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891 results for “apoptosis”
MELAN-A EXPRESSION RELATED TO APOPTOSIS OF MELANOCYTES IN SEGMENTAL AND NONSEGMENTAL VITILIGO
<p><strong>Abstract</strong></p> <p><strong>Background: </strong>Vitiligo is a progressive depigmentation of the skin with unclear etiology. Cell-mediated immunity has been suggested to play an important role in the pathogenesis of vitiligo’s progression. Melan-A has a high affinity for specific CD8+ T cells and is one of the critical markers for detecting damage to melanocytes. </p> <p><strong>Aim: </strong>Our study aims to demonstrate the differences of Melan-A expression associated with apoptosis of melanocytes in patients with segmental vitiligo (SV) and those with non-segmental vitiligo (NSV). </p> <p><strong>Methods:</strong> The subjects consisted of 64 patients diagnosed with vitiligo, of whom 33 were with NSV and 31 with SV. Skin biopsy and direct immunofluorescence were used to examine Melan-A, and the TUNEL method was performed to examine melanocyte apoptosis in both groups. Group comparisons were conducted using appropriate statistical methods. </p> <p><strong>Results: </strong>Melan-A expression was significantly higher in the NSV group than in the SV group, and there was a significant difference between two groups (p = 0.001). The median of melanocyte apoptosis in the NSV group was relatively higher than in the SV group, and a significant difference was found between the two groups (p = 0.001). The Spearman’s rank correlation test between Melan-A expression and melanocyte apoptosis in the NSV group was 0.767 (76.7%) and showed a significant relationship (p <0.05). The same test in the SV group was 0.583 (58.3%) and showed a significant relationship (p <0.05). In both groups, the higher the Melan-A expression, the higher the melanocyte apoptosis. </p> <p><strong>Conclusion:</strong> Melan-A expression and melanocyte apoptosis are correlated. The higher Melan-A expression and melanocyte apoptosis in NSV indicates more severe vitiligo disease compared to SV. </p>
Pterostilbene Protects Cochlea from Ototoxicity in Streptozotocin-Induced Diabetic Rats by Inhibiting Apoptosis
<p>Diabetes mellitus (DM) causes ototoxicity by inducing oxidative stress, microangiopathy, and apoptosis in the cochlear sensory hair cells. The natural anti-oxidant pterostilbene (PTS) (trans-3,5-dimethoxy-4-hydroxystylbene) has been reported to relieve oxidative stress and apoptosis in DM, but its role in diabetic-induced ototoxicity is unclear. This study aimed to investigate the effects of dose-dependent PTS on the cochlear cells of streptozotocin (STZ)-induced diabetic rats. The study included 30 albino male Wistar rats that were randomized into five groups: non-diabetic control (Control), diabetic control (DM), and diabetic rats treated with intraperitoneal PTS at 10, 20, or 40 mg/kg/day during the four-week experimental period (DM + PTS10, DM + PTS20, and DM + PTS40). Distortion product otoacoustic emission (DPOAE) tests were performed at the beginning and end of the study. At the end of the experimental period, apoptosis in the rat cochlea was investigated using caspase-8, cytochrome-c, and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin end labeling (TUNEL). Quantitative real-time polymerase chain reaction was used to assess the mRNA expression levels of the following genes: CASP-3, BCL-associated X protein (BAX), and BCL-2. Body weight, blood glucose, serum insulin, and malondialdehyde (MDA) levels in the rat groups were evaluated. The mean DPOAE amplitude in the DM group was significantly lower than the means of the other groups (0.9–8 kHz; P < 0.001 for all). A dose-dependent increase of the mean DPOAE amplitudes was observed with PTS treatment (P < 0.05 for all). The Caspase-8 and Cytochrome-c protein expressions and the number of TUNEL-positive cells in the hair cells of the Corti organs of the DM rat group were significantly higher than those of the PTS treatment and control groups (DM > DM + PTS10 > DM + PTS20 > DM + PTS40 > Control; P < 0.05 for all). PTS treatment also reduced cell apoptosis in a dose-dependent manner by increasing the mRNA expression of the anti-apoptosis BCL2 gene and by decreasing the mRNA expressions of both the pro-apoptosis BAX gene and its effector CASP-3 and the ratio of BAX/BCL-2 in a dose-dependent manner (P < 0.05 compared to DM for all). PTS treatment significantly improved the metabolic parameters of the diabetic rats, such as body weight, blood glucose, serum insulin, and MDA levels, consistent with our other findings (P < 0.05 compared to DM for all). PTS decreased the cochlear damage caused by diabetes, as confirmed by DPOAE, biochemical, histopathological, immunohistochemical, and molecular findings. This study reports the first in vivo findings to suggest that PTS may be a protective therapeutic agent against diabetes-induced ototoxicity.</p>
Raw data: Patterned apoptosis has an instructive role for local growth and tissue shape regulation in a fast-growing epithelium
<p>What regulates organ size and shape remains one fundamental mystery of modern biology. Research in this area has primarily focused on deciphering the regulation in time and space of growth and cell division, while the contribution of cell death has been overall neglected. This includes studies of the <i>Drosophila</i> wing, one of the best characterised systems for the study of growth and patterning, undergoing massive growth during larval stage and important morphogenetic remodeling during pupal stage. So far, it has been assumed that cell death was relatively neglectable in this tissue both during larval and pupal stage and as a result the pattern of growth was usually attributed to the distribution of cell division. Here, using systematic mapping and registration combined with quantitative assessment of clone size and disappearance as well as live imaging, we outline a persistent pattern of cell death and clone elimination emerging in the larval wing disc and persisting during pupal wing morphogenesis. Local variation of cell death is associated with local variation of clone size, pointing to an impact of cell death on local growth which is not fully compensated by proliferation. Using morphometric analyses of adult wing shape and genetic perturbations, we provide evidence that patterned death affects locally and globally adult wing shape and size. This study describes a roadmap for precise assessment of the contribution of cell death to tissue shape, and outlines an important instructive role of cell death in modulating quantitatively local growth and morphogenesis of a fast-growing tissue.</p><p>This repository contains the raw data (local projection images, ROI and quantificatiosn) of the Current Biology article "<strong>Patterned apoptosis has an instructive role for local growth and tissue shape regulation in a fast-growing epithelium".</strong></p>
An intranuclear bacterial parasite of deep-sea mussels expresses apoptosis inhibitors acquired from its host
<p><span>Only a few bacteria are able to colonize the nuclei of eukaryotes and nearly all of these are known from protists. One bacterial clade, however, “<em>Candidatus</em> Endonucleobacter”, infects the nuclei of deep-sea mussels, where it replicates to ≥ 80,000 bacteria per nucleus and causes nuclei to swell to 50 times their original size. How these parasites are able to replicate so massively and avoid apoptosis is not known. </span><span>Dual RNA-seq transcriptomes of infected nuclei isolated using laser-capture microdissection revealed </span><span>that in contrast to previous assumptions, “</span><em><span>Ca. </span></em><span>Endonucleobacter” does not gain most of its nutrition from nuclear DNA or RNA. Instead, “<em>Ca.</em> Endonucleobacter” upregulated genes for importing sugars, lipids, amino acids and possibly mucin from its host, and digested these nutrients. “<em>Ca.</em> Endonucleobacter” likely prevents apoptosis of host cells by upregulating 7-13 inhibitors of apoptosis (IAPs), proteins previously only known from animals and a few invertebrate viruses. Comparative phylogenetic analyses revealed that “<em>Ca.</em> Endonucleobacter” acquired IAPs repeatedly through horizontal gene transfer (HGT) from their hosts in </span><span>convergent acquisition. HGT from eukaryotes to bacteria, although assumed to be rare, may be more common than currently recognized, particularly in bacteria that live in intimate associations with eukaryotic hosts.</span></p>
SI: A Guide to Automated Apoptosis Detection
<p>supplementary information of the article:</p> <p>"A Guide to Automated Apoptosis Detection:</p> <p>How to Make Sense of Imaging Flow Cytometry Data"</p> <p>D. Pischel et al., 2018</p>
Figure 4 in Evaluation of nickel-induced brain injuries in rats via oxidative stress and apoptosis: attenuating effects of hyperoside
Figure 4. Morphology and location of PAS granules of brain tissues of control (A), Hyp-treated (B), Ni-treated (C), and Ni + Hyp-treated (D) rats. Homogeneous PAS staining was observed in the control group (A) and the Hyp-treated (B) groups. Clusters of granules shown inside square (C) and by black arrow (D), respectively (200× magnification).
Figure 3 in Evaluation of nickel-induced brain injuries in rats via oxidative stress and apoptosis: attenuating effects of hyperoside
Figure 3. Histological views of brain tissues of control (A), Hyp-treated (B), Ni-treated (C), and Ni + Hyp-treated (D) rats. Small blood vessels (BV) from pia mater penetrate the cerebral cortex substance pyramidal cells (PC) with apical dendrites closely associated with smaller, round glial cells (GC) (A and B). Perivascular inflammation around a blood vessel (inside square) (C) and perivascular inflammatory cell infiltrates in hematoxylin and eosin-stained brain tissue (D) (200× magnification).
Figure 5 in Evaluation of nickel-induced brain injuries in rats via oxidative stress and apoptosis: attenuating effects of hyperoside
Figure 5. Brain tissues of control (A) and Hyp (B) groups were negative for Congo red. Amyloid deposits in brain parenchyma and around blood vessels shown inside square (C) and marked by black arrows (D) (200× magnification). Differences in measured parameters among the groups were analyzed with a nonparametric test (Kruskal–Wallis). Dual comparisons between groups exhibiting significant values were evaluated with a Mann–Whitney U test (P <0.05).
Figure 1 in Evaluation of nickel-induced brain injuries in rats via oxidative stress and apoptosis: attenuating effects of hyperoside
Figure 1. Effect of Ni administration on body weight gain. Data are presented as mean ± standard error of mean (SEM) (n = 7). a Significant differences between other studied groups and control (a4 P <0.0001). b Significant differences between other groups studied and Hyp group (b1 P <0.05, b4 P <0.0001). c Significant differences between other groups studied and Ni + Hyp group (c3 P <0.001) by Tukey's multiple range tests.
Expression quantitative trait loci influence DNA damage-induced apoptosis in cancer
<p><strong>Exposure expression quantitative trait loci (e2QTL)</strong></p> <p>The analysis of e2QTL allows for the identification of context-specific eQTL effects (Kim-Hellmuth et al. (2017), PMID: 28814792). To evaluate how inter-individual genetic variability influences the regulation of DNA damage-induced apoptosis, we performed e2QTL analysis of CD8+ T cells from 461 healthy European participants stimulated with high doses of 5 different carcinogens. These include Methyl-methanesulfonate (MMS), tert-butyl-hydroperoxide (TBOOH), benzo(a)pyrene-7,8-diol-9,10-epoxide (BPDE), 4-hydroxycyclophosphamide (HC) and UVC radiation.</p> <p><code>eQTL_DNA_damage_induced_apoptosis.csv:</code> eQTL data. FastQTL was used to analyze cis-eQTL within a 1 MB window of a gene’s transcription start site. Filtering and normalization of expression data was performed as described by the Genotype Tissue Expression (GTEx) project (The GTEx Consortium (2015), PMID: 25954001) including 60 PEER factors, top 3 genotype PCs and sex as covariates. Genotypes were filtered by PHWE > 10-6 and MAF > 5 %. Adjusted p-values were generated using 1,000 to 10,000 permutations. Variant IDs (CHR:POS:REF:ALT) are based on GRCh38.</p> <p><code>e2QTL_DNA_damage_induced_apoptosis.csv:</code> e2QTL data. The most significant variant for each analyzed gene was determined based on eQTL data to calculate e2QTL in a z-test that were corrected for multiple testing using Bonferroni correction as described by Kim-Hellmuth et al. (2017). Variant IDs (CHR:POS:REF:ALT) are based on GRCh38.</p> <p> </p>
Hydroxyurea inhibits proliferation and stimulates apoptosis through inducible nitric oxide synthase in erythroid cells.
<p><a name="_Hlk164856369"></a><span>Hydroxyurea (HU) arrests cells in S-phase through the inhibition of ribonucleotide reductase and DNA synthesis, which is contributed significantly by the release of nitric oxide (NO). </span><span><span>W</span></span><span><span>e investigated the mediation of inducible NO synthase (NOS2) in HU c</span></span><span><span>ytostatic effects</span></span><span><span>, <a name="_Hlk165036602"></a>using <em>in vitro</em> shRNA-induced knock-down of NOS2 or </span></span><span><span><span>specific</span></span></span><span><span><span> </span></span></span><span><span><span>NOS2 inhibitor (1400W), and supported by Nos2 knockout mice (Nos2<sup>-/-</sup>) to observe <em>ex vivo</em> murine erythroid progenitors (mERP).</span></span><a name="_Hlk165036694"></a></span><span><span><span>As a long-term effect, HU increased NOS2 expression in human erythroleukemic HEL92.1.7 cells (via NFκB signaling) and mERP. As a short-term result, HU increased the activity of purified and HEL92.1.7 cell-derived NOS2</span></span></span><span><span>, as confirmed by NO / citrulline production and <em>in silico</em> molecular docking via hydrogen bonds.</span> </span><span><span>Molecular dynamic simulation showed a slight decrease in NOS2 receptor rigidity upon HU binding, confirming the stability of HU at the active site of the NOS2 receptor. Both 1400W and shRNA prevented the <em>in vitro</em> reduction of proliferation and induction of apoptosis of HEL92.1.7 cells by HU. Thus, shRNA blocked preferentially early apoptosis and only shRNA overcame HU-induced S-phase arrest of HEL92.1.7 cells. Both 1400W and Nos2 knockout prevented the <em>in vivo</em> decrease in proliferation and induction of apoptosis of mERP by HU from wild-type and Nos2-/- mice, respectively. Therefore, HU increased NOS2 activity and expression via NFκB signaling. This study demonstrated the NOS2 dependance in the HU inhibition of</span></span><span><span> </span></span><span><span>proliferation and stimulation of</span></span><span><span> apoptosis of erythroid cells. </span></span></p>
Fig 2 in Soluble total antigen derived from Toxoplasma gondii RH strain prevents apoptosis, but induces anti-apoptosis in human monocyte cell line
Fig 2. This schematic overview suggests signaling pathways of apoptosis. Apoptosis is induced through either the extrinsic pathway or intrinsic pathway. Toxoplasma gondii can prevent cell apoptosis via inhibition of cytochrome c release from the mitochondria into the cytosol, inhibition of cas-3, -6, -7, and -9 via blocking the mitochondrial pathway, and blocking cas-8 by external pathways. The parasite may also suppress pro-apoptotic protein (Bax) and induce anti-apoptotic Bcl-2 proteins and is able to activate transcription factors STAT6 and STAT3-miR-17-92-Bim pathway to inhibit apoptosis. Some proteins of T. gondii such as ROP18 plays a role in Fas/ CD95-mediated apoptosis to inhibit this process. Similarly ROP16 phosphorylates STAT3 and STAT6 to inhibit cell death. Original (S. Nemati).
Fig 1 in Soluble total antigen derived from Toxoplasma gondii RH strain prevents apoptosis, but induces anti-apoptosis in human monocyte cell line
Fig 1. The comparison of the expression levels of Bcl-2 (A), Mcl-1 (B), Cas-7 (C), Cas-3 (D), and Bax (E) in THP-1 cell line regarding different concentrations of the soluble total antigen of Toxoplasma gondii (Nicolle et Manceaux, 1908) STAg. NS: not significant; * P value <0.05; ** P value <0.01; *** P value <0.001.
Supplement Tables of Recombinant Klotho protein protects pulmonary alveolar epithelial cells against sepsis-induced apoptosis by inhibiting the Bcl-2/Bax/caspase-3 pathway
<p>This is Supplement Tables of Recombinant Klotho protein protects pulmonary alveolar epithelial cells against sepsis-induced apoptosis by inhibiting the Bcl-2/Bax/caspase-3 pathway.</p>
Data from: Drosophila medulla neuroblast termination via apoptosis, differentiation and gliogenic switch is scheduled by the depletion of the neuroepithelial stem cell pool
<p>The brain is consisted of diverse neurons arising from a limited number of neural stem cells. <em>Drosophila</em> neural stem cells called neuroblasts (NBs) produces specific neural lineages of various lineage sizes depending on their location in the brain. In the <em>Drosophila</em> visual processing centre - the optic lobes (OLs), medulla NBs derived from the neuroepithelium (NE) give rise to neurons and glia cells of the medulla cortex. The timing and the mechanisms responsible for the cessation of medulla NBs are so far not known. In this study, we show that the termination of medulla NBs during early pupal development is determined by the exhaustion of the NE stem cell pool. Hence, altering NE-NB transition during larval neurogenesis disrupts the timely termination of medulla NBs. Medulla NBs terminate neurogenesis via a combination of apoptosis, terminal symmetric division via Prospero, and a switch to gliogenesis via Glial Cell Missing (Gcm), however, these processes occur independently of each other. We also show that temporal progression of the medulla NBs is mostly not required for their termination. As the <em>Drosophila</em> OL shares a similar mode of division with mammalian neurogenesis, understanding when and how these progenitors cease proliferation during development can have important implications for mammalian brain size determination and regulation of its overall function.</p>
Data for: HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer
<p>The membrane-associated RING-CH-type finger ubiquitin ligase MARCHF8 is a human homolog of the viral ubiquitin ligases Kaposi's sarcoma herpesvirus K3 and K5 that promote host immune evasion. Previous studies have shown that MARCHF8 ubiquitinates several immune receptors, such as the major histocompatibility complex II and CD86. While human papillomavirus (HPV) does not encode any ubiquitin ligase, the viral oncoproteins E6 and E7 are known to regulate host ubiquitin ligases. Here, we report that MARCHF8 expression is upregulated in HPV-positive head and neck cancer (HNC) patients but not in HPV-negative HNC patients compared to normal individuals. The MARCHF8 promoter is highly activated by HPV oncoprotein E6-induced MYC/MAX transcriptional activation. The knockdown of MARCHF8 expression in human HPV-positive HNC cells restores cell surface expression of the tumor necrosis factor receptor superfamily (TNFRSF) death receptors, FAS, TRAIL-R1, and TRAIL-R2, and enhances apoptosis. MARCHF8 protein directly interacts with and ubiquitinates the TNFRSF death receptors. Further, MARCHF8 knockout in mouse oral cancer cells expressing HPV16 E6 and E7 augments cancer cell apoptosis and suppresses tumor growth in vivo. Our findings suggest that HPV inhibits host cell apoptosis by upregulating MARCHF8 and degrading TNFRSF death receptors in HPV-positive HNC cells.</p>
Molecular Targeting of 15-Lipoxygenase-1 (15-LOX-1) for Apoptosis Induction in Human Colorectal Cancers
ClinicalTrials.gov study NCT00503035. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Anesthesia and Lymphocytes Apoptosis
ClinicalTrials.gov study NCT01461551. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data for: HPV upregulates MARCHF8 ubiquitin ligase and inhibits apoptosis by degrading the death receptors in head and neck cancer
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Blockade of IKK signaling induces RIPK1-independent apoptosis in human macrophages
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