Biological Species and Environment Study in Microsystins Causing Apotosis in Heart

2014 ◽  
Vol 886 ◽  
pp. 341-344
Author(s):  
Tong Qiu
Keyword(s):  
Caspase 3 ◽  
Apoptotic Cell ◽  
Cell Number ◽  
Biological Species ◽  
Freshwater Ecosystems ◽  
Cyanobacterial Blooms ◽  
Caspase 9 ◽  
Gene Expressions ◽  
Genes Expression ◽  
Environment Study

The occurrence of heavy cyanobacterial blooms in eutrophic freshwater ecosystems has been a worldwide problem. Microcystins, the predominant toxins of cyanobacterial blooms, are associated with mortality and illness in both animals and human. In present study, we monitored the apoptosis of heart from MCs intoxication, and evaluated the roles of main apoptosis-related genes expression in cardiotoxic effects. The results revealed that MCs exposure led to the gradually rise in apoptotic cell number. Meanwhile, Bax, Bcl-2, p53, Caspase-3 and Caspase-9 gene expressions were significantly elevated simultaneously with the extension of the time. It suggested that MCs can cause damage to heart directly.

scholarly journals Ailanthone decreases cell viability in tongue squamous cell carcinoma via PI3K/AKT pathway

2021 ◽  
Author(s):  
shuhan wang ◽  
Xiaoyu Chen ◽  
Xuejie Zhu ◽  
Kehao Lin ◽  
Qixiao Cui ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Cyclin B1 ◽  
Cell Number ◽  
Tongue Squamous Cell Carcinoma ◽  
Caspase 9

Abstract To investigate the anti-tumor effect and mechanisms of ailanthone (AIL) in tongue squamous cell carcinoma (TSCC). The viability and apoptotic cell number of TCA8113 and Cal-27 cells declined and increased considerably following AIL. Hoechst 33258 staining revealed chromatin aggregation after exposure to AIL. Along with an accumulation of cleaved caspase-9, caspase-3, and PARP1, Bcl-2/Bax ratio and the levels of caspase-3, caspase-9 and PARP1 reduced after exposure to AIL treatment. Subjecting Cal-27 cells to AIL treatment led to the arrestment of the cell cycle at the G2/M phase. Nevertheless, the cell cycle of AIL-treated TCA8113 cells did not change significantly. Following AIL treatment, a decline in the expression of CDK1 and cyclin B1 was manifested by Western Blot. The p-AKT as well as the expression level of p-PI3K underwent a significant downregulation by AIL in both cells. The outcome furnishes a valuable understanding of the potential applications of AIL in treating TSCC.

Proinflammatory phenotype of coronary arteries promotes endothelial apoptosis in aging

2004 ◽  
Vol 17 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Anna Csiszar ◽  
Zoltan Ungvari ◽  
Akos Koller ◽  
John G. Edwards ◽  
Gabor Kaley
Keyword(s):  
Cell Death ◽  
Coronary Arteries ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
The Elderly ◽  
Apoptotic Cell Death ◽  
Caspase 9 ◽  
No Donor ◽  
Endothelial Apoptosis ◽  
Age Related

Previously we demonstrated that aging in coronary arteries is associated with proinflammatory phenotypic changes and decreased NO bioavailability, which, we hypothesized, promotes vascular disease by enhancing endothelial apoptosis. To test this hypothesis we characterized proapoptotic alterations in the phenotype of coronary arteries of aged (26 mo old) and young (3 mo old) F344 rats. DNA fragmentation analysis and TUNEL assay showed that in aged vessels there was an approximately fivefold increase in the number of apoptotic endothelial cells. In aged coronary arteries there was an increased expression of TNFα, TNFβ, and caspase 9 (microarray, real-time PCR), as well as increased caspase 9 and caspase 3 activity, whereas expression of TNFR1, TNFα-converting enzyme (TACE), Bcl-2, Bcl-X(L), Bid, Bax, caspase 8, and caspase 3 were unchanged. In vessel culture (18 h) incubation of aged coronary arteries with a TNF blocking antibody or the NO donor S-nitroso-penicillamine (SNAP) decreased apoptotic cell death. Incubation of young arteries with exogenous TNFα increased caspase 9 activity and elicited endothelial apoptosis, which was attenuated by SNAP. Inhibition of NO synthesis in cultured young coronary arteries also induced apoptotic cell death and potentiated the apoptotic effect of TNFα. Thus we propose that age-related upregulation of TNFα and caspase 9 and decreased bioavailability of NO promote endothelial apoptosis in coronary arteries that may lead to impaired endothelial function and ischemic heart disease in the elderly.

Berberine Induces Apoptotic Cell Death via Activation of Caspase-3 and -8 in HL-60 Human Leukemia Cells: Nuclear Localization and Structure–Activity Relationships

2017 ◽  
Vol 45 (07) ◽  
pp. 1497-1511 ◽  
Author(s):  
Shinya Okubo ◽  
Takuhiro Uto ◽  
Aya Goto ◽  
Hiroyuki Tanaka ◽  
Tsuyoshi Nishioku ◽  
...  
Keyword(s):  
Cell Death ◽  
Dna Fragmentation ◽  
Antiproliferative Activity ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Leukemia Cells ◽  
Caspase 8 ◽  
Human Leukemia ◽  
Caspase 9

Berberine (BBR), an isoquinoline alkaloid, is a well-known bioactive compound contained in medicinal plants used in traditional and folk medicines. In this study, we investigated the subcellular localization and the apoptotic mechanisms of BBR were elucidated. First, we confirmed the incorporation of BBR into the cell visually. BBR showed antiproliferative activity and promptly localized to the nucleus from 5[Formula: see text]min to 15[Formula: see text]min after BBR treatment in HL-60 human promyelocytic leukemia cells. Next, we examined the antiproliferative activity of BBR (1) and its biosynthetically related compounds (2-7) in HL-60 cells. BBR exerted strongest antiproliferative activity among 1-7 and the results of structures and activity relation suggested that a methylenedioxyl group in ring A, an [Formula: see text]-alkyl group at C-9 position, and the frame of isoquinoline may be necessary for antiproliferative activity. Moreover, BBR showed the most potent antiproliferative activity in HL-60 cells among human cancer and normal cell lines tested. Next, we examined the effect of BBR on molecular events known as apoptosis induction. In HL-60 cells, BBR induced chromatin condensation and DNA fragmentation, and triggered the activation of PARP, caspase-3 and caspase-8 without the activation of caspase-9. BBR-induced DNA fragmentation was abolished by pretreatment with inhibitors against caspase-3 and caspase-8, but not against caspase-9. ERK and p38 were promptly phosphorylated after 15 min of BBR treatment, and this was correlated with time of localization to the nucleus of BBR. These results demonstrated that BBR translocated into nucleus immediately after treatments and induced apoptotic cell death by activation of caspase-3 and caspase-8.

scholarly journals MicroRNA-155 Promotes Myocardial Infarction-Induced Apoptosis by Targeting RNA-Binding Protein QKI

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jing Guo ◽  
Hui-Bin Liu ◽  
Chuan Sun ◽  
Xiu-Qing Yan ◽  
Juan Hu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Rna Binding ◽  
Apoptotic Cell ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Cell Number ◽  
Neonatal Rat

Acute myocardial infarction (AMI) is the leading cause of sudden death worldwide. MicroRNA-155 (miR-155) has been reported to target antiapoptotic genes in various diseases models, but the functional role of miR-155 in response to MI injury needs further investigations. This study investigated the role of miR-155 in myocardial ischemia injury. TUNEL and flow cytometry were performed to measure cell apoptosis. Western blot analysis was employed to detect protein expressions of Bcl-2, XIAP, Bax, and caspase-3. qRT-PCR was used to quantify miRNA levels. We showed that miR-155 was dynamically elevated in murine hearts subjected to MI and in neonatal rat ventricular cardiomyocyte (NRVM) injury induced by hydrogen peroxide (H2O2). In response to H2O2, the silencing of miR-155 using AMO-155 (antisense inhibitor oligodeoxyribonucleotides) significantly increased cell viability and reduced cell apoptosis. Moreover, AMO-155 reversed the H2O2-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3. Further study revealed that AMO-155 resulted in a decrease of H2O2-induced JC-1-labelled monomeric cell number. In addition, AMO-155 markedly decreased infarct size, ameliorated impaired cardiac function, and significantly reduced apoptotic cell percentages in MI mice heart. The RNA-binding protein Quaking (QKI) was predicted as a target gene of miR-155 through bioinformatic analysis, and AMO-155 attenuated the downregulation of QKI in H2O2-treated cardiomyocytes and MI mice heart. Knockdown of QKI by siRNA abolished the antiapoptotic effects of AMO-155. Taken together, miR-155 is upregulated in the MI heart and NRVMs in response to H2O2 stress, and downregulating of miR-155 protects cardiomyocytes against apoptosis. Mechanistically, it is probably due to the repression of QKI signaling pathway.

Depletion of BIRC6 leads to retarded bovine early embryonic development and blastocyst formation in vitro

2010 ◽  
Vol 22 (3) ◽  
pp. 564 ◽  
Author(s):  
Dessie Salilew-Wondim ◽  
Micheal Hölker ◽  
Franca Rings ◽  
Chirawath Phatsara ◽  
Abdollah Mohammadi-Sangcheshmeh ◽  
...  
Keyword(s):  
Embryo Development ◽  
Preimplantation Embryo ◽  
Apoptotic Cell ◽  
Cell Number ◽  
Blastocyst Formation ◽  
Caspase 9 ◽  
Embryo Survival ◽  
Double Stranded Rna ◽  
Preimplantation Embryo Development

Baculoviral inhibitors of apoptosis repeat-containing 6 (BIRC6) is believed to inhibit apoptosis by targeting key cell-death proteins. To understand its involvement during bovine preimplantation embryo development, two consecutive experiments were conducted by targeted knockdown of its mRNA and protein using RNA interference. In Experiment 1, the effect of BIRC6 knockdown during the early stages of preimplantation embryo development was assessed by injecting zygotes with long double-stranded RNA (ldsRNA) and short hairpin RNA (shRNA) against BIRC6 mRNA followed by in vitro culturing until 96 h post insemination (hpi). The results showed that in RNA-injected zygote groups, reduced levels of BIRC6 mRNA and protein were accompanied by an increase (P < 0.05) in the proportion of 2- and 4-cell and uncleaved embryos and a corresponding decrease (P < 0.05) in the number of 8-cell embryos. In Experiment 2, the effect of BIRC6 knockdown on blastocyst formation, blastocyst total cell number and the extent of apoptosis was investigated. Consequently, zygotes injected with ldsRNA and shRNA resulted in lower (P < 0.05) blastocyst formation and total blastocyst cell number. Moreover, the apoptotic cell ratio, CASPASE 3 and 7 activity, BAX to BCL-2 ratio and levels of SMAC and CASPASE 9 were higher in blastocysts derived from the ldsRNA and shRNA groups, suggesting increased apoptosis in those blastocysts. The results of this study reveal the importance of BIRC6 expression for embryo survival during bovine preimplantation embryo development. However, whether BIRC6 is essential for implantation and fetal development during bovine pregnancy needs further research.

scholarly journals Insight into OroxylinA-7-O-β-d-Glucuronide-Enriched Oroxylum indicum Bark Extract in Oral Cancer HSC-3 Cell Apoptotic Mechanism: Role of Mitochondrial Microenvironment

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7430
Author(s):  
Sharmila Kameyanda Poonacha ◽  
Madhyastha Harishkumar ◽  
Madhyastha Radha ◽  
Remya Varadarajan ◽  
Suchetha Kumari Nalilu ◽  
...  
Keyword(s):  
Incubation Time ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Squamous Carcinoma ◽  
Stem Bark ◽  
Cell Number ◽  
Bark Extract ◽  
Dna Ladder ◽  
Oroxylum Indicum ◽  
Squamous Carcinoma Cells

Oroxylum indicum, of the Bignoniaceae family, has various ethnomedical uses such as an astringent, anti-inflammatory, anti-bronchitis, anti-helminthic and anti-microbial, including anticancer properties. The druggability of OI stem bark extract was determined by its molecular docking interactions with PARP and Caspase-3, two proteins involved in cell survival and death. Note that 50 µg/mL of Oroxylum indicum extract (OIE) showed a significant (p < 0.05%) toxicity to HSC-3 cells. MTT aided cell viability and proliferation assay demonstrated that 50 µg/mL of OIE displayed significant (p < 0.5%) reduction in cell number at 4 h of incubation time. Cell elongation and spindle formation was noticed when HSC-3 cells were treated with 50 µg/mL of OIE. OIE initiated DNA breakage and apoptosis in HSC-3 cells, as evident from DNA ladder assay and calcein/EB staining. Apoptosis potential of OIE is confirmed by flow cytometer and triple-staining (live cell/apoptosis/necrosis) assay. Caspase-3/7 fluorescence quenching (LANCE) assay demonstrated that 50 µg/mL of OIE significantly enhanced the RFU of caspases-3/7, indicating that the apoptosis potential of OIE is probably through the activation of caspases. Immuno-cytochemistry of HSC-3 cells treated with 50 µg/mL of OIE showed a significant reduction in mitochondrial bodies as well as a reduction in RFU in 60 min of incubation time. Immunoblotting studies clearly showed that treatment of HSC-3 cells with OI extract caused caspase-3 activation and PARP deactivation, resulting in apoptotic cell death. Overall, our data indicate that OIE is an effective apoptotic agent for human squamous carcinoma cells and it could be a future cancer chemotherapeutic target.

Fisetin Inhibits Cell Proliferation through the Induction of G0/G1 Phase Arrest and Caspase-3-Mediated Apoptosis in Mouse Leukemia Cells

2019 ◽  
Vol 47 (04) ◽  
pp. 841-863 ◽  
Author(s):  
Yu-Hsiang Tsai ◽  
Jen-Jyh Lin ◽  
Yi-Shih Ma ◽  
Shu-Fen Peng ◽  
An-Cheng Huang ◽  
...  
Keyword(s):  
Fruits And Vegetables ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Human Cancer ◽  
Cell Number ◽  
Viable Cell Number ◽  
Mouse Leukemia ◽  
Human Cancer Cell Lines ◽  
Phase Arrest ◽  
Apoptotic Protein

Fisetin, a naturally occurring flavonoid, is found in common fruits and vegetables and has been shown to induce cytotoxic effects in many human cancer cell lines. No information has shown that fisetin induced cell cycle arrest and apoptosis in mouse leukemia WEHI-3 cells. We found that fisetin decreased total viable cells through G0/G1 phase arrest and induced sub-G1 phase (apoptosis). We have confirmed fisetin induced cell apoptosis by the formation of DNA fragmentation and induction of apoptotic cell death. Results indicated that fisetin induced intracellular Ca[Formula: see text] increase but decreased the ROS production and the levels of [Formula: see text]m in WEHI-3 cells. Fisetin increased the activities of caspase-3, -8 and -9. Cells were pre-treated with inhibitors of caspase-3, -8 and -9 and then treated with fisetin and results showed increased viable cell number when compared to fisetin treated only. Fisetin reduced expressions of cdc25a but increased p-p53, Chk1, p21 and p27 that may lead to G0/G1 phase arrest. Fisetin inhibited anti-apoptotic protein Bcl-2 and Bcl-xL and increased pro-apoptotic protein Bax and Bak. Furthermore, fisetin increased the protein expression of cytochrome c and AIF. Fisetin decreased cell number through G0/G1 phase arrest via the inhibition of cdc25c and induction of apoptosis through caspase-dependent and mitochondria-dependent pathways. Therefore, fisetin may be useful as a potential therapeutic agent for leukemia.

Prostacyclin-induced peroxisome proliferator-activated receptor-α translocation attenuates NF-κB and TNF-α activation after renal ischemia-reperfusion injury

2009 ◽  
Vol 297 (4) ◽  
pp. F1109-F1118 ◽  
Author(s):  
Hsi-Hsien Chen ◽  
Tzen-Wen Chen ◽  
Heng Lin
Keyword(s):  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Apoptotic Cell ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Cell Number ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nitrogen Levels ◽  
Tnf Α

Prostacyclin and peroxisome proliferator-activated receptors (PPAR) protect against ischemia-reperfusion (I/R) injury by the induction of an anti-inflammatory pathway. In this study, we examined the prostacyclin-enhanced protective effect of PPARα in I/R-induced kidney injury. PPAR-α reduced the NF-κB-induced overexpression of TNF-α and apoptosis in cultured kidney cells. In a murine model, pretreating wild-type (WT) mice with a PPAR-α activator, docosahexaenoic acid (DHA), significantly reduced I/R-induced renal dysfunction (lowered serum creatinine and urea nitrogen levels), apoptotic responses (decreased apoptotic cell number and caspase-3, -8 activation), and NF-κB activation. By comparison, I/R-induced injury was exacerbated in PPAR-α knockout mice. This indicated that PPAR-α attenuated renal I/R injury via NF-κB-induced TNF-α overexpression. Overexpression of prostacyclin using an adenovirus could also induce PPAR-α translocation from the cytosol into the nucleus to inhibit caspase-3 activation. This prostacyclin/PPAR-α pathway attenuated TNF-α promoter activity by binding to NF-κB. Using a cAMP inhibitor (CAY10441) and a prostacyclin receptor antibody, we also found that there was another prostacyclin/IP receptor/cAMP pathway that could inhibit TNF-α production. Taken together, our results demonstrate for the first time that prostacyclin induces the translocation of PPAR-α from the cytosol into the nucleus and attenuates NF-κB-induced TNF-α activation following renal I/R injury. Treatments that can augment prostacyclin, PPAR-α, or the associated signaling pathways may ameliorate conditions associated with renal I/R injury.

scholarly journals Effect of N-acetyl cysteine on enterocyte apoptosis and intracellular signalling pathways' response to oxidative stress in weaned piglets

2013 ◽  
Vol 110 (11) ◽  
pp. 1938-1947 ◽  
Author(s):  
Lihui Zhu ◽  
Xuan Cai ◽  
Qi Guo ◽  
Xiaolian Chen ◽  
Suwen Zhu ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Intracellular Signalling ◽  
Signalling Pathways ◽  
Caspase 8 ◽  
Weaned Piglets ◽  
Caspase 9 ◽  
Gene Expressions ◽  
Intracellular Signalling Pathways ◽  
Enterocyte Apoptosis ◽  
Acetyl Cysteine

N-acetyl cysteine (NAC) has been widely used for preventing reactive oxygen species-induced damage. However, little is known as to whether dietary NAC supplementation would alleviate intestinal injury in weaned piglets. The present study evaluated the effect of NAC on enterocyte apoptosis and intracellular signalling pathways' response to weaning stress. The control piglets were normally suckling, and piglets in the weaning and NAC groups were fed the basal diet and basal+NAC diet from 14 to 25 d of age, respectively. Compared with the control piglets, weaning increased cortisol concentrations (P< 0·05), decreased superoxide dismutase and glutathione peroxidase activities (P< 0·05), increased malondialdehyde content (P< 0·05) in serum and enhanced enterocyte apoptosis index (AI) and concentrations of caspase-3, caspase-8 and caspase-9 (P< 0·05). Gene expression analyses indicated that weaning induced apoptosis via Fas signalling and mitochondrial pathways in weaned piglets. Dietary NAC supplementation decreased (P< 0·05) cortisol concentrations and the AI, increased (P< 0·05) antioxidant status in serum and alleviated histopathological changes in the intestine. It also inhibited Fas, caspase-3, caspase-8 and integrin αvβ6 (αvβ6) gene expressions in the NAC-treated piglets. However, no significant decrease (P>0·10) in caspase-3, caspase-8 and caspase-9 concentrations was observed in the NAC group compared with the weaning group. In conclusion, weaning may induce enterocyte apoptosis via the activation of Fas-dependent and mitochondria-dependent apoptosis. Although NAC had no effect on caspase concentrations, it was clearly beneficial for preserving morphological integrity in weaned piglets via the regulation of cell apoptosis and the inhibition of Fas-dependent apoptosis and αvβ6 expression.

scholarly journals Ailanthone Promotes Human Vestibular Schwannoma Cell Apoptosis and Autophagy by Downregulation of miR-21

2018 ◽  
Vol 26 (6) ◽  
pp. 941-948 ◽  
Author(s):  
Peizhen Yang ◽  
Dezhong Sun ◽  
Fei Jiang
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Ailanthus Altissima ◽  
Antitumor Activities ◽  
Caspase 9 ◽  
Chinese Medicinal Herb ◽  
Induced Apoptosis ◽  
Functional Actions

Ailanthone (AIL) is a quassinoid isolated from the traditional Chinese medicinal herb Ailanthus altissima. The antitumor activities of AIL have been reported in several cancers. The purpose of the present study was to explore the effect of AIL on vestibular schwannomas (VSs). Various concentrations of AIL (0‐1 μM) were used to treat human primary VS cells, and then cell viability, proliferation, apoptosis, and autophagy were assessed. Expression of miR-21 in VS cells was altered by miRNA transfection. The functional actions of AIL on miR-21 dysregulated cells were also assessed. AIL significantly reduced the viability of VS cells, and the IC50 value was 0.48 ± 0.023 μM. In response to 0.6 μM AIL, BrdU+ cell rate and cyclin D1 expression were reduced, apoptotic cell rate was increased, caspase 3 and caspase 9 were cleaved, Beclin-1 and LC3-II were accumulated, and p62 was downregulated. miR-21 was lowly expressed in AIL-treated cells, and AIL-induced apoptosis and autophagy were attenuated by miR-21 overexpression. In addition, AIL downregulated Ras and Raf and deactivated MEK, ERK, mTOR, and p70S6K, while the downregulation and deactivation induced by AIL were reversed by miR-21 overexpression. To conclude, AIL inhibited VS cell proliferation and induced apoptosis and autophagy. The antitumor activities of AIL in VS cells were realized possibly via downregulation of miR-21 and blocking the Ras/Raf/MEK/ERK and mTOR pathways.

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