γ-Rays-generated ROS induce apoptosis via mitochondrial and cell cycle alteration in smooth muscle cells

Claro, Sandra; Oshiro, Maria E.M.; Mortara, Renato Arruda; Paredes‐Gamero, Edgar Julian; Pereira, Gustavo José Silva; Smaili, Soraya Soubhi; Ferreira, Alice Teixeira

doi:10.3109/09553002.2014.911988

Cited by 19 publications

(7 citation statements)

References 67 publications

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“…To elucidate the mechanism responsible for miR-214 down regulation in erythroid cells in response to stress, we investigated the relationship between miR-214 expression and ROS production. In agreement with previous studies [49,50], Co-60γ radiation and Fe-NTA gave rise to ROS generation by 2-3 folds, compared to untreated control ( Fig. 2A and C), whereas the expression of miR-214 decreased significantly ( Fig.…”

Section: Ros-dependent Downregulation Of Mir-214 In Erythroid Cellssupporting

confidence: 93%

miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

Gao

Liu

Chen

et al. 2016

Free Radical Biology and Medicine

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Section: Ros-dependent Downregulation Of Mir-214 In Erythroid Cellssupporting

confidence: 93%

miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

Gao

Liu

Chen

et al. 2016

Free Radical Biology and Medicine

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“…Reactive oxygen species (ROS) produced during irradiation to kill tumor cells, and these cells were also involved in the development of radiation-induced normal tissue damage (RINTD). Oxidative stress induced by irradiation [ 83 ] caused liver inflammation, fibrosis, and apoptosis [ 84 ]. Gene expression profiling revealed radiation changes metabolic pathways responsible for adaptation and maintenance of homeostasis in mice [ 85 ].…”

Section: Discussionmentioning

confidence: 99%

Low Molecular Weight Fucoidan Prevents Radiation-Induced Fibrosis and Secondary Tumors in a Zebrafish Model

Yang

Cheng

et al. 2020

Cancers

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Radiotherapy often causes unwanted side effects such as radiation-induced fibrosis and second malignancies. Fucoidan, a sulfated polysaccharide extracted from brown seaweed, has many biological effects including anti-inflammation and anti-tumor. In the present study, we investigated the radioprotective effect of Oligo-Fucoidan (OF) using a zebrafish animal model. Adult zebrafish of wild-type and transgenic fish with hepatocellular carcinoma were orally fed with Oligo-Fucoidan before irradiation. Quantitative PCR, Sirius red stain, hematoxylin, and eosin stain were used for molecular and pathological analysis. Whole genomic microarrays were used to discover the global program of gene expression after Oligo-Fucoidan treatment and identified distinct classes of up- and downregulated genes/pathways during this process. Using Oligo-Fucoidan oral gavage in adult wild-type zebrafish, we found Oligo-Fucoidan pretreatment decreased irradiation-induced fibrosis in hepatocyte. Using hepatitis B virus X antigen (HBx), Src and HBx, Src, p53−/+ transgenic zebrafish liver cancer model, we found that Oligo-Fucoidan pretreatment before irradiation could lower the expression of lipogenic factors and enzymes, fibrosis, and cell cycle/proliferation markers, which eventually reduced formation of liver cancer compared to irradiation alone. Gene ontology analysis revealed that Oligo-Fucoidan pretreatment increased the expression of genes involved in oxidoreductase activity in zebrafish irradiation. Oligo-Fucoidan also decreased the expression of genes involved in transferase activity in wild-type fish without irradiation (WT), nuclear outer membrane-endoplasmic reticulum membrane network, and non-homologous end-joining (NHEJ) in hepatocellular carcinoma (HCC) transgenic fish. Rescue of those genes can prevent liver cancer formation. Conclusions: Our results provide evidence for the ability of Oligo-Fucoidan to prevent radiation-induced fibrosis and second malignancies in zebrafish.

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“…f. The proteins involved in apoptosis were measured by immunofluorescence by specific antibodies, anti-: caspase 3, cyclin A, cyclin B2, cyclin E, PKCα, PKCε, TNFα, BAX, cytochrome c, BAG-1, BCL-2, and BCL-xL ( [20,32]).…”

Section: Immunofluorescence Analysismentioning

confidence: 99%

Radiation-Generated ROS Induce Apoptosis via Mitochondrial

Claro¹,

Ferreira²,

Oshiro³

2020

Free Radical Medicine and Biology

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Ionizing radiation (IR) causes an increase in intracellular calcium, alters contractility, and triggers apoptosis via the activation of PKCα and-ε in irradiated smooth muscle cells. The present study investigated the role of the mitochondria in these processes and characterized the proteins involved in IR-induced apoptosis. Intestinal smooth muscle cells were exposed to 10-50 Gy from a γ-source. ROS and H 2 O 2 levels were measured with colourimetry and a DCFH-DA probe, and protein expression was analyzed by immunoblotting and immunofluorescence. The IR-induced generation of ROS was inhibited by glutathione, and apoptosis was mediated by the mitochondria via BAX, cytochrome c, and caspase 3. IR increased the expression of the cyclins A, B2, and E, and led to unbalanced cellular growth in an absorption dose-dependent manner. However, radiation did not induce alterations in the mitochondrial ultrastructure or in KΨ mito. In contrast, IR increased the nuclear expression of BAG-1, TNFα, PKCα, and-ε and cyclins A and E. In conclusion, IR triggers the activation of antiapoptotic proteins and enhances the risk of a second type of cancer in patients undergoing radiotherapy. In addition to increasing the radioresistance of cells, antiapoptotic proteins can also stimulate uncontrolled cell proliferation that culminates in mutagenesis.

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γ-Rays-generated ROS induce apoptosis via mitochondrial and cell cycle alteration in smooth muscle cells

Abstract: Smooth muscle cells subjected to IR undergo mitochondrial-mediated apoptosis that involves oncoproteins activation and preserves mitochondrial structure. IR also cause alterations in the expression and localization of both pro- and anti-apoptotic proteins.

Cited by 19 publications

References 67 publications

miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

Low Molecular Weight Fucoidan Prevents Radiation-Induced Fibrosis and Secondary Tumors in a Zebrafish Model

Radiation-Generated ROS Induce Apoptosis via Mitochondrial

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