Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
enabled [disable] Abstract
Number of results

Results found: 10

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  DIFFERENTIATION
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
EN
The secretion of interleukin (IL)-2 is a key event in T cell activation. IL-2 allows T cells to enter into the S phase of the cell cycle and divide. After the activation phase takes place, T lymphocytes proliferate and differentiate to generate effector T cells. Thereby, T helper (Th) precursor cells, which are functionally immature, may become Th1 or Th2 effector cells. These subsets are responsible for cell-mediated immunity and humoral responses, respectively. Both, T cell activation and Th differentiation are processes that depend on changes in the pattern of gene expression. The expression and changes in the genes responsible for these events are regulated by transcription factors. This review will focus on both transcription factors involved in the control of IL-2, as well as those that are key in T helper differentiation.
EN
The role of response gene to complement (RGC)-32 as a cell cycle regulator has been attributed to its ability to activate cdc2 kinases and to induce S-phase entry and mitosis. However, recent studies revealed novel functions for RGC-32 in diverse processes such as cellular differentiation, inflammation, and fibrosis. Besides responding to C5b-9 stimulation, RGC-32 expression is also induced by growth factors, hormones, and cytokines. Transforming growth factor ? activates RGC-32 through Smad and RhoA signaling, thus initiating smooth muscle cell differentiation. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human malignancies, hyper-immunoglobulin E syndrome, and fibrosis. RCG-32 expression is up-regulated in cutaneous T cell lymphoma and colon, ovarian, and breast cancer, but down-regulated in invasive prostate cancer, multiple myeloma, and drug-resistant glioblastoma. A better understanding of the mechanism by which RGC-32 contributes to the pathogenesis of these diseases will provide new insights into its therapeutic potential. In this review we provide an overview of this field and discuss the most recent research on RGC-32.
EN
Conditioned medium obtained from B104 neuroblastoma cells (B104CM) has been used widely for inducing oligodendrocyte progenitor cells (OPCs) from neural precursor cells (NPCs). Our previous studies have demonstrated that E16 rat spinal cord-derived NPCs could be induced to differentiate into OPCs using a combination of B104CM and basic fibroblast growth factor (bFGF). Here we report the development of a more efficient and reliable approach to generate large quantities of highly purified OPCs from spinal cord-derived NPCs using a combination of platelet derived growth factor (PDGF) and bFGF. We demonstrated that, after the two factors application, over 90% cells displayed typical bipolar or tripolar morphology and expressed markers for OPCs including A2B5 (90.36 +/- 4.59%), NG2 (93.63 +/- 3.37%) and platelet derived growth factor alpha receptor (PDGFR; 90.35 +/- 1.95%). Our results indicated that the PDGF/bFGF combination is more efficient in generating OPCs than the B104CM/bFGF. And it is a more potent combination of factors in promoting proliferation of OPCs.
EN
Palmitoylcarnitine is synthesized through the action of palmitoylcarnitine transferase I - an enzyme specifically inhibited by etomoxir. An increase of the intracellular content of palmitoylcarnitine in neuroblastoma NB-2a cells after administration of carnitine was correlated with an inhibition of cell proliferation and a concomitant promotion of differentiation processes. The activity of protein kinase C was measured in vivo, with cells permeabilized through the use of streptolysin O and a peptide substrate. Palmitoylcarnitine inhibited the phorbol ester stimulated reaction of the peptide phosphorylation in a concentration dependent way. The degree of protein kinase C inhibition was correlated with intracellular increase of the palmitoylcarnitine content, pointing to this compound as a natural modulator of protein kinase C activity.
EN
Introduction: The relative contributions of CD4+ and CD8+ T cells to transplant rejection remains unknown. The authors integrated a previous model of CD4-mediated graft rejection with a complementary model of CD8-mediated rejection to directly compare the function of graft-reactive CD4+ and CD8+ lymphocytes in vivo in a model where rejection requires transgenic T cells. These studies allow direct comparison of CD4 and CD8 T cell responses to the same antigen without the confounding effects of T cell depletion or homeostatic proliferation. Materials and Methods: Clone 4 and TS1 mice possess MHC class I- and II-restricted CD8+ and CD4+ T cells, respectively, which express transgenic T cell receptors that recognize the influenza hemagglutinin antigen (HA). We compared the in vivo response of CFSE-labeled, HA-specific transgenic CD8+ and CD4+ T cells after adoptive transfer into syngeneic BALB/c mice grafted with HA-expressing skin. Results: As in the authors' CD4+ model, HA104 skin was consistently rejected by both Clone 4 mice (n=9, MST: 14.2) and by 5x105 Clone 4 lymphocytes transferred to naive BALB/c hosts that do not otherwise reject HA+ grafts. Rejection correlated with extensive proliferation of either graft-reactive T cell subset in the draining lymph nodes, and antigen-specific CD4+ and CD8+ cells acquired effector function and proliferated with similar kinetics.Conclusions: These data extend the authors' unique transgenic transplantation model to the investigation of CD8 T cell function. The initial results confirm fundamental functional similarity between the CD4 and CD8 T cell subsets and provide insight into the considerable redundancy underlying T cell mechanisms mediating allograft rejection.
EN
Recent studies have uncovered many aspects of the repair processes that follow airway epithelial injury. Although the repair process has common elements among various epithelia, such as the ones lining the airways, skin, and gut, there are differences based on their diverse functions. Whenever possible, similarities are pointed out that could help researchers further investigate their application to airway epithelia, although it would be beyond the scope of this review to cover the processes that may occur during the repair of all types of epithelia. In general, five major steps are involved in the recovery of airway epithelia from injury: 1) epithelial cells migrate to cover denuded areas within minutes, and certain proteins, such as the trefoil factor family proteins, are crucial to this process; 2) epithelial cells start to proliferate in order to replace injured cells and to differentiate to establish squamous or mucous cell metaplasia; 3) because more epithelial cells are present after proliferation, some of the cells must be discarded to restore the epithelium to the original condition; 4) once the cell numbers have been reduced to those found in unexposed individuals, the normal proportions of cell types are restored; 5) finally, studies from exposures of rats to ozone show that epithelial cells can adapt and develop a memory of the chronic exposure to which they were exposed. This adaptation allows the epithelium to respond quickly, thus minimizing further injury. Although the molecular mechanisms involved in these major steps of the recovery process are largely unknown, disruption of these steps clearly causes the permanent changes observed in diseases such as asthma, chronic bronchitis, and cancer; therefore, extensive research in these areas may provide ideas for novel therapies.
EN
The paper deals with time as a physical (space-time coordinate with specific properties and measure methods) as well as biological concept. Biological time is running differently taking in account various organizational levels like cell, cell organelles, whole organism and, finally, population or species. Time is a factor that regulates plant ontogenesis. In many plant species, time regulates seed dormancy and plant vernalization, photoperiodism and circadian rhythms. Time sets in motion the 'biological clock' which controls physiological and biochemical processes in plant, particularly the rate of enzymatic reactions, oscillation processes (circadian or annual rhythms), as well as internal 'cell clock' deciding upon the length of cell life as well as the rate of cell ageing processes. Senescence or death of particular cells do not mean death of the whole organism. In numerous plant species, death of individual cell is even a factor determining survival of the whole plant. The plant senescence is regulated by phytohormones such as abscisic acid, cytokinins or auxins. Time gathers new meaning in in vitro cultures. It may differ with respect to stable cell suspension culture in many cases maintaining an ability for cell multiplication for many years as compared to another fast regenerating cultures. The influence of various stress factors under in vitro conditions enables the'switching on' the clock controlling the processes of cell multiplication and differentiation.
EN
In the present study the functional role of SH groups in the Ca2+ -independent K+ selective channel activity in the membrane of bovine adrenal gland chromaffin granules has been studied. Ionic channel activity has been estimated using 86Rb+, a K+ analogue, flux measurements. The inhibition of chromaffin granules K+ channel by SH modifying agents, such as N ethylmaleimide, mersalyl and phenylarsenoxide, is described.
EN
Jasmonic acid (JA), methyl jasmonate (JA-Me) and their related compounds which are designated as jasmonates, are widely distributed in the plant kingdom and show various important biological activities in the regulation of plant growth and development, resulting in a consideration that they are putative new plant hormones. Endogenous levels of jasmonates, mainly JA, increase rapidly and transiently in plants or their organs under both abiotic and biotic stress conditions. Jasmonates consist of an integral part of the signal transduction chain between stress signal(s) and stress response(s). In this article, we focused on and reviewed the role of jasmonates in control of differentiation processes in tissue cultures, regeneration and micropropagation, somatic embryo formation, tuber initiation and formation. The involvement of jasmonates in tuberization, tuberous root formation and bulb formation was inferred from their ability to induce the processes in vitro, and from changes in the levels of endogenous jasmonates during the growth of the plants which can account for the initiation of tuberization. The tuberization and the expansion of cells induced by jasmonates always involve the reorientation of cortical microtubules. Differential effect of jasmonic acid on cell cycle progression is also presented. It is still an open question about interactions between jasmonates and other hormones (auxin, ethylene, cytokinins, abscisic acid) in the regulation of meristem activities, cell cycle and other physiological processes.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.