  
...  
Keyword(s):  
Proliferating Cells ◽  
Epidermal Keratinocyte ◽  
Nuclear Expression ◽  
Differentiated Cells

scholarly journals Changes in the mechanism of Ca2+ mobilization during the differentiation of BC3H1 muscle cells

1991 ◽  
Vol 273 (1) ◽  
pp. 219-223 ◽  
Author(s):  
H De Smedt ◽  
J B Parys ◽  
B Himpens ◽  
L Missiaen ◽  
R Borghgraef
Keyword(s):  
Cell Differentiation ◽  
Muscle Cell ◽  
Muscle Cells ◽  
Proliferating Cells ◽  
Muscle Cell Differentiation ◽  
Differentiated Cells

Ca2+ sequestration and release in BC3H1 muscle cells is strongly dependent on the stage of differentiation. In proliferating cells, more than 90% of the sequestered Ca2+ was Ins(1,4,5)P3-sensitive and 25% was caffeine-sensitive. In differentiated cells, the Ca2+ accumulation was 5-fold higher and was InsP3-insensitive, but about 60% of the sequestered Ca2+ was caffeine-sensitive. These changes were reversible upon addition of growth stimuli. Similarly, by measuring the intracellular Ca2+ concentration in single intact BC3H1 cells, it was found that the number of histamine-responsive cells decreased and the number of caffeine-responsive cells increased during muscle cell differentiation. These data indicate that the development of the muscle phenotype in BC3H1 myoblasts induces a major rearrangement of the mechanisms for Ca2+ mobilization.

scholarly journals Emergence of proto-organisms from bistable stochastic differentiation and adhesion

2016 ◽  
Vol 13 (117) ◽  
pp. 20160108 ◽  
Author(s):  
Salva Duran-Nebreda ◽  
Adriano Bonforti ◽  
Raúl Montañez ◽  
Sergi Valverde ◽  
Ricard Solé
Keyword(s):  
Evolutionary Biology ◽  
Spatial Organization ◽  
Organizational Complexity ◽  
Differentiated Cells ◽  
Differential Adhesion ◽  
Multicellular Aggregates ◽  
Conflict Mediation ◽  
Evolution Of Life ◽  
Living Organisms ◽  
High Degree

The rise of multicellularity in the early evolution of life represents a major challenge for evolutionary biology. Guidance for finding answers has emerged from disparate fields, from phylogenetics to modelling and synthetic biology, but little is known about the potential origins of multicellular aggregates before genetic programmes took full control of developmental processes. Such aggregates should involve spatial organization of differentiated cells and the modification of flows and concentrations of metabolites within well-defined boundaries. Here, we show that, in an environment where limited nutrients and toxic metabolites are introduced, a population of cells capable of stochastic differentiation and differential adhesion can develop into multicellular aggregates with conflict mediation mechanisms and a complex internal structure. The morphospace of possible patterns is shown to be very rich, including proto-organisms that display a high degree of organizational complexity, far beyond simple heterogeneous populations of cells. Our findings reveal that there is a potentially enormous richness of organismal complexity between simple mixed cooperators and embodied living organisms.

scholarly journals Differentiation-Induced Radioresistance in Muscle Cells

2004 ◽  
Vol 24 (14) ◽  
pp. 6350-6361 ◽  
Author(s):  
Lucia Latella ◽  
Jiri Lukas ◽  
Cristiano Simone ◽  
Pier Lorenzo Puri ◽  
Jiri Bartek
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Double Strand Breaks ◽  
Proliferating Cells ◽  
Histone H2ax ◽  
Selective Blockade ◽  
Differentiated Cells ◽  
Dna Damage Signaling ◽  
Ataxia Teleangiectasia ◽  
Associated Proteins

ABSTRACT DNA damage induces cell cycle arrest and DNA repair or apoptosis in proliferating cells. Terminally differentiated cells are permanently withdrawn from the cell cycle and partly resistant to apoptosis. To investigate the effects of genotoxic agents in postmitotic cells, we compared DNA damage-activated responses in mouse and human proliferating myoblasts and their differentiated counterparts, the myotubes. DNA double-strand breaks caused by ionizing radiation (IR) induced rapid activating autophosphorylation of ataxia-teleangiectasia-mutated (ATM), phosphorylation of histone H2AX, recruitment of repair-associated proteins MRE11 and Nbs1, and activation of Chk2 in both myoblasts and myotubes. However, IR-activated, ATM-mediated phosphorylation of p53 at serine 15 (human) or 18 (mouse) [Ser15(h)/18(m)], and apoptosis occurred in myoblasts but was impaired in myotubes. This phosphorylation could be enforced in myotubes by the anthracycline derivative doxorubicin, leading to selective activation of proapoptotic genes. Unexpectedly, the abundance of autophosphorylated ATM was indistinguishable after exposure of myotubes to IR (10 Gy) or doxorubicin (1 μM/24 h) despite efficient phosphorylation of p53 Ser15(h)/18(m), and apoptosis occurred only in response to doxorubicin. These results suggest that radioresistance in myotubes might reflect a differentiation-associated, pathway-selective blockade of DNA damage signaling downstream of ATM. This mechanism appears to preserve IR-induced activation of the ATM-H2AX-MRE11/Rad50/Nbs1 lesion processing and repair pathway yet restrain ATM-p53-mediated apoptosis, thereby contributing to life-long maintenance of differentiated muscle tissues.

K562. A Human Cellular System Capable of Undergoing In Vitro Differentiation: Measurement of Genotoxic Parameters Useful for Cytotoxicity Evaluation

1993 ◽  
Vol 21 (1) ◽  
pp. 50-56
Author(s):  
Orazio Sapora ◽  
Antonella Maggi ◽  
Barbara Maione ◽  
Simonetta Pazzaglia ◽  
Maria-Antonella Tabocchini
Keyword(s):  
K562 Cells ◽  
Relative Sensitivity ◽  
Cellular System ◽  
Time Interval ◽  
Proliferating Cells ◽  
Differentiated Cells ◽  
Repair Enzymes ◽  
Initial Damage ◽  
Residual Damage

The initial damage produced by ionising radiation and its subsequent repair have been studied in a cellular system. K562 cells are used which are capable of undergoing in vitro pseudoerythroid differentiation in the presence of 2mM butyric acid. The level of initial damage is similar in actively growing and 48-hour differentiated cells, while it is lower by a factor of two in cells irradiated after exposure to the inducer for 72 hours. In differentiated cells, the kinetics of repair measured up to 60 minutes is slower than that in actively growing cells. These findings suggest that the genome of actively proliferating cells is not only more susceptible to radiation-induced damage, but also more accessible to repair enzymes than the more compact genome of differentiated cells. Repair after a longer time interval has also been investigated. After 24 hours of repair, the amount of residual damage is higher in actively proliferating cells than in differentiated ones. However, in proliferating cells, DNA synthesis can interfere with repair of the lesions or vice versa, while in differentiated cells, due to the lack of proliferation, damage occurring in non-transcribing genes can presumably be sustained for longer periods without biological consequences. A method to evaluate the relative sensitivity of non-duplicating differentiated cells is proposed. It is based on measurement of the residual damage, detected after 24 hours of repair, and on the assumption that a relationship exists between unrepaired DNA damage (residual damage) and the ability of the cell to survive.

scholarly journals Immature Human Megakaryocytes Produce Nuclear-Associated Acetylcholinesterase

Blood ◽  
1997 ◽  
Vol 89 (10) ◽  
pp. 3644-3653 ◽  
Author(s):  
Efrat Lev-Lehman ◽  
Varda Deutsch ◽  
Amiram Eldor ◽  
Hermona Soreq
Keyword(s):  
Bone Marrow ◽  
Ache Activity ◽  
Pcr Amplification ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Medium Size ◽  
Proliferating Cells ◽  
Differentiated Cells ◽  
Idiopathic Thrombocytopenia Purpura ◽  
Species Specific

Abstract Acetylcholinesterase (AChE) is expressed in murine megakaryocytes (MK), where its antisense inhibition suppresses differentiation, yet was never detected in human MK. Here, we report that AChE is produced in normal human bone marrow MK and in cell lines derived thereof. Reverse transcriptase-polymerase chain reaction (RT-PCR) amplification showed two ACHEmRNA forms in human megakaryoblastic DAMI cells. In situ hybridization demonstrated ACHEmRNA surrounding the nucleus of small DAMI cells and the nuclear lobes of large, polyploid cells. Differentiation induction with phorbol ester and exposure to recombinant human thrombopoietin suppressed both ACHEmRNA and AChE activity. The residual AChE in mature differentiated cells acquired higher stability and detergent-sensitivity as compared with AChE in small proliferating cells. AChE activity was primarily associated with nuclei of both DAMI cells and small (10 μm) primary proliferating human bone marrow MK identified with GPIIb/IIIa antibodies. This activity was significantly reduced in medium size MK (10 to 25 μm) and was almost undetectable in large MK (<25 μm), yet was twofold more abundant in some large MK from idiopathic thrombocytopenia purpura (ITP) patients with accelerated MK maturation. The loss of AChE activity at the transition from proliferating to differentiating MK highlights species-specific differences in its expression, suggesting a distinct role for AChE in human MK development.

scholarly journals Cellular Senescence in the Lung: The Central Role of Senescent Epithelial Cells

2020 ◽  
Vol 21 (9) ◽  
pp. 3279 ◽  
Author(s):  
Christine Hansel ◽  
Verena Jendrossek ◽  
Diana Klein
Keyword(s):  
Cell Cycle ◽  
Cellular Senescence ◽  
Inflammatory Diseases ◽  
Cancer Tissue ◽  
Gene Expressions ◽  
Proliferating Cells ◽  
Differentiated Cells ◽  
Tissue Degeneration ◽  
Age Related

Cellular senescence is a key process in physiological dysfunction developing upon aging or following diverse stressors including ionizing radiation. It describes the state of a permanent cell cycle arrest, in which proliferating cells become resistant to growth-stimulating factors. Senescent cells differ from quiescent cells, which can re-enter the cell cycle and from finally differentiated cells: morphological and metabolic changes, restructuring of chromatin, changes in gene expressions and the appropriation of an inflammation-promoting phenotype, called the senescence-associated secretory phenotype (SASP), characterize cellular senescence. The biological role of senescence is complex, since both protective and harmful effects have been described for senescent cells. While initially described as a mechanism to avoid malignant transformation of damaged cells, senescence can even contribute to many age-related diseases, including cancer, tissue degeneration, and inflammatory diseases, particularly when senescent cells persist in damaged tissues. Due to overwhelming evidence about the important contribution of cellular senescence to the pathogenesis of different lung diseases, specific targeting of senescent cells or of pathology-promoting SASP factors has been suggested as a potential therapeutic approach. In this review, we summarize recent advances regarding the role of cellular (fibroblastic, endothelial, and epithelial) senescence in lung pathologies, with a focus on radiation-induced senescence. Among the different cells here, a central role of epithelial senescence is suggested.

scholarly journals The HSP90/R2TP assembly chaperone promotes cell proliferation in the intestinal epithelium

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chloé Maurizy ◽  
Claire Abeza ◽  
Bénédicte Lemmers ◽  
Monica Gabola ◽  
Ciro Longobardi ◽  
...  
Keyword(s):  
Rna Polymerase Ii ◽  
Intestinal Epithelium ◽  
Core Component ◽  
Proliferating Cells ◽  
Knock Out ◽  
Differentiated Cells ◽  
Adult Mice ◽  
Cycle Arrest ◽  
Small Intestinal ◽  
Knock Out Mice

AbstractThe R2TP chaperone cooperates with HSP90 to integrate newly synthesized proteins into multi-subunit complexes, yet its role in tissue homeostasis is unknown. Here, we generated conditional, inducible knock-out mice for Rpap3 to inactivate this core component of R2TP in the intestinal epithelium. In adult mice, Rpap3 invalidation caused destruction of the small intestinal epithelium and death within 10 days. Levels of R2TP substrates decreased, with strong effects on mTOR, ATM and ATR. Proliferative stem cells and progenitors deficient for Rpap3 failed to import RNA polymerase II into the nucleus and they induced p53, cell cycle arrest and apoptosis. Post-mitotic, differentiated cells did not display these alterations, suggesting that R2TP clients are preferentially built in actively proliferating cells. In addition, high RPAP3 levels in colorectal tumors from patients correlate with bad prognosis. Here, we show that, in the intestine, the R2TP chaperone plays essential roles in normal and tumoral proliferation.

Cancer and Evolution

2006 ◽  
Vol 52 (3-4) ◽  
pp. 233-245 ◽  
Author(s):  
Walter. F. Bodmer
Keyword(s):  
Stem Cells ◽  
Germ Line ◽  
Evolutionary Process ◽  
Current Evidence ◽  
Benign Tumors ◽  
Proliferating Cells ◽  
Genetic Changes ◽  
Differentiated Cells ◽  
Selective Forces

Cancer mostly is a disease of old age. Evolutionary pressures have pushed the somatic "error rate", especially the mutation rate, down to a level where for most organisms cancer is no longer of any selective significance. This appears to be a by-product of the selection that gives rise to senescence, following the arguments of Medawar, Holliday, and Kirkwood. The development of a cancer is discussed from an evolutionary viewpoint, emphasising the role of selection versus mutation and the fact that each cancer is an independent evolutionary process. The nature of the selective advantages associated with the somatic genetic changes during a cancer's evolution can sometimes be inferred by reference to the known types of mutations found in cancers. Examples are given using colorectal cancer as a model. The major selective forces involve the balance between selection for increased growth rate and against apoptosis. There are strong arguments against the much discussed role of genomic instability as a requirement for cancer. Current evidence suggests that instability is a byproduct of selection against apoptosis. There is an important contrast between germ line and somatic changes, the former being the basis for inherited susceptibilities to cancer, while the latter are the fundamental changes that turn a normal cell into a cancer cell. Tissue stem cells, as in the colonic crypt, provide the source, through division and differentiation, of the differentiated cells in a crypt. Mathematical models can provide an explanation for how the balance in a crypt between stem cells, intermediate proliferating cells, and non-proliferating differentiated cells is maintained. Perturbations of the renewal parameters in the model can explain the evolution of benign tumors, namely polyps or adenomas, and the eventually exponential growth of cells resulting in a fully developed carcinoma. It seems probable that the origin of most carcinomas is in the intermediate proliferating cells, and that these are therefore the likely source of cancer stem cells.

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