PKC and MAPKs Pathways Mediate EGF-induced Stimulation of 2-Deoxyglucose Uptake in Mouse Embryonic Stem Cells

Heo, Jung Sun; Han, Ho Jae

doi:10.1159/000092076

Cited by 23 publications

(19 citation statements)

References 56 publications

(50 reference statements)

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“…Our study demonstrates the reduced c-Fos expression in PI treated OC precursor cells, which suggested cause by the impaired activation of NFATc1 responsible for the inhibition of RANKL-induced OCs formation. Moreover, MAPKs family members (p38, ERK and JNK) are proline-directed serine/threonine kinases that play important roles in OCs growth, differentiation, and apoptosis [27]. In that, ERK signaling is involved in the cell proliferation and differentiation, and the expression of p-ERK can induce the OCs proliferation and differentiation [28].…”

Section: Discussionmentioning

confidence: 99%

Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production

Kong¹,

Wang²,

Yang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Osteoporosis is a metabolic bone disorder that tortures about millions of people worldwide. Recent study demonstrated agents derived from picrasma quassioides is a promising drug for targets multiple signaling pathways. However its potential in treatment of bone loss has not been fully understood. Methods: The bone marrow macrophages (BMMs) were cultured and induced with M-CSF and RANKL followed by picrasidine I (PI) treatment. Then the effects of PI on osteoclast formation were evaluated by counting tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Moreover, effects of PI on bone resorption activity of mature osteoclast were studied through bone resorption pit counting and actin ring structure analysis. Further, the involved potential signaling pathways cross-talking were investigated by performed Western blotting and quantitative real-time PCR examination. Results: Results demonstrated PI strongly inhibited RANKL induced osteoclast formation from its precursors. Mechanistically, the inhibitory effect of PI on osteoclast differentiation was due to the suppression of osteoclastogenic transcription factors, c-Fos and NFATc1. Moreover, PI markedly blocked the RANKL-induced osteoclastogenesis by attenuating MAPKs and NF-κB signaling pathways. In addition, PI decreased the ROS generation in osteoclast and osteoblast. Conclusion: Taken together our data demonstrate that PI has antiosteoclastogenic effect by inhibiting inflammation induced activation of MAPKs, NF-κB and ROS generation followed by suppressing the gene expression of c-Fos and NFATc1 in osteoclast precursors.

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Section: Discussionmentioning

confidence: 99%

Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production

Kong¹,

Wang²,

Yang³

et al. 2017

Cell Physiol Biochem

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“…None of these concentrations affected the proportion of embryos developing to the blastocyst stage by 96 h post-hCG, so 10 mM were selected for experiments. CHX (2 mg/l CHX, Sigma-Aldrich (Heo & Han 2006)), and a-amanitin (1 mg/l aAA, Fluka, 06422 from Sigma-Aldrich (Liu et al 2004)), were used to inhibit translation and transcription respectively. DPI (Sigma-Aldrich), an irreversible inhibitor of flavoenzymes, particularly activated NADPH oxidase, with tenfold lower potency for NADH oxidase (Morre 2002), inhibits the production of peroxide by the blockade of several NADPdependent enzymes in the pentose phosphate pathway and tricarboxylic acid cycle.…”

Section: Media Chemicals and Buffersmentioning

confidence: 99%

Glucose deprivation, oxidative stress and peroxisome proliferator-activated receptor-α (PPARA) cause peroxisome proliferation in preimplantation mouse embryos

Jansen

Cashman²,

Thompson³

et al. 2009

Reproduction

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Ex vivo two-cell mouse embryos deprived of glucose in vitro can develop to blastocysts by increasing their pyruvate consumption; however, zygotes when glucose-deprived cannot adapt this metabolic profile and degenerate as morulae. Prior to their death, these glucose-deprived morulae exhibit upregulation of the H C -monocarboxylate co-transporter SLC16A7 and catalase, which partly co-localize in peroxisomes. SLC16A7 has been linked to redox shuttling for peroxisomal b-oxidation. Peroxisomal function is unclear during preimplantation development, but as a peroxisomal transporter in embryos, SLC16A7 may be involved and influenced by peroxisome proliferators such as peroxisome proliferator-activated receptor-a (PPARA). PCR confirmed Ppara mRNA expression in mouse embryos. Zygotes were cultured with or without glucose and with the PPARA-selective agonist WY14643 and the developing embryos assessed for expression of PPARA and phospho-PPARA in relation to the upregulation of SLC16A7 and catalase driven by glucose deprivation, indicative of peroxisomal proliferation. Reactive oxygen species (ROS) production and relationship to PPARA expression were also analysed. In glucose-deprived zygotes, ROS was elevated within 2 h, as were PPARA expression within 8 h and catalase and SLC16A7 after 12-24 h compared with glucose-supplied embryos. Inhibition of ROS production prevented this induction of PPARA and SLC16A7. Selective PPARA agonism with WY14643 also induced SLC16A7 and catalase expression in the presence of glucose. These data suggest that glucose-deprived cleavage stage embryos, although supplied with sufficient monocarboxylate-derived energy, undergo oxidative stress and exhibit elevated ROS, which in turn upregulates PPARA, catalase and SLC16A7 in a classical peroxisomal proliferation response.

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“…The stimulation of PKC-activated p38 mitogen-activated protein kinase (MAPK) or ERK1/2 MAPK, is linked to the induction of blastocyst development. 4,29,30 To test this link, we studied the phosphorylated (p-) of p38 or ERK1/2 and their transport between the cytoplasm and nucleus using an immunofluorescence confocal technique. As shown in Figure 5B, p-p38 translocated to the nucleus of TEs in blastocysts that were transfected with scrambled (control) RNA.…”

Section: Fgfr2 In Tes Is Required For Expanded Blastocyst Formationmentioning

confidence: 99%

Binding of FGF2 to FGFR2 in an autocrine mode in trophectoderm cells is indispensable for mouse blastocyst formation through PKC-p38 pathway

Yang

Zhang

et al. 2015

Cell Cycle

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(2015) Binding of FGF2 to FGFR2 in an autocrine mode in trophectoderm cells is indispensable for mouse blastocyst formation through PKC-p38 pathway, Cell Cycle, 14:20, 3318-3330, DOI: 10.1080/15384101.2015 Keywords: blastocyst formation, fibroblast growth factor 2 (FGF2), fibroblast growth factor receptor 2 (FGFR2), protein kinase C (PKC), p38 MAPK Fibroblast growth factors (FGF1, FGF2 and FGF4) and fibroblast growth factor receptors (FGFR1, FGFR2, FGFR3 and FGFR4) have been reported to be expressed in preimplantation embryos and be required for their development. However, the functions of these molecules in trophectoderm cells (TEs) that lead to the formation of the blastocyst as well as the underlying mechanism have not been elucidated. The present study has demonstrated for the first time that endogenous FGF2 secreted by TEs can regulate protein expression and distribution in TEs via the FGFR2-mediated activation of PKC and p38, which are important for the development of expanded blastocysts. This finding provides the first explanation for the long-observed phenomenon that only high concentrations of exogenous FGFs have effects on embryonic development, but in vivo the amount of endogenous FGFs are trace. Besides, the present results suggest that FGF2/FGFR2 may act in an autocrine fashion and activate the downstream PKC/p38 pathway in TEs during expanded blastocyst formation.

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PKC and MAPKs Pathways Mediate EGF-induced Stimulation of 2-Deoxyglucose Uptake in Mouse Embryonic Stem Cells

Cited by 23 publications

References 56 publications

Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production

Picrasidine I from Picrasma Quassioides Suppresses Osteoclastogenesis via Inhibition of RANKL Induced Signaling Pathways and Attenuation of ROS Production

Glucose deprivation, oxidative stress and peroxisome proliferator-activated receptor-α (PPARA) cause peroxisome proliferation in preimplantation mouse embryos

Binding of FGF2 to FGFR2 in an autocrine mode in trophectoderm cells is indispensable for mouse blastocyst formation through PKC-p38 pathway

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