scholarly journals Lipid Mediators and Human Leukemic Blasts

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Rémi Fiancette ◽  
Christelle Vincent-Fabert ◽  
Estelle Guerin ◽  
Franck Trimoreau ◽  
Yves Denizot
Keyword(s):  
Cell Proliferation ◽  
Inflammatory Mediators ◽  
Current Knowledge ◽  
Wide Spectrum ◽  
Platelet Activating Factor ◽  
Lipid Mediators ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Membrane Bound ◽  
Specific Membrane

Some of the most potent inflammatory mediators share a lipid origin. They regulate a wide spectrum of cellular processes including cell proliferation and apoptosis. However, the precise roles and ways (if any) in which these compounds impact the growth and apoptosis of leukemic blasts remain incompletely resolved. In spite of this, significant advances have been recently made. Here we briefly review the current knowledge about the production of lipid mediators (prostaglandins, leukotrienes, platelet-activating factor) by leukemic blasts, the enzymatic activities (phospholipaseA2, cyclooxygenases, lipoxygenases) involved in their productions and their effects (through specific membrane bound receptors) on the growth, and apoptosis of leukemic blasts.

scholarly journals Endotoxins and the importance of procalcitonin

2019 ◽  
Vol 67 (1) ◽  
pp. 169-170
Author(s):  
Paola Andrea Yasnó-Navia ◽  
Luisa Fernanda Zuñiga-Ceron ◽  
Jhan Sebastián Saavedra-Torres ◽  
María Virginia Pinzón-Fernández
Keyword(s):  
Septic Shock ◽  
Immune Response ◽  
Cell Wall ◽  
Outer Membrane ◽  
Inflammatory Mediators ◽  
Platelet Activating Factor ◽  
Cellular Level ◽  
Lipid Mediators ◽  
The State ◽  
Gram Negative

Gram-negative bacilli and cocci bacteria produce and release endotoxins, which are lipopolysaccharides found in the outer membrane of the cell wall. These endotoxins are responsible for releasing a series of inflammatory mediators such as IL1, TNFα and proteases, as well as lipid mediators such as prostaglandins, leukotrienes, thromboxanes and platelet-activating factor, ultimately activitating immune response cells like leukocytes, macrophages and platelets. These cells amplify the response to shock, generate a procoagulant state and produce alterations at the cellular level, for example, damage to the endothelium, which in the end benefit and worsen the state of septic shock (Figure 1).

Malignant Nonhematological Effusion Characterization by Flow Cytometry

2016 ◽  
Vol 60 (4) ◽  
pp. 365-371 ◽  
Author(s):  
Ben Davidson
Keyword(s):  
Flow Cytometry ◽  
Cancer Biology ◽  
Current Knowledge ◽  
Quantitative Detection ◽  
Routine Practice ◽  
Stem Cell Markers ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Malignant Effusions ◽  
Monitoring Treatment

With the exception of hematological malignancies, flow cytometry (FC) is infrequently applied as an ancillary tool in the diagnosis of malignant effusions in most institutions. However, FC may be effectively used to differentiate between epithelial cells, mesothelial cells and leukocytes using antibodies against both cell surface and intracellular proteins, offering the advantage of quantitative analysis. Additionally, FC may be applied to the quantitative detection of cancer-associated molecules, including stem cell markers, as well as assessment of critical cellular processes, such as proliferation and apoptosis. Some of the latter tests may have relevance for monitoring treatment response in the presence of metastatic disease, although this does not constitute routine practice to date. This review summarizes current knowledge regarding the application of FC to serous effusions in the diagnostic setting, as well as in research into cancer biology focusing on clinical specimens. The studies published to date suggest a role for this method in the clinical setting in the context of diagnosis, prediction and prognosis.

scholarly journals MicroRNAs as Novel Regulators of Neuroinflammation

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Dominika Justyna Ksiazek-Winiarek ◽  
Magdalena Justyna Kacperska ◽  
Andrzej Glabinski
Keyword(s):  
Multiple Sclerosis ◽  
Current Knowledge ◽  
Neurological Diseases ◽  
Small Noncoding Rnas ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Genetic And Environmental Factors ◽  
Ms Pathogenesis ◽  
Fine Tune

MicroRNAs are relatively recently discovered class of small noncoding RNAs, which function as important regulators of gene expression. They fine-tune protein expression either by translational inhibition or mRNA degradation. MicroRNAs act as regulators of diverse cellular processes, such as cell differentiation, proliferation, and apoptosis. Their defective biogenesis or function has been identified in various pathological conditions, like inflammation, neurodegeneration, or autoimmunity. Multiple sclerosis is one of the predominated debilitating neurological diseases affecting mainly young adults. It is a multifactorial disorder of as yet unknown aetiology. As far, it is suggested that interplay between genetic and environmental factors is responsible for MS pathogenesis. The role of microRNAs in this pathology is now extensively studied. Here, we want to review the current knowledge of microRNAs role in multiple sclerosis.

scholarly journals Glucocorticoid inhibits cell proliferation in differentiating osteoblasts by microRNA-199a targeting of WNT signaling

2015 ◽  
Vol 54 (3) ◽  
pp. 325-337 ◽  
Author(s):  
Changgui Shi ◽  
Ping Huang ◽  
Hui Kang ◽  
Bo Hu ◽  
Jin Qi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Transcriptional Repression ◽  
Wnt Signaling Pathway ◽  
Luciferase Reporter ◽  
Osteoblast Proliferation ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Proliferation Assays

The inhibition of osteoblast proliferation by glucocorticoids (GCs) is very important in the etiology of GC-induced osteoporosis. The mechanisms of this process are still not fully understood. The results of recent studies have indicated an important role for microRNAs in GC-mediated responses in various cellular processes, including cell proliferation and apoptosis. Therefore, we developed the hypothesis that these regulatory molecules might be involved in GC-decreased osteoblast proliferation. Western blotting, quantitative real-time PCR, cell proliferation assays, and luciferase assays were employed to investigate the role of miRNAs in GC-inhibited osteoblast proliferation. microRNA-199a-5p was significantly increased in osteoblasts treated with dexamethasone (Dex). To delineate the role of microRNA-199a-5p, we silenced and overexpressed microRNA-199a-5p in osteoblasts. We found that overexpressing microRNA-199a-5p remarkably increased the inhibition effect of Dex on osteoblast proliferation, and depleting microRNA-199a-5p significantly attenuated Dex-inhibited osteoblast proliferation. Results of mechanistic studies indicated that microRNA-199a-5p inhibited FZD4 and WNT2 expression through a microRNA-199a-5p binding site within the 3′-UTR of FZD4 and WNT2. The post-transcriptional repression of FZD4 and WNT2 were further confirmed by luciferase reporter assay. These results indicated that microRNA-199a-5p may play a significant role in GC-inhibited osteoblast proliferation by regulating the WNT signaling pathway.

scholarly journals An emerging potential therapeutic target for osteoporosis: LncRNA H19/miR-29a-3p axis

2020 ◽  
Vol 64 (4) ◽  
Author(s):  
Ziqi Li ◽  
Zhinan Hong ◽  
Yuesheng Zheng ◽  
Yongwei Dong ◽  
Wei He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Inflammatory Mediators ◽  
Therapeutic Target ◽  
Systemic Disease ◽  
Bone Fragility ◽  
Potential Therapeutic Target ◽  
Health Control ◽  
Proliferation And Apoptosis ◽  
Increase Risk

Osteoporosis (OP) is a complex systemic disease characterized by a loss of bone density, leading to bone fragility and an increase risk of fractures of the hip, spine and wrist. The clinical therapeutic effect is still far from satisfactory. Thus, further studies are urgently needed to explore the pathogenesis of OP. In this study, our aim is to explore the underlying molecular mechanism of lncRNA H19/miR-29a-3p axis for regulating of inflammation, proliferation and apoptosis in OP. The expression of lncRNA H19 was significantly upregulated in OP samples compared with the health control. Subsequently, we found that miR-29a-3p is the target of lncRNA H19 in OP. Furthermore, the knockdown of lncRNA H19 was validated to promote the expression of pro-inflammatory mediators, repress cell proliferation and inhibit cell apoptosis in vitro. Moreover, the modulating effects of lncRNA-H19 on the expressions of pro-inflammatory mediators, cell proliferation and apoptosis in vitro were diminished after co-transfecting with miR-29a-3p inhibitor and siRNA-H19. Thus, we concluded that lncRNA H19/miR-29a-3p axis was involved in the development of OP. This study might provide a better understanding of OP development and a potential therapeutic target for OP intervention.

scholarly journals The Manifold Cellular Functions of von Willebrand Factor

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2351
Author(s):  
Angelika Mojzisch ◽  
Maria A. Brehm
Keyword(s):  
Cell Proliferation ◽  
Von Willebrand Factor ◽  
Current Knowledge ◽  
Coagulation Factor ◽  
Cellular Functions ◽  
Cellular Processes ◽  
Cargo Proteins ◽  
Plasma Glycoprotein ◽  
Von Willebrand ◽  
Willebrand Factor

The plasma glycoprotein von Willebrand factor (VWF) is exclusively synthesized in endothelial cells (ECs) and megakaryocytes, the precursor cells of platelets. Its primary function lies in hemostasis. However, VWF is much more than just a “fishing hook” for platelets and a transporter for coagulation factor VIII. VWF is a true multitasker when it comes to its many roles in cellular processes. In ECs, VWF coordinates the formation of Weibel–Palade bodies and guides several cargo proteins to these storage organelles, which control the release of hemostatic, inflammatory and angiogenic factors. Leukocytes employ VWF to assist their rolling on, adhesion to and passage through the endothelium. Vascular smooth muscle cell proliferation is supported by VWF, and it regulates angiogenesis. The life cycle of platelets is accompanied by VWF from their budding from megakaryocytes to adhesion, activation and aggregation until the end in apoptosis. Some tumor cells acquire the ability to produce VWF to promote metastasis and hide in a shell of VWF and platelets, and even the maturation of osteoclasts is regulated by VWF. This review summarizes the current knowledge on VWF’s versatile cellular functions and the resulting pathophysiological consequences of their dysregulation.

Some Aspects of the Polyhexamethyleneguanidine Salts Effect on Cell Cultures

2014 ◽  
Vol 1 (1) ◽  
pp. 62-67 ◽  
Author(s):  
M. Mandygra ◽  
A. Lysytsia
Keyword(s):  
Proliferative Activity ◽  
Cell Monolayer ◽  
Eukaryotic Cell ◽  
Culture Methods ◽  
Cellular Processes ◽  
Negative Effect ◽  
Membrane Bound ◽  
Membrane Bound Enzymes ◽  
Anion Type ◽  
Cell Culture Methods

Aim. To investigate the effect of polyhexamethyleneguanidine (PHMG) to eukaryotic cell culture. Methods. The passaged bovine tracheal cells culture (TCC) and primary culture of chicken embryo fi broblasts (FCE) were used in the experiments. TCC and FCE monolayers were treated with aqueous solutions of PHMG chloride or succinate. The method of PHMG polycation adsorption to the cells’ plasma membrane together with microscopy were applied. Results. The dependence of PHMG effect on the eukaryotic cells on the agent concentration, duration of exposure and the anion type has been fi xed. The PHMG concentration of 10 –5 per cent (0.1 μg/ml) never causes degradation of the previously formed cell monolayer, while the higher concentrations damage it. The conditions of the PHMG chloride and succinate’s negative effect on cell proliferation and inhibition of monolayer formation were determined. The hypothesis that under certain conditions PHMG stimulates the proliferative activity of the cells has been confi rmed. Stimulation may be associated with non-specifi c stress adaptation of cells. In this case, it is due to modifi cations of the cell membrane after PHMG adsorption to it. Conclusions. PHMG polycation binds with the membrane’s phosphoglycerides fi rmly and irreversibly. A portion of the lipids are removed from participation in the normal cellular processes at that. At the same time, the synthesis of new lipids and membrane-bound enzymes is probably accelerated. The phospholip ids’ neogenesis acceleration can stimulate mitosis under certain conditions. The obtained results can be used in the biotechnologies.

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