Pro-death signaling of cytoprotective heat shock factor 1: upregulation of NOXA leading to apoptosis in heat-sensitive cells

Janus, Patryk; Toma-Jonik, Agnieszka; Vydra, Natalia; Mrowiec, Katarzyna; Korfanty, Joanna; Chadalski, Marek; Widłak, Piotr; Dudek, Karolina; Paszek, Anna; Rusin, Marek; Polańska, Joanna; Widłak, Wiesława

doi:10.1038/s41418-020-0501-8

Cited by 23 publications

(14 citation statements)

References 53 publications

(71 reference statements)

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“…BCL2L14 markedly increased in our project is regarded as facilitator of apoptosis [ 28 ] and PMAIP1 is a pro-apoptotic gene and functions to neutralize anti-apoptotic activity of MCL1 and BCL2A1. This explains the down-regulation of anti-apoptotic gene activity in our result [ 29 ]. Apoptosis evaluated on cell line of oral squamous cell carcinoma claimed higher expression of BAX gene and p53 gene but the level of BCL2 anti-apoptosis gene was suppressed resembling our data [ 30 ].…”

Section: Discussionsupporting

confidence: 52%

Effect of glucose mediated oxidative stress on apoptotic gene expression in gingival mesenchymal stem cells

et al. 2021

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Background Diabetes is a common disease that causes gingival and periodontal problems. Stem cells isolated from dental sources are an emerging area of research with a potential to facilitate regenerative medicine. The stem cells retain the property of self-renewal and the ones isolated from dental sources are mainly multipotent mesenchymal stem cells that have the ability to self-renew as well as differentiation towards multiple lineages. Objectives We aimed to isolate and characterize gingival mesenchymal stem cells by pluripotency markers and investigated the effect of oxidative stress on growth kinetics and apoptotic gene expression of gingival cells exposed to glucose mediated oxidative stress. Methods In this study, we isolated gingival mesenchymal stem cells from gingiva. This was followed by morphologic analysis using inverted phase contrast microscopy and molecular profiling of these cells for the mRNA expression of specific genes. The isolated cells were cultured till passage 3 and then exposed to oxidative stress (high glucose concentration). We measured the apoptotic gene expression and compared their growth kinetics. Results The results showed that oxidative stress produced by glucose reduced growth kinetics and increased apoptotic gene expression in gingival mesenchymal stem cells. According to the genetic results, glucose activated TNF family to initiate apoptosis. Conclusion In conclusion, the present study demonstrated that high glucose obliterated cellular proliferation testified by evaluating growth kinetics and induced apoptotic gene expression in gingival mesenchymal stem cells. This initiated extrinsic apoptotic pathway mediated by TNF family. Therefore, in diabetes oral health condition is compromised and periodontal disease is common.

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Section: Discussionsupporting

confidence: 52%

Effect of glucose mediated oxidative stress on apoptotic gene expression in gingival mesenchymal stem cells

et al. 2021

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“…However, despite the downregulation of p38, its inhibiting impact was probably diminished by an overexpression of apoptosis initiator caspase—CASP10—and executioner caspases—CASP3 and CASP7—which indicates the onset of programmed cell death. Additionally, we identified an increased expression of pro-apoptotic sensitizer/de-repressor—PMAIP1—which neutralizes anti-apoptotic agents and promotes efflux of apoptogenic proteins [ 73 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Profiling of Femoral Veins in Deep Vein Thrombosis in a Porcine Model

Gromadziński

Paukszto

Skowrońska

et al. 2021

Cells

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Deep vein thrombosis (DVT) is a severe disease affecting the human venous system, accompanied by high morbidity and mortality rates caused by early and late complications. The study aimed at analyzing the changes in the transcriptome of the femoral vein caused by DVT in the porcine model based on the formation of the thrombus in vivo. The study was performed on 11 castrated male pigs: a thrombus was formed in each left femoral vein in six animals; the remaining five served as a control group. Total RNA was isolated from the left femoral veins of the experimental and control animals. High-throughput RNA sequencing was used to analyze the global changes in the transcriptome of veins with induced DVT. Applied multistep bioinformatics revealed 1474 differentially expressed genes (DEGs): 1019 upregulated and 455 downregulated. Functional Gene Ontology annotated 1220 of DEGs into 225 biological processes, 30 molecular functions and 40 cellular components categories. KEGG analysis disclosed TNF, NF-κB and apoptosis pathways’ overexpression in DVT samples. A thorough analysis of the detected DEGs indicated that a dysregulated inflammatory response and disturbed balance between clotting and anti-clotting factors play a crucial role in the process of DVT.

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“…CCK-8 Assay. Transfected cells were seeded into 96-well plates and cultured for 24 h. Next, 10 μL of the CCK-8 solution was added to each well, and the cells were incubated for 2 h. After incubation, absorbance was measured at 450 nm using a microplate reader (Bio-Rad, USA) [36].…”

Section: Oxygen-glucose Deprivation (Ogd) Followed Bymentioning

confidence: 99%

Coronary Endothelium No‐Reflow Injury Is Associated with ROS‐Modified Mitochondrial Fission through the JNK‐Drp1 Signaling Pathway

Chen

Liu

Zhou

et al. 2021

Oxidative Medicine and Cellular Longevity

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Coronary artery no-reflow is a complex problem in the area of reperfusion therapy, and the molecular mechanisms underlying coronary artery no-reflow injury have not been fully elucidated. In the present study, we explored whether oxidative stress caused damage to coronary endothelial cells by inducing mitochondrial fission and activating the JNK pathway. The hypoxia/reoxygenation (H/R) model was induced in vitro to mimic coronary endothelial no-reflow injury, and mitochondrial fission, mitochondrial function, and endothelial cell viability were analyzed using western blotting, quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence. Our data indicated that reactive oxygen species (ROS) were significantly induced upon H/R injury, and this was followed by decreased endothelial cell viability. Mitochondrial fission was induced and mitochondrial bioenergetics were impaired in cardiac endothelial cells after H/R injury. Neutralization of ROS reduced mitochondrial fission and protected mitochondrial function against H/R injury. Our results also demonstrated that ROS stimulated mitochondrial fission via JNK-mediated Drp1 phosphorylation. These findings indicate that the ROS-JNK-Drp1 signaling pathway may be one of the molecular mechanisms underlying endothelial cell damage during H/R injury. Novel treatments for coronary no-reflow injury may involve targeting mitochondrial fission and the JNK-Drp1 signaling pathway.

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Pro-death signaling of cytoprotective heat shock factor 1: upregulation of NOXA leading to apoptosis in heat-sensitive cells

Cited by 23 publications

References 53 publications

Effect of glucose mediated oxidative stress on apoptotic gene expression in gingival mesenchymal stem cells

Effect of glucose mediated oxidative stress on apoptotic gene expression in gingival mesenchymal stem cells

Transcriptomic Profiling of Femoral Veins in Deep Vein Thrombosis in a Porcine Model

Coronary Endothelium No‐Reflow Injury Is Associated with ROS‐Modified Mitochondrial Fission through the JNK‐Drp1 Signaling Pathway

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