Release of cellular cholesterol: molecular mechanism for cholesterol homeostasis in cells and in the body

2000 ◽  
Vol 1529 (1-3) ◽  
pp. 231-244 ◽  
Author(s):  
S Yokoyama
Keyword(s):  
Molecular Mechanism ◽  
The Body ◽  
Cholesterol Homeostasis ◽  
Cellular Cholesterol ◽  
In Cells

scholarly journals Epithelial Protein Lost in Neoplasm, EPLIN, the Cellular and Molecular Prospects in Cancers

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1038
Author(s):  
Jianyuan Zeng ◽  
Wen G. Jiang ◽  
Andrew J. Sanders
Keyword(s):  
The Body ◽  
Early Years ◽  
Actin Binding ◽  
Cell Cycle Gene ◽  
Lim Domain ◽  
The Past ◽  
Concise Review ◽  
Cancerous Cell ◽  
Cytoskeletal Dynamics ◽  
In Cells

Epithelial Protein Lost In Neoplasm (EPLIN), also known as LIMA1 (LIM Domain And Actin Binding 1), was first discovered as a protein differentially expressed in normal and cancerous cell lines. It is now known to be key to the progression and metastasis of certain solid tumours. Despite a slow pace in understanding the biological role in cells and body systems, as well as its clinical implications in the early years since its discovery, recent years have witnessed a rapid progress in understanding the mechanisms of this protein in cells, diseases and indeed the body. EPLIN has drawn more attention over the past few years with its roles expanding from cell migration and cytoskeletal dynamics, to cell cycle, gene regulation, angiogenesis/lymphangiogenesis and lipid metabolism. This concise review summarises and discusses the recent progress in understanding EPLIN in biological processes and its implications in cancer.

d-threo-1-Phenyl-2-decanoylamino-3-morpholino-1-propanol Alters Cellular Cholesterol Homeostasis by Modulating the Endosome Lipid Domains†

Biochemistry ◽  
2006 ◽  
Vol 45 (14) ◽  
pp. 4530-4541 ◽  
Author(s):  
Asami Makino ◽  
Kumiko Ishii ◽  
Motohide Murate ◽  
Tomohiro Hayakawa ◽  
Yusuke Suzuki ◽  
...  
Keyword(s):  
Cholesterol Homeostasis ◽  
Lipid Domains ◽  
Cellular Cholesterol

scholarly journals Insights into genome recoding from the mechanism of a classic +1-frameshifting tRNA

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Howard Gamper ◽  
Haixing Li ◽  
Isao Masuda ◽  
D. Miklos Robkis ◽  
Thomas Christian ◽  
...  
Keyword(s):  
Amino Acids ◽  
Conformational Change ◽  
Molecular Mechanism ◽  
Late Stage ◽  
Anticodon Loop ◽  
Pairing Mechanism ◽  
Extra Nucleotide ◽  
In Cells

AbstractWhile genome recoding using quadruplet codons to incorporate non-proteinogenic amino acids is attractive for biotechnology and bioengineering purposes, the mechanism through which such codons are translated is poorly understood. Here we investigate translation of quadruplet codons by a +1-frameshifting tRNA, SufB2, that contains an extra nucleotide in its anticodon loop. Natural post-transcriptional modification of SufB2 in cells prevents it from frameshifting using a quadruplet-pairing mechanism such that it preferentially employs a triplet-slippage mechanism. We show that SufB2 uses triplet anticodon-codon pairing in the 0-frame to initially decode the quadruplet codon, but subsequently shifts to the +1-frame during tRNA-mRNA translocation. SufB2 frameshifting involves perturbation of an essential ribosome conformational change that facilitates tRNA-mRNA movements at a late stage of the translocation reaction. Our results provide a molecular mechanism for SufB2-induced +1 frameshifting and suggest that engineering of a specific ribosome conformational change can improve the efficiency of genome recoding.

scholarly journals Nedd4-2 but not Nedd4-1 is critical for protein kinase C-regulated ubiquitination, expression, and transport activity of human organic anion transporter 1

2016 ◽  
Vol 310 (9) ◽  
pp. F821-F831 ◽  
Author(s):  
Da Xu ◽  
Haoxun Wang ◽  
Qiang Zhang ◽  
Guofeng You
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Surface ◽  
Organic Anion ◽  
The Body ◽  
Organic Anion Transporter ◽  
Transport Activity ◽  
Kinase C ◽  
Anion Transporter ◽  
In Cells

Human organic anion transporter 1 (hOAT1) expressed at the membrane of the kidney proximal tubule cells mediates the body disposition of a diverse array of clinically important drugs, including anti-HIV therapeutics, antitumor drugs, antibiotics, antihypertensives, and antiinflammatories. Therefore, understanding the regulation of hOAT1 will provide significant insights into kidney function and dysfunction. We previously established that hOAT1 transport activity is inhibited by activation of protein kinase C (PKC) through accelerating hOAT1 internalization from cell surface into intracellular endosomes and subsequent degradation. We further established that PKC-induced hOAT1 ubiquitination is an important step preceding hOAT1 internalization. In the current study, we identified two closely related E3 ubiquitin ligases, neural precursor cell expressed, developmentally downregulated 4-1 and 4-2 (Nedd4-1 and Nedd4-2), as important regulators for hOAT1: overexpression of Nedd4-1 or Nedd4-2 enhanced hOAT1 ubiquitination, reduced the hOAT1 amount at the cell surface, and suppressed hOAT1 transport activity. In further exploring the relationship among PKC, Nedd4-1, and Nedd4-2, we discovered that PKC-dependent changes in hOAT1 ubiquitination, expression, and transport activity were significantly blocked in cells transfected with the ligase-dead mutant of Nedd4-2 (Nedd4-2/C821A) or with Nedd4-2-specific siRNA to knockdown endogenous Nedd4-2 but not in cells transfected with the ligase-dead mutant of Nedd4-1 (Nedd4-1/C867S) or with Nedd4-1-specific siRNA to knockdown endogenous Nedd4-1. In conclusion, this is the first demonstration that both Nedd4-1 and Nedd4-2 are important regulators for hOAT1 ubiquitination, expression, and function. Yet they play distinct roles, as Nedd4-2 but not Nedd4-1 is a critical mediator for PKC-regulated hOAT1 ubiquitination, expression, and transport activity.

scholarly journals Toxicity study of new metal nanoparticles functionalized with fluorescein derivatives as novel image systems

2013 ◽  
Vol 19 (S4) ◽  
pp. 25-26 ◽  
Author(s):  
A. Fernandéz-Lodeiro ◽  
J. Fernandéz-Lodeiro ◽  
C. Nuñez ◽  
E. Oliveira ◽  
H.M. Santos ◽  
...  
Keyword(s):  
The Body ◽  
Limited Information ◽  
Glutathione S Transferase ◽  
Ag Nps ◽  
One Pot ◽  
Novel Treatments ◽  
Transmission Electron ◽  
Dying Cells ◽  
Gastro Intestinal Tract ◽  
In Cells

Nanoparticles in general (NPs) and/or nanomaterials offer remarkable opportunities in industrial production, daily consumables, medicine, biotechnology, electronics and numerous other important commercial and economical areas. Among all these areas, nanomedicine has opened novel treatments for problematic diseases such as viral, genetic, cancer, AIDS, etc. There is limited information available regarding translocation and distribution of NPs in the body and in the environment. Additionally, there is also need for more information on NPs toxicity. Recently has been demonstrated that physiological barriers such as pulmonary and gastro-intestinal tract are affected.The main objective of this work is to use functionalized metal NPs, as emissive agent markers, assess their internalization in cells and evaluate toxicity to cells.Using the emissive two probes synthesized in a one-pot reaction using fluoresceine as chromophore, several gold (Au), round shape, and silver (Ag) NPs (round and triangular shapes) were functionalized in organic media and water by Brust and Turkevish methodology, using tetraoctylammonium bromide (TOABr) as a common stabilizer and sodium borohydride as reducing agent. All has been characterized by UV-vis and emission spectroscopy, transmission electron microscopy (TEM) (Figure 1), and Light scattering. To study the route of internalization into the cell NP-complexes were injected intraperitoneally in fish (Carassius auratus). After 48 hour fish were sampled and sacrificed and liver and intestine processed for histology examination. Additional sub-samples were stored at – 80ºC for enzymatic analysis (glutathione-S-transferase and catalase). Blood was also collected from healthy non-injected fish, for leucocyte separation followed by incubation with the metal NPs and cell viability assays. The presence of emissive NPs in cells was examined by microscopy using a Leica microscope (ATC 2000) adapted for epifluorescence (EF).The microscopy analysis showed that apparently both metal NPs were internalized by leucocytes and intestine cells (Figure 2a and 2b) but apparently not by hepatocytes. However, it is still to clarify if NPs internalization occurred in dead or dying cells only, with more permeable membranes, or also in living cells. Another possibility relates to the detection limits and resolution of the microscope used: the fraction of NPs entering is too low and not detectable with this type of equipment. No significant fluorescence was detected in controls. Viability assays showed higher mortality rates in leucocytes incubated with triangular Ag NPs suggesting that the type of metal and shape have influence in cell toxicity. In general, enzymatic assays indicate low oxidative stress for cells. However, GST results show significant (p > 0.05) differences in livers from fish injected with round Ag NPs. With respect to catalase, significant differences (p > 0.05) were detected in livers from fish injected with round Au NPs. Although the presented results are preliminary they suggest that functionalized NPs are able to penetrate cell membranes. On the other hand, the observed toxicity can be attributed to differences in shape and type of metal NPs.The authors acknowledge the funding by Fundação para a Ciência e Tecnologia through grant PTDC/MAR/119068/2010 and through project no. PEst-C/EQB/LA0006/2011 granted to Requimte.

scholarly journals Membrane Organization and Regulation of Cellular Cholesterol Homeostasis

2010 ◽  
Vol 234 (3) ◽  
pp. 183-194 ◽  
Author(s):  
María S. Jaureguiberry ◽  
M. Alejandra Tricerri ◽  
Susana A. Sanchez ◽  
Horacio A. Garda ◽  
Gabriela S. Finarelli ◽  
...  
Keyword(s):  
Cholesterol Homeostasis ◽  
Membrane Organization ◽  
Cellular Cholesterol

scholarly journals Anti-adipogenic and anti-obesity activities of purpurin in 3T3-L1 preadipocyte cells and in mice fed a high-fat diet

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Woo Nam ◽  
Seok Hyun Nam ◽  
Sung Phil Kim ◽  
Carol Levin ◽  
Mendel Friedman
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Biological Activities ◽  
The Body ◽  
High Fat ◽  
In Vivo Models ◽  
Triglyceride Accumulation ◽  
In Cells

Abstract Background The body responds to overnutrition by converting stem cells to adipocytes. In vitro and in vivo studies have shown polyphenols and other natural compounds to be anti-adipogenic, presumably due in part to their antioxidant properties. Purpurin is a highly antioxidative anthraquinone and previous studies on anthraquinones have reported numerous biological activities in cells and animals. Anthraquinones have also been used to stimulate osteoblast differentiation, an inversely-related process to that of adipocyte differentiation. We propose that due to its high antioxidative properties, purpurin administration might attenuate adipogenesis in cells and in mice. Methods Our study will test the effect purpurin has on adipogenesis using both in vitro and in vivo models. The in vitro model consists of tracking with various biomarkers, the differentiation of pre-adipocyte to adipocytes in cell culture. The compound will then be tested in mice fed a high-fat diet. Murine 3T3-L1 preadipocyte cells were stimulated to differentiate in the presence or absence of purpurin. The following cellular parameters were measured: intracellular reactive oxygen species (ROS), membrane potential of the mitochondria, ATP production, activation of AMPK (adenosine 5′-monophosphate-activated protein kinase), insulin-induced lipid accumulation, triglyceride accumulation, and expression of PPARγ (peroxisome proliferator activated receptor-γ) and C/EBPα (CCAAT enhancer binding protein α). In vivo, mice were fed high fat diets supplemented with various levels of purpurin. Data collected from the animals included anthropometric data, glucose tolerance test results, and postmortem plasma glucose, lipid levels, and organ examinations. Results The administration of purpurin at 50 and 100 μM in 3T3-L1 cells, and at 40 and 80 mg/kg in mice proved to be a sensitive range: the lower concentrations affected several measured parameters, whereas at the higher doses purpurin consistently mitigated biomarkers associated with adipogenesis, and weight gain in mice. Purpurin appears to be an effective antiadipogenic compound. Conclusion The anthraquinone purpurin has potent in vitro anti-adipogenic effects in cells and in vivo anti-obesity effects in mice consuming a high-fat diet. Differentiation of 3T3-L1 cells was dose-dependently inhibited by purpurin, apparently by AMPK activation. Mice on a high-fat diet experienced a dose-dependent reduction in induced weight gain of up to 55%.

scholarly journals Cellular cholesterol homeostasis in vascular endothelial cells

2006 ◽  
Vol 22 ◽  
pp. 35B-40B ◽  
Author(s):  
Houssein Hajj Hassan ◽  
Maxime Denis ◽  
Larbi Krimbou ◽  
Michel Marcil ◽  
Jacques Genest
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Cholesterol Homeostasis ◽  
Vascular Endothelial ◽  
Cellular Cholesterol
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