scholarly journals Phenylethanoid Glycosides from Cistanche tubulosa Inhibits the Growth of B16-F10 Cells both in Vitro and in Vivo by Induction of Apoptosis via Mitochondria-dependent Pathway

2016 ◽  
Vol 7 (13) ◽  
pp. 1877-1887 ◽  
Author(s):  
Jinyu Li ◽  
Jinyao Li ◽  
Adila Aipire ◽  
Li Gao ◽  
Shixia Huo ◽  
...  
Keyword(s):  
Phenylethanoid Glycosides ◽  
Induction Of Apoptosis ◽  
Cistanche Tubulosa ◽  
Dependent Pathway

scholarly journals Effects of Ubiquinol-10 on MicroRNA-146a Expression In Vitro and In Vivo

2009 ◽  
Vol 2009 ◽  
pp. 1-7 ◽  
Author(s):  
Constance Schmelzer ◽  
Mitsuaki Kitano ◽  
Gerald Rimbach ◽  
Petra Niklowitz ◽  
Thomas Menke ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Biological Processes ◽  
Oxygen Species ◽  
Moderate Reduction ◽  
Suppression Of Gene Expression ◽  
Fine Tune ◽  
Dependent Pathway

MicroRNAs (miRs) are involved in key biological processes via suppression of gene expression at posttranscriptional levels. According to their superior functions, subtle modulation of miR expression by certain compounds or nutrients is desirable under particular conditions. Bacterial lipopolysaccharide (LPS) induces a reactive oxygen species-/NF-κB-dependent pathway which increases the expression of the anti-inflammatory miR-146a. We hypothesized that this induction could be modulated by the antioxidant ubiquinol-10. Preincubation of human monocytic THP-1 cells with ubiquinol-10 reduced the LPS-induced expression level of miR-146a to 78.9±13.22%. In liver samples of mice injected with LPS, supplementation with ubiquinol-10 leads to a reduction of LPS-induced miR-146a expression to 78.12±21.25%. From these consistent in vitro and in vivo data, we conclude that ubiquinol-10 may fine-tune the inflammatory response via moderate reduction of miR-146a expression.

scholarly journals Salmonella-Induced Caspase-2 Activation in Macrophages

2000 ◽  
Vol 192 (7) ◽  
pp. 1035-1046 ◽  
Author(s):  
Veronika Jesenberger ◽  
Katarzyna J. Procyk ◽  
Junying Yuan ◽  
Siegfried Reipert ◽  
Manuela Baccarini
Keyword(s):  
Type Iii Secretion ◽  
Caspase 3 ◽  
Secretion System ◽  
Caspase 1 ◽  
Chemical Inhibition ◽  
Induction Of Apoptosis ◽  
Caspase 2 ◽  
Induced Apoptosis

The enterobacterial pathogen Salmonella induces phagocyte apoptosis in vitro and in vivo. These bacteria use a specialized type III secretion system to export a virulence factor, SipB, which directly activates the host's apoptotic machinery by targeting caspase-1. Caspase-1 is not involved in most apoptotic processes but plays a major role in cytokine maturation. We show that caspase-1–deficient macrophages undergo apoptosis within 4–6 h of infection with invasive bacteria. This process requires SipB, implying that this protein can initiate the apoptotic machinery by regulating components distinct from caspase-1. Invasive Salmonella typhimurium targets caspase-2 simultaneously with, but independently of, caspase-1. Besides caspase-2, the caspase-1–independent pathway involves the activation of caspase-3, -6, and -8 and the release of cytochrome c from mitochondria, none of which occurs during caspase-1–dependent apoptosis. By using caspase-2 knockout macrophages and chemical inhibition, we establish a role for caspase-2 in both caspase-1–dependent and –independent apoptosis. Particularly, activation of caspase-1 during fast Salmonella-induced apoptosis partially relies on caspase-2. The ability of Salmonella to induce caspase-1–independent macrophage apoptosis may play a role in situations in which activation of this protease is either prevented or uncoupled from the induction of apoptosis.

Abstract 230: Lipoprotein X Causes Renal Disease in LCAT Deficiency

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Edward B Neufeld ◽  
Alice Ossoli ◽  
Seth G Thacker ◽  
Boris Vaisman ◽  
Milton Pryor ◽  
...  
Keyword(s):  
Renal Disease ◽  
Plasma Clearance ◽  
Mesangial Cells ◽  
Chemical Properties ◽  
Low Hdl ◽  
Lcat Deficiency ◽  
Physical And Chemical ◽  
Dependent Pathway

Familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is characterized by low HDL, accumulation of an abnormal cholesterol-rich multilamellar particle called lipoprotein-X (LpX) in plasma, and renal disease. The aim of our study was to determine if LpX is nephrotoxic and to gain insight into the pathogenesis of FLD renal disease. We administered a synthetic LpX, nearly identical to endogenous LpX in its physical, and chemical properties, to wild-type and Lcat -/- mice. Our in vitro and in vivo studies demonstrated an apoA-I and LCAT-dependent pathway for LpX conversion to HDL-like particles, which likely mediates normal plasma clearance of LpX. Plasma clearance of exogenous LpX was markedly delayed in Lcat -/- mice, which have low HDL but only minimal amounts of endogenous LpX and do not spontaneously develop renal disease. Chronically administered exogenous LpX deposited in all renal glomerular cellular and matrical compartments of Lcat -/- mice, and induced proteinuria and nephrotoxic gene changes, as well as all of the hallmarks of FLD renal disease as assessed by histological, TEM, and SEM analyses. Extensive in vivo EM studies revealed LpX uptake by macropinocytosis into mouse glomerular endothelial cells, podocytes, and mesangial cells and delivery to lysosomes, where it was degraded. Endocytosed LpX appeared to be degraded by both human podocyte and mesangial cell lysosomal PLA 2 and induced podocyte secretion of pro-inflammatory IL-6 in vitro and renal Cxl10 expression in Lcat -/- mice. In conclusion, LpX is a nephrotoxic particle that in the absence of LCAT induces all of the histological and functional hallmarks of FLD and hence may serve as a biomarker for monitoring recombinant LCAT therapy. In addition, our studies suggest that LpX-induced loss of endothelial barrier function and release of cytokines by renal glomerular cells likely plays a role in the initiation and progression of FLD nephrosis.

scholarly journals Solid lipid nanoparticle induced apoptosis of macrophages via a mitochondrial-dependent pathway in vitro and in vivo

2019 ◽  
Vol Volume 14 ◽  
pp. 3283-3295 ◽  
Author(s):  
Wan-Li Liang ◽  
Lan Xiao ◽  
Hong-Wei Gu ◽  
Xiao-Jun Li ◽  
Yu-Sang Li ◽  
...  
Keyword(s):  
Solid Lipid Nanoparticle ◽  
Solid Lipid ◽  
Lipid Nanoparticle ◽  
Induced Apoptosis ◽  
Dependent Pathway

scholarly journals Induction of apoptosis by in vitro and in vivo plant extracts derived from Menyanthes trifoliata L. in human cancer cells

2019 ◽  
Vol 71 (1) ◽  
pp. 165-180 ◽  
Author(s):  
Tomasz Kowalczyk ◽  
Przemysław Sitarek ◽  
Ewa Skała ◽  
Monika Toma ◽  
Marzena Wielanek ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Plant Extracts ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Induction Of Apoptosis ◽  
Menyanthes Trifoliata

scholarly journals cAMP levels regulate macrophage alternative activation marker expression

2020 ◽  
pp. 175342592097508
Author(s):  
Swamy Polumuri ◽  
Darren J Perkins ◽  
Stefanie N Vogel
Keyword(s):  
G Protein Coupled Receptors ◽  
Alternative Activation ◽  
Marker Genes ◽  
Marker Expression ◽  
Inflammatory Milieu ◽  
G Protein Coupled ◽  
Camp Levels ◽  
Dependent Pathway

The capacity for macrophages to polarize into distinct functional activation states (e.g., M1, M2) is critical to tune an inflammatory response to the relevant infection or injury. Alternative or M2 polarization of macrophages is most often achieved in vitro in response to IL-4/IL-13 and results in the transcriptional up-regulation of a constellation of characteristic M2 marker genes. In vivo, additional signals from the inflammatory milieu can further increase or decrease M2 marker expression. Particularly, activation of cAMP-generating G protein-coupled receptors is reported to increase M2 markers, but whether this is strictly dependent upon cAMP production is unclear. We report herein that increased cAMP alone can increase IL-4-dependent M2 marker expression through a PKA/C/EBPβ/CREB dependent pathway in murine macrophages.

Kinetic evidence for separate systems in transport of D- and L-methionine by rat small intestine

1987 ◽  
Vol 252 (3) ◽  
pp. G320-G324
Author(s):  
P. Brachet ◽  
F. Alvarado ◽  
A. Puigserver
Keyword(s):  
Brush Border Membrane ◽  
Diffusion Constant ◽  
Membrane Vesicles ◽  
Beta Alanine ◽  
Imino Acid ◽  
Methionine Uptake ◽  
Kinetics Of ◽  
Dependent Pathway

The kinetics of D- and L-methionine uptake by rings of everted intestine in vitro are consistent with a saturable Michaelis-Menten component (Km = 11.7 and 1.7 mM; Vmax = 0.53 and 0.74 mumol X g-1 X min-1 for D- and L-methionine, respectively) plus a linear, diffusional one. All the data could be fit with a diffusion constant (Kd = 3.2 microliters X g-1 X min-1), which was essentially the same, independent of whether it was estimated by iteration or by using the extracellular marker, inulin. Similar results were obtained from in vivo perfusion experiments, except that the diffusional term was negligible. D-Methionine was found to inhibit L-methionine uptake by intestinal rings according to fully noncompetitive kinetics (Ki = 45 mM). Another set of experiments with jejunal brush-border membrane vesicles showed that D-methionine uptake is dependent on a Na+ gradient and is significantly inhibited by L-methionine and L-proline, but not by beta-alanine and alpha-methylaminoisobutyric acid. Our results indicate that, in rat jejunum, D-methionine is taken up through a Na+-dependent pathway distinct from the neutral amino acid (L-methionine) carrier and from the imino acid (L-proline, alpha-methylaminoisobutyric acid, beta-alanine) carrier.

Juniperus communis Suppresses Melanoma Tumorigenesis by Inhibiting Tumor Growth and Inducing Apoptosis

2019 ◽  
Vol 47 (05) ◽  
pp. 1171-1191 ◽  
Author(s):  
Hong-Wei Gao ◽  
Xiao-Fan Huang ◽  
Tzi-Peng Yang ◽  
Kai-Fu Chang ◽  
Ling-Wen Yeh ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Death Rate ◽  
Tumor Burden ◽  
Autocrine Signaling ◽  
Juniperus Communis ◽  
Common Skin ◽  
Metastatic Capacity ◽  
Induction Of Apoptosis

Melanoma, which has a high metastatic capacity and death rate, is a common skin cancer in Western countries. The purpose of this study was to address whether Juniperus communis (JCo) extract is effective in the suppression of melanoma and to elucidate the anticancer mechanisms involved in vitro and in vivo. The antitumor capacities of JCo extract on tumor suppression and toxicity were evaluated and the results demonstrated that the tumor burden was reduced via mediation of cell cycle, reduction of autocrine signaling, and induction of apoptosis. Moreover, JCo extract significantly prolonged the survival rate of the test subjects with only low pathological and physiological toxicity. Additionally, JCo extract also reduced cancer stem cell-related angiogenic and metastatic proteins in the process of tumor elimination. Based on these results, this study suggests that JCo extract suppresses tumor growth and induces apoptosis, and JCo extract may be useful for the prevention of melanoma tumorigenesis.

scholarly journals Induction of apoptosis by human Nbk/Bik, a BH3-containing protein that interacts with E1B 19K.

1996 ◽  
Vol 16 (10) ◽  
pp. 5857-5864 ◽  
Author(s):  
J Han ◽  
P Sabbatini ◽  
E White
Keyword(s):  
Apoptotic Cell ◽  
Yeast Two Hybrid ◽  
Nuclear Membranes ◽  
Induction Of Apoptosis ◽  
Low Levels ◽  
Apoptosis Inhibitor ◽  
Apoptosis Proteins ◽  
Two Hybrid

The E1B 19-kilodalton protein (19K protein) is a potent apoptosis inhibitor and the adenovirus homolog of Bcl-2 (E. White, Genes Dev. 10:1-15, 1996). To obtain a better understanding of the biochemical mechanism by which the E1B 19K protein regulates apoptosis, proteins that interact with 19K have been identified; one of these is Bax (J. Han, P. Sabbatini, D. Perez, L. Rao, D. Mohda, and E. White, Genes Dev. 10:461-477, 1996), and another is Bak (S. N. Farrow, J. H. M. White, I. Martinou, T. Raven, K.-T. Pun, C. J. Grinham, J.-C. Martinou, and R. Brown, Nature (London) 374:731-733, 1995). Bax and Bak are Bcl-2 family members which contain Bcl-2 homology regions 1, 2, and 3 (BH1, BH2, and BH3), which interact with E1B 19K and Bcl-2 and promote apoptosis. Like Bax and Bak, Nbk was cloned from a yeast two-hybrid screen for proteins that interact with E1B 19K. Nbk contained BH3 but not BH1 or BH2. It also interacted with Bcl-2 but not with Bax. Both Bcl-2 and E1B 19K interacted with Nbk in vitro, and this interaction was highly specific. In vivo, the Nbk and E1B 19K proteins may colocalize with cytoplasmic and nuclear membranes. Nbk expression functionally antagonized 19K-mediated inhibition of apoptotic cell death and completely prevented transformation by E1A and E1B 19K. Nbk was sufficient for induction of apoptosis in the presence of mutant p53 and thus low levels of Bax, suggesting that Nbk functions independently of Bax to induce apoptosis. Nbk may therefore represent a novel death regulator which contains only a BH3 that interacts with and antagonizes apoptosis inhibitors such as the E1B 19K protein.

Activity of dolastatin 10 against small-cell lung cancer in vitro and in vivo: induction of apoptosis and bcl-2 modification

1999 ◽  
Vol 43 (6) ◽  
pp. 507-515 ◽  
Author(s):  
Gregory P. Kalemkerian ◽  
Xiaolan Ou ◽  
Mohammed R. Adil ◽  
Rita Rosati ◽  
M. Monir Khoulani ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Induction Of Apoptosis ◽  
In Vivo Induction ◽  
Dolastatin 10
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