Brefeldin A inhibits clathrin‐dependent endocytosis and ion transport in <i>Chara</i> internodal cells

Foissner, Ilse; Hoeftberger, Margit; Hoepflinger, Marion C.; Булычев, А. А.

doi:10.1111/boc.202000031

Cited by 13 publications

(11 citation statements)

References 73 publications

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“…JTE013 (8 μM) enhanced both Wnt3a and Wnt5a/b protein levels in BMSCs cultured in osteogenic media compared with BMSCs treated with DMSO from day 3 to day 9 ( Figure 6 M). To further determine whether Wnt3a and Wnt5a/b protein expressions were associated with vesicle trafficking, murine BMSCs were treated with brefeldin A (BFA, an inhibitor of protein trafficking from ER to Golgi) [ 46 , 47 ] or DMSO and cultured in osteogenic media for 6 days. Treatment with BFA suppressed both Wnt3a and Wnt5a/b protein expressions in BMSCs compared with DMSO treatment ( Figure 6 N).…”

Section: Resultsmentioning

confidence: 99%

Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Promoted Osteogenesis by Increasing Vesicle Trafficking, Wnt/Ca2+, and BMP/Smad Signaling

Lin

Pandruvada

2021

IJMS

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Sphingosine-1-phosphate receptor 2 (S1PR2) is a G protein-coupled receptor that regulates various immune responses. Herein, we determine the effects of a S1PR2 antagonist (JTE013) or a S1PR2 shRNA on osteogenesis by culturing murine bone marrow stromal cells (BMSCs) in osteogenic media with JTE013, dimethylsulfoxide (DMSO), a S1PR2 shRNA, or a control shRNA. Treatment with JTE013 or the S1PR2 shRNA increased alkaline phosphatase and alizarin red s staining, and enhanced alkaline phosphatase, RUNX2, osteocalcin, and osterix mRNA levels in BMSCs compared with the controls. Protein analysis revealed that a high dose of JTE013 (4 or 8 μM) increased vesicle trafficking-associated proteins (F-actin, clathrin, Early Endosome Antigen 1 (EEA1), and syntaxin 6) and Wnt/Ca2+ signaling. On the other hand, a low dose of JTE013 (1 to 2 μM) increased BMP/Smad signaling. In contrast, the S1PR2 shRNA reduced vesicle trafficking-associated proteins and attenuated Wnts and BMP/Smad signaling, but enhanced p-CaMKII compared with the control, suggesting that the S1PR2 shRNA influenced osteogenesis via different signaling pathways. Moreover, inhibiting protein trafficking by brefeldin A in BMSCs suppressed Wnts and BMPRs expressions. These data supported that enhanced osteogenesis in JTE013-treated BMSCs is associated with increased vesicle trafficking, which promotes the synthesis and transport of osteogenic protein and matrix vesicles and enhances matrix mineralization.

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Section: Resultsmentioning

confidence: 99%

Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Promoted Osteogenesis by Increasing Vesicle Trafficking, Wnt/Ca2+, and BMP/Smad Signaling

Lin

Pandruvada

2021

IJMS

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“…In addition, cells treated with chlorpromazine (an inhibitor of clathrin-mediated endocytosis), colchicine (an inhibitor of microtubule formation and macropinocytosis), and brefeldin A (an inhibitor of protein transport from the endoplasmic reticulum to the Golgi apparatus) showed a 36%, 39%, and 31% decrease in cellular uptake, respectively as reflected in the decrease in fluorescence signals. The cellular uptake of rhApoE/Cou-6/Aβ-CN-PMs was partially dependent on clathrin-mediated endocytosis, macropinocytosis, and the Golgi apparatus [ 41 – 43 ]. Sodium azide (NaN 3 ) is used to inhibit energy-dependent endocytosis by disrupting ATP production.…”

Section: Resultsmentioning

confidence: 99%

Novel brain-targeted nanomicelles for anti-glioma therapy mediated by the ApoE-enriched protein corona in vivo

Xin

Liu

et al. 2021

J Nanobiotechnol

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Background The interactions between nanoparticles (NPs) and plasma proteins form a protein corona around NPs after entering the biological environment, which provides new biological properties to NPs and mediates their interactions with cells and biological barriers. Given the inevitable interactions, we regard nanoparticle‒protein interactions as a tool for designing protein corona-mediated drug delivery systems. Herein, we demonstrate the successful application of protein corona-mediated brain-targeted nanomicelles in the treatment of glioma, loading them with paclitaxel (PTX), and decorating them with amyloid β-protein (Aβ)-CN peptide (PTX/Aβ-CN-PMs). Aβ-CN peptide, like the Aβ1–42 peptide, specifically binds to the lipid-binding domain of apolipoprotein E (ApoE) in vivo to form the ApoE-enriched protein corona surrounding Aβ-CN-PMs (ApoE/PTX/Aβ-CN-PMs). The receptor-binding domain of the ApoE then combines with low-density lipoprotein receptor (LDLr) and LDLr-related protein 1 receptor (LRP1r) expressed in the blood–brain barrier and glioma, effectively mediating brain-targeted delivery. Methods PTX/Aβ-CN-PMs were prepared using a film hydration method with sonication, which was simple and feasible. The specific formation of the ApoE-enriched protein corona around nanoparticles was characterized by Western blotting analysis and LC–MS/MS. The in vitro physicochemical properties and in vivo anti-glioma effects of PTX/Aβ-CN-PMs were also well studied. Results The average size and zeta potential of PTX/Aβ-CN-PMs and ApoE/PTX/Aβ-CN-PMs were 103.1 nm, 172.3 nm, 7.23 mV, and 0.715 mV, respectively. PTX was efficiently loaded into PTX/Aβ-CN-PMs, and the PTX release from rhApoE/PTX/Aβ-CN-PMs exhibited a sustained-release pattern in vitro. The formation of the ApoE-enriched protein corona significantly improved the cellular uptake of Aβ-CN-PMs on C6 cells and human umbilical vein endothelial cells (HUVECs) and enhanced permeability to the blood–brain tumor barrier in vitro. Meanwhile, PTX/Aβ-CN-PMs with ApoE-enriched protein corona had a greater ability to inhibit cell proliferation and induce cell apoptosis than taxol. Importantly, PTX/Aβ-CN-PMs exhibited better anti-glioma effects and tissue distribution profile with rapid accumulation in glioma tissues in vivo and prolonged median survival of glioma-bearing mice compared to those associated with PMs without the ApoE protein corona. Conclusions The designed PTX/Aβ-CN-PMs exhibited significantly enhanced anti-glioma efficacy. Importantly, this study provided a strategy for the rational design of a protein corona-based brain-targeted drug delivery system. More crucially, we utilized the unfavorable side of the protein corona and converted it into an advantage to achieve brain-targeted drug delivery. Graphical Abstract

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“…The present study showed that BFA inhibited the heat-induced nuclear PA elevation and also nuclear translocation of GAPC. While BFA has been used to block the exocytosis by preventing COP-coated vesicle transport from the ER to Golgi membranes, evidence suggests that it also suppresses the retrograde trafficking in animals, plants, and green algae (Grebe et al, 2003; Jelínková et al, 2015; Zhang et al, 2019b; Foissner et al, 2020). Thus, the data support the model that PA mediates the stress-induced nuclear translocation of GAPC via binding of GAPC and then trafficking of the PA-GAPC-containing vesicles to the nucleus (Figure 8).…”

Section: Discussionmentioning

confidence: 99%

Lipid-mediated nuclear moonlighting of cytosolic glyceraldehyde-3-phosphate dehydrogenase in plant heat response

Wang

Kim

Yao

et al. 2022

Preprint

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Cytosolic glyceraldehyde-3-phosphate dehydrogenase (GAPC) is a glycolytic enzyme, but it undergoes stress-induced nuclear translocation for moonlighting and regulating gene expression. To elucidate how the cytosolic enzyme moves into the nuclei under stress, we show that the plasma membrane-associated phospholipase Dδ (PLDδ) and its product phosphatidic acid (PA) promote heat-induced nuclear translocation of GAPC. The GAPC nuclear accumulation and Arabidopsis seedling tolerance to heat stress were reduced in pldδ, which was restored by genetic complementation with intact PLDδ, but not with catalytically inactive enzyme. GAPC overexpression enhanced the seedling thermotolerance and the expression of heat-inducible genes, but this was not observed when GAPC was overexpressed in the pldδ background. The GAPC nuclear accumulation and seedling thermotolerance were also decreased by application with a vesicle trafficking inhibitor brefeldin A (BFA) or zinc that inhibited the PA-GAPC interaction. Heat stress elevated PA levels in nuclei from wild-type, but not from pldδ and BFA-treated plants. Lipid labeling and fluorescence resonance energy transfer analyses demonstrated heat-induced nuclear co-localization of PA and GAPC, which was impaired by BFA or zinc treatment. Taken together, our data suggest that PLDδ-produced PA mediates nuclear translocation of GAPC via lipid-protein interaction and vesicle trafficking for plants to cope with heat.

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Brefeldin A inhibits clathrin‐dependent endocytosis and ion transport in Chara internodal cells

Cited by 13 publications

References 73 publications

Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Promoted Osteogenesis by Increasing Vesicle Trafficking, Wnt/Ca2+, and BMP/Smad Signaling

Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Promoted Osteogenesis by Increasing Vesicle Trafficking, Wnt/Ca2+, and BMP/Smad Signaling

Novel brain-targeted nanomicelles for anti-glioma therapy mediated by the ApoE-enriched protein corona in vivo

Lipid-mediated nuclear moonlighting of cytosolic glyceraldehyde-3-phosphate dehydrogenase in plant heat response

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