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Journal articles on the topic 'Expressão de caspase 8 e caspase 9'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Demirci, Umut, Melek Yaman, and Umit E. Bagriacik. "Effects of acute doxorubicin exposure on caspase-mediated apoptosis in cardiomyocytes." Journal of Clinical Oncology 31, no. 15_suppl (2013): e12036-e12036. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e12036.

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e12036 Background: Doxorubicin binds to DNA-associated enzymes, intercalates the base pairs of the DNA and induces apoptosis in cancerous and healthy tissues especially in cardiomyocytes. Caspase mediated apoptosis in cardiomyocytes remains largely unknown. We investigated the role of doxorubicin via caspase system on apoptosis of cardiomyocytes. Methods: H9C2ratcardiomyocytes were incubated with doxorubicin a concentration of 10-6 Mfor 4 or 24 hours to perform gene expression and activity of caspases, respectively. Total RNA isolated and expression analysis were performed by real time PCR ass

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Ekonomopoulou, Maria Themistokli, Evaggelos Babas, Eleutheria Mioglou-Kalouptsi, Maria Malandri, and Zafiroula Iakovidou-Kritsi. "Changes in Activities of Caspase-8 and Caspase-9 in Human Cervical Malignancy." International Journal of Gynecologic Cancer 21, no. 3 (2011): 435–38. http://dx.doi.org/10.1097/igc.0b013e31820d3e42.

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IntroductionThe apoptotic process of programmed cell death and its dysfunctions in a variety of human diseases, including cervical cancer, has become the focus of extensive scientific research. Caspases are considered key factors in the execution of apoptosis, although there are many aspects of their role to be elucidated. It has been found that disturbance of initiator caspase-8 and caspase-9 expression or function may contribute to cancer formation/progression, and inactivation of them could promote resistance to current treatment approaches. In our research, the activities of caspase-8 and

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Janečková, Eva, Petra Bíliková, and Eva Matalová. "Osteogenic Potential of Caspases Related to Endochondral Ossification." Journal of Histochemistry & Cytochemistry 66, no. 1 (2017): 47–58. http://dx.doi.org/10.1369/0022155417739283.

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Caspases have functions particularly in apoptosis and inflammation. Increasing evidence indicates novel roles of these proteases in cell differentiation, including those involved in osteogenesis. This investigation provides a complex screening of osteogenic markers affected by pan caspase inhibition in micromass cultures derived from mouse forelimbs. PCR Array analysis showed significant alterations in expression of 49 osteogenic genes after 7 days of inhibition. The largest change was a decrease in CD36 expression, which was confirmed at organ level by caspase inhibition in cultured mouse uln

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Cao, Guodong, Yumin Luo, Tetsuya Nagayama, et al. "Cloning and Characterization of Rat Caspase-9: Implications for a Role in Mediating Caspase-3 Activation and Hippocampal Cell Death after Transient Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 22, no. 5 (2002): 534–46. http://dx.doi.org/10.1097/00004647-200205000-00005.

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Delayed hippocampal neurodegeneration after transient global ischemia is mediated, at least in part, through the activation of terminal caspases, particularly caspase-3, and the subsequent proteolytic degradation of critical cellular proteins. Caspase-3 may be activated by the membrane receptor-initiated caspase-8–dependent extrinsic pathway and the mitochondria-initiated caspase-9–dependent intrinsic pathway; however, the precise role of these deduced apoptosis-signaling pathways in activating caspase-3 in ischemic neurons remains elusive. The authors cloned the caspase-9 gene from the rat br

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Peluffo, Marina C., Richard L. Stouffer, and Marta Tesone. "Activity and expression of different members of the caspase family in the rat corpus luteum during pregnancy and postpartum." American Journal of Physiology-Endocrinology and Metabolism 293, no. 5 (2007): E1215—E1223. http://dx.doi.org/10.1152/ajpendo.00261.2007.

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Studies were designed to examine the expression and activity of four caspases that contribute to the initial (caspases-2, -8, and -9) and final (caspase-3) events in apoptosis in the rat corpus luteum (CL) during pregnancy ( days 7, 17, 19, and 21 of gestation), postpartum ( days 1 and 4), and after injection (0, 8, 16, 24, and 36 h) of the physiological luteolysin PGF2α. In addition, the temporal relationship of caspase expression/activity relative to steroid production and luteal regression was evaluated. During pregnancy, the activity of all four caspases was significantly greater on day 19

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Rathbun, R. Keaney, Tracy A. Christianson, Gregory R. Faulkner та ін. "Interferon-γ–induced apoptotic responses of Fanconi anemia group C hematopoietic progenitor cells involve caspase 8–dependent activation of caspase 3 family members". Blood 96, № 13 (2000): 4204–11. http://dx.doi.org/10.1182/blood.v96.13.4204.h8004204_4204_4211.

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Hematopoietic progenitor cells (HPC) from mice nullizygous at the Fanconi anemia (FA) group C locus and children with Fanconi anemia group C (FA-C) are hypersensitive to interferon-gamma (IFN-γ) and tumor necrosis factor-α. This hypersensitivity results, in part, from the capacity of these cytokines to prime the fas pathway. Because fas-mediated programmed cell death in many cells involves sequential activation of specific caspases, we tested the hypothesis that programmed cell death in FA HPC involves the ordered activation of specific caspase molecules. Lysates from lymphoblasts treated with

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Smith, Mitchell Reed, Fang Jin, and Indira Joshi. "Antibodies to TRAIL Receptors R1 and R2 Induce Apoptosis in Non-Hodgkin’s Lymphoma Cells." Blood 104, no. 11 (2004): 3290. http://dx.doi.org/10.1182/blood.v104.11.3290.3290.

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Abstract Monoclonal antibodies and chemotherapy can be effective, but not curative, therapy for non-Hodgkin s lymphoma (NHL). Rituximab acts by several mechanisms, including directly signaling apoptosis of CD20+ cells via the mitochondrial pathway involving caspase 9. Chemotherapy also activates this apoptotic pathway. TRAIL-R1 and -R2 signaling induces apoptosis via a pathway that activates caspase 8. Thus, we investigated the effects of agonistic monoclonal antibodies to TRAIL-R1 and -R2 on NHL cell lines (DoHH2, WSU-FSCCL and FC-TxFL2, each t(14;18)+, EBV-). TRAIL-R1 (HGS-ETR1) and -R2 (HGS

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Gaddy, Daniel F., and Douglas S. Lyles. "Vesicular Stomatitis Viruses Expressing Wild-Type or Mutant M Proteins Activate Apoptosis through Distinct Pathways." Journal of Virology 79, no. 7 (2005): 4170–79. http://dx.doi.org/10.1128/jvi.79.7.4170-4179.2005.

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ABSTRACT Vesicular stomatitis virus (VSV) induces apoptosis by at least two mechanisms. The viral matrix (M) protein induces apoptosis via the mitochondrial pathway due to the inhibition of host gene expression. However, in some cell types, the inhibition of host gene expression by VSV expressing wild-type (wt) M protein delays VSV-induced apoptosis, indicating that another mechanism is involved. In support of this, the recombinant M51R-M (rM51R-M) virus, expressing a mutant M protein that is defective in its ability to inhibit host gene expression, induces apoptosis much more rapidly in L929

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Rathbun, R. Keaney, Tracy A. Christianson, Gregory R. Faulkner та ін. "Interferon-γ–induced apoptotic responses of Fanconi anemia group C hematopoietic progenitor cells involve caspase 8–dependent activation of caspase 3 family members". Blood 96, № 13 (2000): 4204–11. http://dx.doi.org/10.1182/blood.v96.13.4204.

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Abstract Hematopoietic progenitor cells (HPC) from mice nullizygous at the Fanconi anemia (FA) group C locus and children with Fanconi anemia group C (FA-C) are hypersensitive to interferon-gamma (IFN-γ) and tumor necrosis factor-α. This hypersensitivity results, in part, from the capacity of these cytokines to prime the fas pathway. Because fas-mediated programmed cell death in many cells involves sequential activation of specific caspases, we tested the hypothesis that programmed cell death in FA HPC involves the ordered activation of specific caspase molecules. Lysates from lymphoblasts tre

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Papandile, Adrian, David Tyas, Donald M. O'Malley, and Carol M. Warner. "Analysis of caspase-3, caspase-8 and caspase-9 enzymatic activities in mouse oocytes and zygotes." Zygote 12, no. 1 (2004): 57–64. http://dx.doi.org/10.1017/s0967199404002588.

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The current consensus in the literature is that ovulated oocytes that are not fertilized die by apoptosis, but the details of the proteins involved in the apoptotic pathways have not been elucidated. In this paper we confirm that caspase-3, the executioner of apoptosis, is expressed in mouse oocytes, and show that two initiators of apoptosis, caspase-8 and caspase-9, are expressed in mouse oocytes. Comparisons were made of caspase-3, -8, and -9 activities in superovulated oocytes that were freshly collected or allowed to age in vivo or in vitro. We found that caspase-3 activity significantly i

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Chen, Hexin, Seung Chung, and Saraswati Sukumar. "HOXA5-Induced Apoptosis in Breast Cancer Cells Is Mediated by Caspases 2 and 8." Molecular and Cellular Biology 24, no. 2 (2004): 924–35. http://dx.doi.org/10.1128/mcb.24.2.924-935.2004.

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ABSTRACT HOXA5 is a transcriptional factor whose expression is lost in more than 60% of breast carcinomas. Our previous work demonstrated that the overexpression of HOXA5 in MCF7 cells resulted in cell death through a p53-dependent apoptotic pathway. To determine whether p53-independent apoptotic pathways are involved in HOXA5-induced cell death, we engineered a p53-mutant breast cancer cell line, Hs578T, to inducibly express HOXA5. Induction of HOXA5 expression led to cell death with features typical of apoptosis within 24 h, and the expression levels of mutant p53 and its target genes either

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Keane, Robert W., Susan Kraydieh, George Lotocki, Ofelia F. Alonso, Phillip Aldana, and W. Dalton Dietrich. "Apoptotic and Antiapoptotic Mechanisms after Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 21, no. 10 (2001): 1189–98. http://dx.doi.org/10.1097/00004647-200110000-00007.

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Caspase and inhibitor of apoptosis (IAP) expression was examined in rats subjected to moderate traumatic brain injury (TBI) using a parasagittal fluid-percussion brain insult (1.7 to 2.2 atm). Within 1 hour after injury, caspase-8 and −9, two initiators of apoptosis, were predominantly expressed in superficial cortical areas adjacent to the impact site and in the thalamus. Caspase-3, an effector caspase, was evident at 6 hours throughout the traumatized cerebral cortex and hippocampus. Moreover, the authors observed that XIAP, cIAP-1, and cIAP-2, members of the IAP family, were constitutively

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Martin, Carla A., and Asit Panja. "Cytokine regulation of human intestinal primary epithelial cell susceptibility to Fas-mediated apoptosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 1 (2002): G92—G104. http://dx.doi.org/10.1152/ajpgi.2002.282.1.g92.

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The regulatory mechanisms of nontransformed intestinal epithelial cell apoptosis have not been thoroughly investigated. We determined the susceptibility and mechanism of Fas-mediated apoptosis in nontransformed human intestinal epithelial cells (HIPEC) in the presence and absence of inflammatory cytokines. Despite ample expression of Fas, HIPEC were relatively insensitive to Fas-mediated apoptosis in that agonist anti-Fas antibody (CH11) induced a <25% increase in HIPEC apoptosis. Pretreatment of HIPEC with interferon (IFN)-γ, but not tumor necrosis factor-α or granulocyte-macrophage colony

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Baburamani, Ana A., Yasuka Miyakuni, Regina Vontell, et al. "Does Caspase-6 Have a Role in Perinatal Brain Injury?" Developmental Neuroscience 37, no. 4-5 (2015): 321–37. http://dx.doi.org/10.1159/000375368.

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Apoptotic mechanisms are centre stage for the development of injury in the immature brain, and caspases have been shown to play a pivotal role during brain development and in response to injury. The inhibition of caspases using broad-spectrum agents such as Q-VD-OPh is neuroprotective in the immature brain. Caspase-6, an effector caspase, has been widely researched in neurodevelopmental disorders and found to be important following adult stroke, but its function in the neonatal brain has yet to be detailed. Furthermore, caspases may be important in microglial activation; microglia are required

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El-Sayed, Ibrahim, Khalid Bassiouny, Aziz Nokaly, Ahmed S. Abdelghani та Wael Roshdy. "Influenza A Virus and Influenza B Virus Can Induce Apoptosis via Intrinsic or Extrinsic Pathways and Also via NF-κB in a Time and Dose Dependent Manner". Biochemistry Research International 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/1738237.

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Influenza viruses are able to cause annual epidemics and pandemics due to their mutation rates and reassortment capabilities leading to antigenic shifts and drifts. To identify host response to influenza A and B viruses on A549 and MDCK II cells at low and high MOIs, expressions of MxA and caspases 3, 8, and 9 and BAD, TNFα, and IκBαgenes were measured in the cells supernatants. H1N1 and H3N2 prefer to initially enhance the intrinsic pathway, determined by higher caspase 9 activity in MDCK II cells compared to caspase 8 activity and vice versa in A549 cells at different MOIs, while INF B prefe

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Shibayama, Keigo, Yohei Doi, Naohiro Shibata, et al. "Apoptotic Signaling Pathway Activated byHelicobacter pylori Infection and Increase of Apoptosis-Inducing Activity under Serum-Starved Conditions." Infection and Immunity 69, no. 5 (2001): 3181–89. http://dx.doi.org/10.1128/iai.69.5.3181-3189.2001.

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ABSTRACT The enhanced gastric epithelial cell apoptosis observed during infection with Helicobacter pylori has been suggested to be of significance in the etiology of gastritis, peptic ulcers, and neoplasia. To investigate the cell death signaling induced by H. pylori infection, human gastric epithelial cells were incubated with H. pylori for up to 72 h. H. pyloriinfection induced the activation of caspase -8, -9, and -3 and the expression of the proapoptotic Bcl-2 family proteins Bad and Bid. The peak of the activity of the caspases occurred at 24 h. At this time, the inhibition of caspase-8

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Arroba, Ana I., Laura M. Frago, Jesús Argente, and Julie A. Chowen. "Activation of Caspase 8 in the Pituitaries of Streptozotocin-Induced Diabetic Rats: Implication in Increased Apoptosis of Lactotrophs." Endocrinology 146, no. 10 (2005): 4417–24. http://dx.doi.org/10.1210/en.2005-0517.

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Lactotroph cell death is increased in streptozotocin-induced diabetic rats. To determine the mechanism involved, cell death proteins were accessed in pituitaries of diabetic (streptozotocin at 65 mg/kg, 2 months evolution) and control male rats by Western blot analysis and double immunohistochemistry. The intact and cleaved forms of caspase 9 were increased in diabetic rat pituitaries compared with controls. Although the proforms of caspases 3, 6, and 7 were increased in diabetic rat pituitaries, their activated forms were either unchanged or decreased. Activation of these effector caspases ma

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Chang, Li-Rong, Jin-Ping Liu, Yi-Zhi Song, Tao Lu, Gang Lu, and Yan Wu. "Expression of caspase-8 and caspase-9 in rat hippocampus during postnatal development." Microscopy Research and Technique 74, no. 2 (2011): 153–58. http://dx.doi.org/10.1002/jemt.20886.

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Din, Tengku Ahmad Damitri Al Astani Tengku. "ID:2038 THE ROLE OF THE CASPASE FAMILY in PF4-INDUCED APOPTOSIS IN BREAST CANCER IN VIVO STUDY." Biomedical Research and Therapy 4, S (2017): 69. http://dx.doi.org/10.15419/bmrat.v4is.277.

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Background: Apoptosis is critical to the development and homeostasis of metazoans. Apoptotic dysregulation leads to various human pathologies including cancer, autoimmune and neurodegenerative disorders. Caspases, sub-members of cysteine proteases, are the central components of apoptotic response. The ELR-negative chemokine platelet factor 4 (PF4) was initially identified as an antiangiogenic agent. It inhibits endothelial cell proliferation, migration and angiogenesis in in vitro and in vivo and was further proving in the in vivo models of human colon carcinoma and murine melanoma xenograft m

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Dai, Chunhua, та Sanford B. Krantz. "Interferon γ Induces Upregulation and Activation of Caspases 1, 3, and 8 to Produce Apoptosis in Human Erythroid Progenitor Cells". Blood 93, № 10 (1999): 3309–16. http://dx.doi.org/10.1182/blood.v93.10.3309.410k04_3309_3316.

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Interferon γ (IFNγ) induces apoptosis in purified human erythroid colony-forming cells (ECFC) and inhibits cell growth. Fas (APO-1; CD95) and Fas ligand (FasL) mediate apoptosis induced by IFNγ, because Fas is significantly upregulated by IFNγ, whereas Fas ligand is constitutively present in the ECFC and neutralization of FasL greatly reduces the apoptosis. Because conversion of caspases from their dormant proenzyme forms to active enzymes has a critical role in transducing a cascade leading to apoptosis, we performed further studies of the expression and activation of caspases in normal human

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Nováková, Jana, Pavel Talacko, Petr Novák, and Karel Vališ. "The MEK-ERK-MST1 Axis Potentiates the Activation of the Extrinsic Apoptotic Pathway during GDC-0941 Treatment in Jurkat T Cells." Cells 8, no. 2 (2019): 191. http://dx.doi.org/10.3390/cells8020191.

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The discrete activation of individual caspases is essential during T-cell development, activation, and apoptosis. Humans carrying nonfunctional caspase-8 and caspase-8 conditional knockout mice exhibit several defects in the progression of naive CD4+ T cells to the effector stage. MST1, a key kinase of the Hippo signaling pathway, is often presented as a substrate of caspases, and its cleavage by caspases potentiates its activity. Several studies have focused on the involvement of MST1 in caspase activation and also reported several defects in the immune system function caused by MST1 deficien

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Peluffo, Marina C., Leonardo Bussmann, Richard L. Stouffer, and Marta Tesone. "Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle." Reproduction 132, no. 3 (2006): 465–75. http://dx.doi.org/10.1530/rep.1.00910.

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Apoptosis is associated with the regression of the corpus luteum (CL) in many species. Since caspases play a central role in apoptosis, we studied several initiators (-2, -8, and -9) and the main effector (-3) caspase in the CL during the estrous cycle of the rat. Two different populations of CL (old and new) were identified on ovaries at estrus and diestrus II (DII). Diminished (P< 0.05) luteal progesterone content and P450scc levels suggested that functional luteolysis occurred between the new CL at DII and old CL at estrus, whereas the decline (P< 0.05) in luteal weight indicated that

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Dewson, Grant, Gerald M. Cohen, and Andrew J. Wardlaw. "Interleukin-5 inhibits translocation of Bax to the mitochondria, cytochrome c release, and activation of caspases in human eosinophils." Blood 98, no. 7 (2001): 2239–47. http://dx.doi.org/10.1182/blood.v98.7.2239.

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The apoptosis and subsequent clearance of eosinophils without histotoxic mediator release is thought to be crucial in the resolution of airway inflammation in asthma. Interleukin-5 (IL-5) is a potent suppressor of eosinophil apoptosis. The mechanism by which IL-5 inhibits spontaneous eosinophil apoptosis was investigated. Freshly isolated eosinophils constitutively expressed the conformationally active form of Bax in the cytosol and nucleus. During spontaneous and staurosporine-induced apoptosis, Bax underwent a caspase-independent translocation to the mitochondria, which was inhibited by IL-5

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Muris, Jettie J. F., Saskia A. G. M. Cillessen, Wim Vos, et al. "Immunohistochemical profiling of caspase signaling pathways predicts clinical response to chemotherapy in primary nodal diffuse large B-cell lymphomas." Blood 105, no. 7 (2005): 2916–23. http://dx.doi.org/10.1182/blood-2004-07-2716.

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AbstractWe used biopsy specimens of primary nodal diffuse large B-cell lymphoma (DLBCL) to investigate whether the inhibition of caspase 8 and/or 9 apoptosis signaling pathways predicts clinical outcome. Expression levels of cellular FLICE inhibitory protein (c-Flip) and numbers of active caspase 3-positive lymphoma cells were used to determine the status of the caspase 8-mediated pathway. Expression levels of Bcl-2 and X-linked inhibitor of apoptosis (XIAP) were used to determine the status of the caspase 9-mediated pathway. Expression of c-Flip, XIAP, Bcl-2, and caspase 3 activity all provid

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Kawahara, Tsukasa, Shigetada Teshima, Yuki Kuwano, Ayuko Oka, Kyoichi Kishi, and Kazuhito Rokutan. "Helicobacter pylorilipopolysaccharide induces apoptosis of cultured guinea pig gastric mucosal cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 3 (2001): G726—G734. http://dx.doi.org/10.1152/ajpgi.2001.281.3.g726.

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Helicobacter pylori lipopolysaccharide (LPS) is generally accepted as a low-toxicity virulence. Primary cultures of guinea pig gastric mucosal cells expressed the Toll-like receptor 4 and were sensitive to H. pylori LPS as well as Escherichia coli LPS. H. pylori LPS stimulated phosphorylation of transforming growth factor-β-activated kinase 1 (TAK1), TAK1-binding protein 1 (TAB1), and c-Jun NH2-terminal kinase (JNK) 2. H. pylori LPS at >2.1 endotoxin unit/ml (>1 ng/ml) activated caspase-8, stimulated cytochrome c release from mitochondria, and subsequently activated caspases-9 and -3, le

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Yao, Shihong, Pu Huang, Fen Liu, Fanyang Zeng, Wenxuan Zeng, and Shifeng He. "Preparation of a polymer-modified folate-targeted magnetic nano-delivery system and its inhibitory effect on nasopharyngeal carcinoma." Materials Express 10, no. 8 (2020): 1224–29. http://dx.doi.org/10.1166/mex.2020.1757.

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The aims of this work were to investigate the effect of a polymer-modified folate-targeted magnetic nano-delivery system on growth inhibition of CNE2 cells and expression of Caspase-3 mRNA, and Caspase-3, Caspase-8, and Caspase-9 proteins, and to explore the mechanism used by this nano-delivery system to inhibit proliferation and induce apoptosis of human nasopharyngeal carcinoma cells. The MTT method was used to detect the effect of the polymer-modified folate-targeted magnetic nano-delivery system at different concentrations (0, 0.25, 0.50, 0.75, 1.00, 1.50, 2.00 g/mL) on CNE2 cell prolifera

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Oudejans, Joost J., Jettie J. F. Muris, Gert J. Ossenkoppele, et al. "Profiling of Caspase Signaling Pathways Predicts Clinical Response to Chemotherapy in Diffuse Large B-Cell Lymphomas." Blood 104, no. 11 (2004): 1544. http://dx.doi.org/10.1182/blood.v104.11.1544.1544.

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Abstract Disruption of the apoptosis signaling cascade is a probable cause for resistance to chemotherapy in patients with diffuse large B-cell lymphomas (DLBCL). We investigated whether inhibition of either or both caspase 8 and 9 apoptosis signaling pathways in biopsy specimens of primary nodal (DLBCL) predicts clinical outcome. Expression levels of c-Flip and numbers of active caspase 3 positive lymphoma cells were used to determine the status of the caspase 8 mediated pathway. Expression levels of Bcl-2 and XIAP were used to determine the status of the caspase 9 mediated pathway. Expressio

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Pagliari, Lisa J., Harris Perlman, Hongtao Liu та Richard M. Pope. "Macrophages Require Constitutive NF-κB Activation To Maintain A1 Expression and Mitochondrial Homeostasis". Molecular and Cellular Biology 20, № 23 (2000): 8855–65. http://dx.doi.org/10.1128/mcb.20.23.8855-8865.2000.

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ABSTRACT NF-κB is a critical mediator of macrophage inflammatory responses, but its role in regulating macrophage survival has yet to be elucidated. Here, we demonstrate that constitutive NF-κB activation is essential for macrophage survival. Blocking the constitutive activation of NF-κB with pyrrolidine dithiocarbamate or expression of IκBα induced apoptosis in macrophagelike RAW 264.7 cells and primary human macrophages. This apoptosis was independent of additional death-inducing stimuli, including Fas ligation. Suppression of NF-κB activation induced a time-dependent loss of mitochondrial t

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Giagkousiklidis, Stavros, Meike Vogler, Andrew Westhoff, Hubert Kasperczyk, Klaus-Michael Debatin, and Simone Fulda. "Radiosensitization of Human Cancers by Smac Agonists." Blood 106, no. 11 (2005): 1523. http://dx.doi.org/10.1182/blood.v106.11.1523.1523.

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Abstract Resistance to current treatment regimens such as radiation therapy remains a major concern in oncology and may be caused by defects in apoptosis programs. Since “Inhibitor of apoptosis proteins” (IAPs), which are expressed at high levels in many tumors, block apoptosis at the core of the apoptotic machinery by inhibiting caspases, therapeutic modulation of IAPs could target a key control point in resistance. Here, we report for the first time that full length or mature Smac, an inhibitor of IAPs, significantly enhanced γ-irradiation-induced apoptosis and reduced clonogenic survival in

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Alam, Antoine, Luchino Y. Cohen, Salah Aouad, and Rafick-Pierre Sékaly. "Early Activation of Caspases during T Lymphocyte Stimulation Results in Selective Substrate Cleavage in Nonapoptotic Cells." Journal of Experimental Medicine 190, no. 12 (1999): 1879–90. http://dx.doi.org/10.1084/jem.190.12.1879.

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Apoptosis induced by T cell receptor (TCR) triggering in T lymphocytes involves activation of cysteine proteases of the caspase family through their proteolytic processing. Caspase-3 cleavage was also reported during T cell stimulation in the absence of apoptosis, although the physiological relevance of this response remains unclear. We show here that the caspase inhibitor benzyloxycarbonyl (Cbz)-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD) blocks proliferation, major histocompatibility complex class II expression, and blastic transformation during stimulation of peripheral blood lymphocytes. Mo

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Won, Jong-Heon, Kyung-Sook Chung, Eun-Young Park, et al. "23-Hydroxyursolic Acid Isolated from the Stem Bark of Cussonia bancoensis Induces Apoptosis through Fas/Caspase-8-Dependent Pathway in HL-60 Human Promyelocytic Leukemia Cells." Molecules 23, no. 12 (2018): 3306. http://dx.doi.org/10.3390/molecules23123306.

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The natural product 23-hydroxyursolic acid (23-HUA) is a derivative of ursolic acid, which is known to induce cancer cell apoptosis. However, apoptotic effects and mechanisms of 23-HUA have not been well characterized yet. Herein, we investigated the molecular mechanisms of 23-HUA-induced apoptosis in HL-60 human promyelocytic leukemia cells. 23-HUA-treated HL-60 cells showed apoptotic features including internucleosomal DNA condensation and fragmentation as well as externalization of phosphatidylserine residues. 23-HUA induced a series of mitochondrial events including disruption of mitochond

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Ruefli, Astrid A., Mark J. Smyth, and Ricky W. Johnstone. "HMBA induces activation of a caspase-independent cell death pathway to overcome P-glycoprotein-mediated multidrug resistance." Blood 95, no. 7 (2000): 2378–85. http://dx.doi.org/10.1182/blood.v95.7.2378.

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Abstract Multidrug resistance (MDR) is often characterized by the expression of P-glycoprotein (P-gp), a 170-kd ATP-dependent drug efflux protein. As well as effluxing xenotoxins, functional P-gp can confer resistance to caspase-dependent apoptosis induced by a range of different stimuli, including Fas ligand, tumor necrosis factor, UV irradiation, and serum starvation. However, P-gp-positive cells remain sensitive to caspase-independent death induced by cytotoxic T-cell granule proteins, perforin, and granzyme B. It is, therefore, possible that agents that induce cell death in a caspase-indep

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Ruefli, Astrid A., Mark J. Smyth, and Ricky W. Johnstone. "HMBA induces activation of a caspase-independent cell death pathway to overcome P-glycoprotein-mediated multidrug resistance." Blood 95, no. 7 (2000): 2378–85. http://dx.doi.org/10.1182/blood.v95.7.2378.007k10_2378_2385.

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Multidrug resistance (MDR) is often characterized by the expression of P-glycoprotein (P-gp), a 170-kd ATP-dependent drug efflux protein. As well as effluxing xenotoxins, functional P-gp can confer resistance to caspase-dependent apoptosis induced by a range of different stimuli, including Fas ligand, tumor necrosis factor, UV irradiation, and serum starvation. However, P-gp-positive cells remain sensitive to caspase-independent death induced by cytotoxic T-cell granule proteins, perforin, and granzyme B. It is, therefore, possible that agents that induce cell death in a caspase-independent ma

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Jin, Dandan, David M. Ojcius, Dexter Sun, et al. "Leptospira interrogans Induces Apoptosis in Macrophages via Caspase-8- and Caspase-3-Dependent Pathways." Infection and Immunity 77, no. 2 (2008): 799–809. http://dx.doi.org/10.1128/iai.00914-08.

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ABSTRACT Apoptosis of host cells plays an important role in modulating the pathogenesis of many infectious diseases. It has been reported that Leptospira interrogans, the causal agent of leptospirosis, induces apoptosis in macrophages and hepatocytes. However, the molecular mechanisms responsible for host cell death remained largely unknown. Here we demonstrate that L. interrogans induced apoptosis in a macrophage-like cell line, J774A.1, and primary murine macrophages in a time- and dose-dependent manner. Apoptosis was associated with the activation of cysteine aspartic acid-specific protease

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35

Mondello, Cristina, Chiara Stassi, Letteria Minutoli, et al. "Caspase 9 and Caspase 3 Immunohistochemical Pattern in Skeletal and Cardiac Muscles at Different Times after Death: An Experimental Study on PMI Estimation." Diagnostics 11, no. 6 (2021): 1062. http://dx.doi.org/10.3390/diagnostics11061062.

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(1) Background: The estimation of the post mortem interval (PMI) is a challenge for forensic pathologists because data emerging from methods commonly applied are not always conclusive, since several conditions exist that may affect the reliability of these parameters. Thus, new approaches have been proposed to overcome such a limit. In recent years, several studies have been performed on proteins analyzing their expression/degradation patterns in relation to the progressing of the post mortem interval. (2) Methods: The immunoreactivity patterns of two apoptosis mediators—Caspase 9 and Caspase

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Keyes, William M., and Esmond J. Sanders. "Regulation of apoptosis in the endocardial cushions of the developing chick heart." American Journal of Physiology-Cell Physiology 282, no. 6 (2002): C1348—C1360. http://dx.doi.org/10.1152/ajpcell.00509.2001.

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During the early stages of heart development, there are two main foci of cell death: outflow tract (OT) and atrioventricular (AV) endocardial cushions. These tissues contribute to the septa and valves of the mature heart and receive cell populations from neural crest (NC) cell migration and epicardial cell invasion. We examined embryonic chick hearts for expression, in the cushions, of bcl-2 family members, caspase-9, and the caspase substrate poly(ADP-ribose) polymerase. Antiapoptotic bcl-2 is expressed heavily in the OT and AV regions throughout embryonic days (ED) 4–7, with a decrease in le

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Sawaya, Marty E., Ulrike Blume-Peytavi, Diane L. Mullins, et al. "Effects of Finasteride on Apoptosis and Regulation of the Human Hair Cycle." Journal of Cutaneous Medicine and Surgery 6, no. 1 (2002): 1–9. http://dx.doi.org/10.1177/120347540200600101.

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Background: A number of studies have provided evidence that apoptosis is a central element in the regulation of hair follicle regression. In androgenetic alopecia (AGA), the exact location and control of key players in the apoptotic pathways remains obscure. Objective: In the present study, we used a panel of antibodies and investigated the spatial and cellular pattern of expression of caspases and inhibitors of apoptosis (IAPs), such as XIAP and FLIP, in men with normal scalp and in men with AGA before and after 6 months of treatment with 1 mg oral finasteride treatment. Methods and Results:

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Gao, Han, Yan Sun, Hai Tao Yu, and Chun Jing Zhang. "Mechanism of Ginsenoside Rh2 Inhibit Non-Small Cell Lung Cancer." Advanced Materials Research 749 (August 2013): 167–71. http://dx.doi.org/10.4028/www.scientific.net/amr.749.167.

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To study function and relativity of autophagy in NSCLC treated with ginsenoside Rh2, and to explore some molecular mechanism that ginsenoside Rh2 induces A549 cell lines of NSCLC apoptosis. Methods: Immunofluorescence assays detects activity of caspase-8 / 9 and expression of autophagy-related molecules Beclin-1 and LC3. Results: Immunofluorescence assays shows that, 20μg/mL ginsenoside Rh2 acts 3h, fluorescent intensity that marks activity of caspase-8 and expression level of Beclin-1 significantly increases, it means that activity of caspase-8 significantly rises and expression level of Becl

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Mungunsukh, Ognoon, Autumn J. Griffin, Young H. Lee, and Regina M. Day. "Bleomycin induces the extrinsic apoptotic pathway in pulmonary endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 5 (2010): L696—L703. http://dx.doi.org/10.1152/ajplung.00322.2009.

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Bleomycin, a chemotherapeutic agent, can cause pulmonary fibrosis in humans and is commonly used to induce experimental pulmonary fibrosis in rodents. In cell culture, bleomycin causes single- and double-stranded DNA breaks and produces reactive oxidative species, both of which require iron (Fe2+) and O2. The mechanism of bleomycin-induced apoptosis is controversial due to its complexity. We investigated bleomycin apoptotic signaling events in primary pulmonary endothelial cells. Time course experiments revealed that bleomycin induced apoptosis within 4 h. Caspase-8, the initiator caspase for

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Taranukhin, A. G., E. Y. Taranukhina, P. Saransaari, I. M. Djatchkova, M. Pelto-Huikko, and S. S. Oja. "Taurine reduces caspase-8 and caspase-9 expression induced by ischemia in the mouse hypothalamic nuclei." Amino Acids 34, no. 1 (2007): 169–74. http://dx.doi.org/10.1007/s00726-006-0405-z.

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Mitsiades, Nicholas, Constantine S. Mitsiades, Vassiliki Poulaki, Kenneth C. Anderson, and Steven P. Treon. "Intracellular regulation of tumor necrosis factor–related apoptosis-inducing ligand–induced apoptosis in human multiple myeloma cells." Blood 99, no. 6 (2002): 2162–71. http://dx.doi.org/10.1182/blood.v99.6.2162.

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Abstract Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL, Apo2 ligand) effectively kills multiple myeloma (MM) cells in vitro irrespective of refractoriness to dexamethasone and chemotherapy. Because clinical trials with this anticancer agent are expected shortly, we investigated the signaling pathway of TRAIL-induced apoptosis in MM. We detected rapid cleavage of caspases-8, -9, -3, and -6, as well as the caspase substrates poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor-45 (DFF45), but not caspase-10, upon TRAIL treatment in sensitive MM cells, pointing to casp

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Wallach-Dayan, Shulamit B., Gabriel Izbicki, Pazit Y. Cohen, Regina Gerstl-Golan, Alan Fine, and Raphael Breuer. "Bleomycin initiates apoptosis of lung epithelial cells by ROS but not by Fas/FasL pathway." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 4 (2006): L790—L796. http://dx.doi.org/10.1152/ajplung.00300.2004.

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Epithelial cells are considered to be a main target of bleomycin-induced lung injury, which leads to fibrosis in vivo. We studied the characteristics of in vitro bleomycin-induced apoptosis in a mouse lung epithelial (MLE) cell line. Bleomycin caused an increase of reactive oxygen species (ROS) resulting in oxidative stress, mitochondrial leakage, and apoptosis. These were associated with elevated caspase-8 and resultant caspase-9 activity and with upregulation of Fas expression. Glutathione and inhibitors of caspase-8 or caspase-9, but not of FasL, inhibited these effects, suggesting their de

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Poiroux, Guillaume, Annick Barre, Mathias Simplicien, et al. "Morniga-G, a T/Tn-Specific Lectin, Induces Leukemic Cell Death via Caspase and DR5 Receptor-Dependent Pathways." International Journal of Molecular Sciences 20, no. 1 (2019): 230. http://dx.doi.org/10.3390/ijms20010230.

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Morniga-G, the Gal-specific black mulberry (Morus nigra) lectin, displays high affinity for T (CD176) and Tn (CD175) antigens, frequently expressed at the cancer cell surface. The effects of Morniga-G were investigated on a Tn-positive leukemic Jurkat cell line. The lectin, used in a concentration range between 5–20 μg/mL, induced cell death in leukemic Jurkat cells. Microscopic and cytofluorometric analyses indicated that Jurkat cell death was essentially apoptotic, associated with an increase in the ceramide content and a depolarization of the mitochondrial transmembrane potential. This lect

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Carvalho, Tatiane F., Núbia Braga Pereira, Camila Raianna Justiniana Rocha, Camila Couto Figueiredo, Milene Alvarenga Rachid, and Anilton C. Vasconcelos. "Apoptose e maturação placentária bovina: um estudo imunohistoquímico e morfométrico." Pesquisa Veterinária Brasileira 36, no. 3 (2016): 237–46. http://dx.doi.org/10.1590/s0100-736x2016000300014.

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Resumo: A liberação da placenta após o parto envolve a perda da adesão materno-fetal e ocorre somente após a maturação completa do placentoma, que está relacionada com a diminuição da celularidade dos tecidos fetal e materno. A apoptose é requerida tanto para a maturação quanto para a liberação normal da placenta após o parto. O objetivo do presente estudo foi avaliar a ocorrência de apoptose em amostras de placenta de vacas em diferentes fases de gestação. Amostras de placentomas de 15 vacas saudáveis com 4 (n=5), 6 (n=5) e 9 (n=5) meses de gestação foram colhidas e processadas rotineiramente

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Asch, Rebecca J., Nisha Shah, and Tucker W. LeBien. "Role of Individual Amino Acids in the Action of Caspase Inhibitors as Proapoptotic Peptides for Human Leukemia." Blood 104, no. 11 (2004): 1998. http://dx.doi.org/10.1182/blood.v104.11.1998.1998.

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Abstract Three to five amino acid caspase inhibitors have been extensively used to identify the role of specific caspases in apoptotic pathways triggered by a wide range of cellular insults. Unexpectedly, we have recently demonstrated that the irreversible caspase-9 inhibitor (C9i) Z-LEHD-FMK can promote apoptosis in selected stressed and non-stressed human leukemic cells, and that inhibition of caspase-9 protein expression does not render cells more resistant to stress-induced apoptosis (Shah et al., Blood, in press 11/15/04). The goal of the current study was to analyze the role of caspase-9

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Kawakami, Atsushi, Tomoki Nakashima, Hideaki Sakai та ін. "Inhibition of Caspase Cascade by HTLV-I Tax Through Induction of NF-κB Nuclear Translocation". Blood 94, № 11 (1999): 3847–54. http://dx.doi.org/10.1182/blood.v94.11.3847.

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Abstract NF-κB is required for prevention of apoptosis. We examined the importance of human T-cell leukemia virus–I (HTLV-I) Tax protein to stimulate NF-κB nuclear translocation, thus preventing apoptosis. Jurkat cells and JPX-9 cells in which the inducible Tax expression plasmid vector was stably transfected were used in the present study. Both Jurkat and Tax− JPX-9 cells had small amounts of basal nuclear NF-κB activity. The addition of NF-κB inhibitors suppressed NF-κB nuclear translocation of the cells, thus inducing apoptosis. Sequential activation of caspases from caspase-8 to caspase-3

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Kawakami, Atsushi, Tomoki Nakashima, Hideaki Sakai та ін. "Inhibition of Caspase Cascade by HTLV-I Tax Through Induction of NF-κB Nuclear Translocation". Blood 94, № 11 (1999): 3847–54. http://dx.doi.org/10.1182/blood.v94.11.3847.423a24_3847_3854.

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NF-κB is required for prevention of apoptosis. We examined the importance of human T-cell leukemia virus–I (HTLV-I) Tax protein to stimulate NF-κB nuclear translocation, thus preventing apoptosis. Jurkat cells and JPX-9 cells in which the inducible Tax expression plasmid vector was stably transfected were used in the present study. Both Jurkat and Tax− JPX-9 cells had small amounts of basal nuclear NF-κB activity. The addition of NF-κB inhibitors suppressed NF-κB nuclear translocation of the cells, thus inducing apoptosis. Sequential activation of caspases from caspase-8 to caspase-3 was shown

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Wang, Xinlu, Xuanxuan Hao, Youping Wang, et al. "Protective Effects of Shenfuyixin Granule on H2O2-Induced Apoptosis in Neonatal Rat Cardiomyocytes." Evidence-Based Complementary and Alternative Medicine 2021 (January 29, 2021): 1–10. http://dx.doi.org/10.1155/2021/6654457.

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Shenfuyixin granule (SFYXG, i.e., Xinshuaikang granule) is a prescription, commonly used in the clinical experience, which plays a significant role in the treatment of heart failure. The purpose of this present research was to investigate the protective effect of SFYXG, and the mechanism about anti-H2O2-induced oxidative stress and apoptosis in the neonatal rat cardiomyocytes. Myocardial cells, as is well known, were divided into 4 groups: normal, model, SFYXG, and coenzyme Q10 group, respectively. Cells viability was determined by MTT assay. Flow cytometry and AO/EB staining were implemented

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Lee, Sang-Yun, Rama P. Cherla, Isa Caliskan, and Vernon L. Tesh. "Shiga Toxin 1 Induces Apoptosis in the Human Myelogenous Leukemia Cell Line THP-1 by a Caspase-8-Dependent, Tumor Necrosis Factor Receptor-Independent Mechanism." Infection and Immunity 73, no. 8 (2005): 5115–26. http://dx.doi.org/10.1128/iai.73.8.5115-5126.2005.

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ABSTRACT Shiga toxins (Stxs) induce apoptosis in a variety of cell types. Here, we show that Stx1 induces apoptosis in the undifferentiated myelogenous leukemia cell line THP-1 in the absence of tumor necrosis factor alpha (TNF-α) or death receptor (TNF receptor or Fas) expression. Caspase-8 and -3 inhibitors blocked, and caspase-6 and -9 inhibitors partially blocked, Stx1-induced apoptosis. Stx1 induced the mitochondrial pathway of apoptosis, as activation of caspase-8 triggered the (i) cleavage of Bid, (ii) disruption of mitochondrial membrane potential, and (iii) release of cytochrome c int

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Scholz, Christian, Antje Richter, Mario Lehmann, Klaus Schulze-Osthoff, Bernd Dörken, and Peter T. Daniel. "Arsenic Trioxide Induces Regulated, Death Receptor- and Caspase-Independent Cell Death through the Mitochondrial Death Pathway." Blood 106, no. 11 (2005): 4421. http://dx.doi.org/10.1182/blood.v106.11.4421.4421.

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Abstract Arsenic trioxide (As2O3, arsenite) efficiently kills cells from various hematologic malignancies and has successfully been employed especially for the treatment of acute promyelocytic leukemia. There, and in lymphoid cells we demonstrated that arsenite induces cell death in a caspase-2 and -9-independent fashion. Here, we address a potential role of death receptor signaling through the FADD/caspase-8 death inducing signaling complex in arsenite-induced cell death. In detail, we demonstrate that arsenite induces cell death independently of caspase-8 or FADD and cannot be blocked by dis

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