AutoTube: a novel software for the automated morphometric analysis of vascular networks in tissues

Montoya-Zegarra, Javier A.; Russo, Erica; Runge, Peter; Jadhav, Maria; Willrodt, Ann-Helen; Stoma, Szymon; Nørrelykke, Simon F.; Detmar, Michael; Halin, Cornelia

doi:10.1007/s10456-018-9652-3

Cited by 50 publications

(40 citation statements)

References 38 publications

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“…SOD, GSH, and GPX were antioxidants which were downregulated by Mst1 overexpression and were reversed to near-normal levels with DRP1 knockdown. *p < 0.05 vs. ad-ctrl group; # p < 0.05 vs. ad-Mst1 + si-ctrl group injury, endothelial oxidative stress (Zhu et al 2018), fatty liver disease, and acute kidney injury (Montoya-Zegarra et al 2019). In the present study, we observed that mitochondrial division was activated by Mst1 overexpression, an effect that was accompanied by mitochondrial membrane potential reduction and cyt-c release.…”

Section: Discussionsupporting

confidence: 55%

Hippo/Mst1 overexpression induces mitochondrial death in head and neck squamous cell carcinoma via activating β-catenin/Drp1 pathway

Fan

Wang

et al. 2019

Cell Stress and Chaperones

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Mammalian Ste20-like kinase 1 (Mst1) is associated with cell apoptosis. In the current study, we explored the regulatory effects of Mst1 on squamous cell carcinoma of the head and neck (SCCHN) in vitro. SCCHN Cal27 cells and Tu686 cells were transfected with adenovirus-loaded Mst1 to detect the role of Mst1 in cell viability. Then, siRNA against Drp1 was transfected into cells to evaluate the influence of mitochondrial fission in cancer survival. Our data illustrated that Mst1 overexpression promoted SCCHN Cal27 cell and Tu686 cell death via activating mitochondria-related apoptosis. Cells transfected with adenovirus-loaded Mst1 have increased expression of DRP1 and higher DRP1 promoted mitochondrial fission. Active mitochondrial fission mediated mitochondrial damage, as evidenced by increased mitochondrial oxidative stress, decreased mitochondrial energy production, and reduced mitochondrial respiratory complex function. Moreover, Mst1 overexpression triggered mitochondria-dependent cell apoptosis via DRP1-related mitochondrial fission. Further, we found that Mst1 overexpression controlled mitochondrial fission via the β-catenin/DRP1 pathways; inhibition of β-catenin and/or knockdown of DRP1 abolished the pro-apoptotic effects of Mst1 overexpression on SCCHN Cal27 cells and Tu686 cells, leading to the survival of cancer cells in vitro. In sum, our results illustrate that Mst1/β-catenin/DRP1 axis affects SCCHN Cal27 cell and Tu686 cell viability via controlling mitochondrial dynamics balance. This finding identifies Mst1 activation might be an effective therapeutic target for the treatment of SCCHN.

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Section: Discussionsupporting

confidence: 55%

Hippo/Mst1 overexpression induces mitochondrial death in head and neck squamous cell carcinoma via activating β-catenin/Drp1 pathway

Fan

Wang

et al. 2019

Cell Stress and Chaperones

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“…death. Interestingly, Exenatide treatment attenuated ER stress, thereby sustaining cardiomyocyte contractile functions and favoring cardiomyocyte survival [38,39]. These results identified ER stress as a downstream target of Exenatide treatment.…”

Section: Agingmentioning

confidence: 86%

Exenatide inhibits NF-κB and attenuates ER stress in diabetic cardiomyocyte models

Mui

Zhu

et al. 2020

Aging

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Exenatide is used to treat patients with type-2 diabetes and it also exerts cardioprotective effects. Here, we tested whether Exenatide attenuates hyperglycemia-related cardiomyocyte damage by inhibiting endoplasmic reticulum (ER) stress and the NF-κB signaling pathway. Our results demonstrated that hyperglycemia activates the NF-κB signaling pathway, eliciting ER stress. We also observed cardiomyocyte contractile dysfunction, inflammation, and cell apoptosis induced by hyperglycemia. Exenatide treatment inhibited inflammation, improved cardiomyocyte contractile function, and rescued cardiomyocyte viability. Notably, re-activation of the NF-κB signaling pathway abolished Exenatide's protective effects on hyperglycemic cardiomyocytes. Taken together, our results demonstrate that Exenatide directly reduces hyperglycemia-induced cardiomyocyte damage by inhibiting ER stress and inactivating the NF-κB signaling pathway.

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“…In the present study, we reported that Akt activity and Parkin expression were rapidly downregulated in response to inflammation response. 66 Interestingly, overexpression of TrxR2 could reverse the activity of the Akt-Parkin pathway. These data support the functional importance of the redox balance in regulating the Akt-Parkin pathway.…”

Section: Discussionmentioning

confidence: 99%

TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt–Parkin pathway

Gao¹,

Li²,

Li³

et al. 2019

Toxicology Research

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Neuronal death caused by inflammatory cytokine-mediated neuroinflammation is being extensively explored. Thioredoxin reductase (TrxR) 2 is a novel mediator of inflammation response. In the current study, we focus on the mechanisms of TrxR2 overexpression in inflammation-mediated neuronal death. LPS was used to induce neuroinflammation in N2a cells in vitro. Adenovirus-loaded TrxR2 was transfected into N2a cells to up-regulate TrxR2 expression. Then, cell viability was determined via MTT assay and TUNEL assay. Apoptosis was measured via western blotting and ELISA. Oxidative stress was detected via ELISA and flow cytometry. A pathway inhibitor was used to verify the role of the Akt–Parkin pathway in the LPS-mediated N2a cell death in the presence of TrxR2 overexpression. With the help of immunofluorescence assay and western blotting, we found that TrxR2 expression was significantly reduced in response to LPS treatment, and this effect was associated with N2a cell death via apoptosis. At the molecular level, TrxR2 overexpression elevated the activity of the Akt–Parkin pathway, as evidenced by the increased expression of p-Akt and Parkin. Interestingly, inhibition of the Akt–Parkin pathway abolished the regulatory effect of TrxR2 on LPS-treated N2a cells, as evidenced by the decreased cell viability and increased apoptotic ratio. Besides, TrxR2 overexpression also reduced oxidative stress, inflammation factor transcription and mitochondrial apoptosis. However, inhibition of Akt–Parkin axis abrogated the protective effects of TrxR2 on redox balance, mitochondrial performance and cell survival. LPS-mediated neuronal death was linked to a drop in TrxR2 overexpression and the inactivation of the Akt–Parkin pathway. Overexpression of TrxR2 sustained mitochondrial function, inhibited oxidative stress, repressed inflammation response, and blocked mitochondrial apoptosis, finally sending a pro-survival signal for the N2a cells in the setting of LPS-mediated inflammation environment.

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AutoTube: a novel software for the automated morphometric analysis of vascular networks in tissues

Cited by 50 publications

References 38 publications

Hippo/Mst1 overexpression induces mitochondrial death in head and neck squamous cell carcinoma via activating β-catenin/Drp1 pathway

Hippo/Mst1 overexpression induces mitochondrial death in head and neck squamous cell carcinoma via activating β-catenin/Drp1 pathway

Exenatide inhibits NF-κB and attenuates ER stress in diabetic cardiomyocyte models

TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt–Parkin pathway

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