Browsing by Subject "Cell differentiation"

Now showing 1 - 5 of 5
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    Markers of senescence are often associated with neuronal differentiation in the developing sensory systems
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Mera Rodríguez, José Antonio; Álvarez Hernán, Guadalupe; Gañán, Yolanda; Solana Fajardo, Jorge; Martín Partido, Gervasio; Rodríguez León, Joaquín; Francisco Morcillo, Javier
    It has been shown that senescent cells accumulate in transient structures of the embryo that normally degenerate during tissue development. A collection of biomarkers is generally accepted to define senescence in embryonic tissues. The histochemical detection of β-galactosidase activity at pH 6.0 (β-galpH6) is the most widely used assay for cellular senescence. Immunohistochemical detection of common mediators of senescence which block cell cycle progression, including p16, p21, p63, p15 or p27, has also been used to characterize senescent cells in the embryo. However, the reliability of this techniques has been discussed in recent publications because nonsenescent cells are also labelled during development. Indeed, increased levels of senescent markers promote differentiation over apoptosis in developing neurons, suggesting that machinery used for the establishment of cellular senescence is also involved in neuronal maturation. Notably, it has recently been argued that a comparable state of cellular senescence might be adopted by terminally differentiated neurons. The developing sensory systems provide excellent models for studying if canonical markers of senescence are associated with terminal neuronal differentiation.
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    Pancreas is a preeminent source of ghrelin after sleeve gastrectomy in Wistar rats
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Camacho Ramírez, Alonso; Mayo Ossorio, María Ángeles; Pacheco García, José Manuel; Almorza Gomar, David; Ribelles García, Antonio; Belmonte Núñez, Ana; Prada Oliveira, J. Arturo; Pérez Arana, Gonzalo M.
    Many surgical techniques are employed in the treatment of severe obesity. A main consequence of these techniques is the improvement of type 2 Diabetes mellitus. Ghrelin is a gut hormone released in the gastric fundus and corpus, which has been related to diabetic improvement as mentioned in these papers. Sleeve gastrectomy and Roux-en Y Gastric Bypass are surgical techniques broadly employed in humans; both severely reduce the gastric surface. Paradoxically, the serum level of ghrelin in patients is preserved. We hypothesized about the role of embryonic pancreatic epsilon cells, which have the capacity to release ghrelin. We studied the changes in the epsilon cells and differentiation markers with immunostaining and ghrelin serum level and after surgery. We employed euglycemic male Wistar rats: two surgical groups (Sleeve gastrectomy and Roux- en Y Gastric Bypass) and two control groups. We reported a significant increase of ghrelin epsilon-cells in the pancreas and basal serum after Sleeve gastrectomy versus the control groups. The epsilon cellular increment was related to neogenesis, as the neurogenin-3 marker revealed. The Roux-en Y Gastric Bypass showed neither epsilon cell increase nor basal serum changes in ghrelin release. As a conclusion, we reported that the severe suppression of the fundus gastric produced the recovery of ghrelin released by the epsilon cells, which was indicative of an ontogenic embryonic pancreatic function
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    Significance of proneural basic helix-loop-helix transcription factors in neuroendocrine differentiation of fetal lung epithelial cells and lung carcinoma cells
    (Murcia : F. Hernández, 2001) Ito, T.; Udaka, N.; Ikeda, M.; Yazawa, T.; Kageyama, R.; Kitamura, H.
    In this brief review article, we describe how cell fate determination by which the airway epithelial cells become neuroendocrine or non-neuroendocrine is regulated by a network of basic helix-loop-helix transcription (bHLH) factors in a similar manner to neurona1 differentiation, and how this system could work to determine cell differentiation of human lung carcinomas. Immunohistochemical studies reveal that mammalina achaete-scute complex homologue (Mash)l is expressed in pulmonary neuroendocrine cells (PNEC), while hairy and Enhancer of split (Hes)l is expressed in pulmonary non-neuroendocrine cells (non-PNEC). Studies using gene-deficient mice for the bHLH factors revealed that in Mashl homozygous null mice no PNEC are detected, while PNEC increase markedly in Hesl homozygous null mice. These obse~at ionss uggest that Mashl is an essential positive factor for neuroendocrine differentiation of lung epithelium, and that Hesl is one of the repressive factors for neuroendocrine differentiation. Moreover, immunohistochemical studies revealed that Notch receptors are detected in non-PNEC, and thus the Notch signalling pathway could play a role in the determination of airway epithelial cell differentiation. In human lung carcinomas, a similar bHLH network should operate to determine cell differentiation phenotypes. Generally, expression of the human homologue of Mashl (HASH1) is detected in small cell carcinoma and carcinoids, while Hesl seems to be expressed mainly in non-small cell carcinoma. Thus, proneuronal bHLH factors may play roles in cell fate determination of the airway epithelial system, and may regulate human airway epithelial cells in diseased conditions.
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    Symmetry applied to nuclear microanatomy: a review of gene function and cell differentiation
    (Murcia : F. Hernández, 2004) Bell, C.D.
    The purpose of this paper is to review current knowledge and understandings of gene control and cell differentiation, based upon an appreciation of a possible role that nuclear microanatomy and considerations of steric symmetry might play. Metaphase sister chromatids have identical base codes but show a mirror image symmetry of higher order coiling. Chromosomes in the interphase nucleus have spatially well defined domains and are anatomically distinct and ordered. Chromosomes are known to have interactions i.e. sex chromosome inactivation, PEV etc An hypothesis of gene activation is made based on steric interactions among chromosomes and between chromosomes and activating and repressor proteins. These interactions may be influenced by the handedness of higher order chromatid coiling, since homologues show mirror-image symmetrical coiling in metaphase, which might be retained to a certain degree in interphase. This may result in a binary switching of genes. All possible combinations of chromatids in the interphase nucleus, would be enabled by a differential segregation of homologous chromatids at mitosis. To conserve patterns of interchromatid interactions, there must be a programmed segregation of chromatids towards one of the two spindle pole attachments. This orientation might be effected by preferential attachment of microtubules to kinetochore attachment sites, by steric hindrance of the kinetochore by condensed chromatin which initially allows only unidirectional tubule attachment, or possibly by a tethering of interacting chromatids which would migrate en masse. An attempt to apply this hypothesis to some illustrative pathological conditions is made.
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    The emerging role of DOT1L in cell proliferation and differentiation: Friend or foe
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Wu, Di; Zhang, Jing; Jun, Yang; Liu, Li; Huang, Cuiyuan; Wang, Wei; Yang, Chaojun; Xiang, Zujin; Wu, Jingyi; Huang, Yifan; Meng, Di; Yang, Zishu; Zhou, Xiaoyan; Cheng, Chen; Yang, Jian
    Cell proliferation and differentiation are the basic physiological activities of cells. Mistakes in these processes may affect cell survival, or cause cell cycle dysregulation, such as tumorigenesis, birth defects and degenerative diseases. In recent years, it has been found that histone methyltransferase DOT1L is the only H3 lysine 79 methyltransferase, which plays an important role in the process of cell fate determination through monomethylation, dimethylation and trimethylation of H3K79. DOT1L has a pro-proliferative effect in leukemia cells; however, loss of heart-specific DOT1L leads to increased proliferation of cardiac tissue. Additionally, DOT1L has carcinogenic or tumor suppressive effects in different neoplasms. At present, some DOT1L inhibitors for the treatment of MLL-driven leukemia have achieved promising results in clinical trials, but completely blocking DOT1L will also bring some side effects. Thus, this uncertainty suggests that DOT1L has a unique function in cell physiology. In this review, we summarize the primary findings of DOT1L in regulating cell proliferation and differentiation. Correlations between DOT1L and cell fate specification might suggest DOT1L as a therapeutic target for diseases.