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P75NTR-/- mice exhibit an alveolar bone loss phenotype and inhibited PI3K/Akt/?-catenin pathway.

ABSTRACT: OBJECTIVES:The aim of this study was to investigate the role of p75 neurotrophin receptor (p75NTR) in regulating the mouse alveolar bone development and the mineralization potential of murine ectomesenchymal stem cells (EMSCs). Moreover, we tried to explore the underlying mechanisms associated with the PI3K/Akt/?-catenin pathway. MATERIALS AND METHODS:p75NTR knockout (p75NTR-/- ) mice and wild-type (WT) littermates were used. E12.5d p75NTR-/- and WT EMSCs were isolated in the same pregnant p75NTR-/+ mice from embryonic maxillofacial processes separately. Mouse alveolar bone mass was evaluated using micro-CT. Differential osteogenic differentiation pathways between p75NTR-/- and WT EMSCs were analysed by RNA-sequencing. The PI3K inhibitor LY294002 and PI3K agonist 740Y-P were used to regulate the PI3K/Akt pathway in EMSCs. p75NTR overexpression lentiviruses, p75NTR knock-down lentiviruses and recombined mouse NGF were used to transfect cells. RESULTS:The alveolar bone mass was found reduced in the p75NTR knockout mouse comparing to the WT mouse. During mineralization induction, p75NTR-/- EMSCs displayed decreased osteogenic capacity and downregulated PI3K/Akt/?-catenin signalling. The PI3K/Akt/?-catenin pathway positively regulates the potential of differential mineralization in EMSCs. The promotive effect of p75NTR overexpression can be attenuated by LY294002, while the inhibitory effect of p75NTR knock-down on Runx2 and Col1 expression can be reversed by 740Y-P. CONCLUSION:Deletion of p75NTR reduced alveolar bone mass in mice. P75NTR positively regulated the osteogenic differentiation of EMSCs via enhancing the PI3K/Akt/?-catenin pathway.

SUBMITTER: Wang Y

PROVIDER: S-EPMC7162804 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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p75NTR<sup>-/-</sup> mice exhibit an alveolar bone loss phenotype and inhibited PI3K/Akt/β-catenin pathway.

Wang Yingying Y Yang Kun K Li Gang G Liu Rui R Liu Junyu J Li Jun J Tang Mengying M Zhao Manzhu M Song Jinlin J Wen Xiujie X

Cell proliferation 20200325 4

<h4>Objectives</h4>The aim of this study was to investigate the role of p75 neurotrophin receptor (p75NTR) in regulating the mouse alveolar bone development and the mineralization potential of murine ectomesenchymal stem cells (EMSCs). Moreover, we tried to explore the underlying mechanisms associated with the PI3K/Akt/β-catenin pathway.<h4>Materials and methods</h4>p75NTR knockout (p75NTR<sup>-/-</sup> ) mice and wild-type (WT) littermates were used. E12.5d p75NTR<sup>-/-</sup> and WT EMSCs wer ...[more]

PMID: 32215984

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Project description:Meloxicam is a non-steroidal anti-inflammatory drug and has been used to relieve pain and control inflammation in cows with metritis and endometritis. Meloxicam has been found to be effective in inhibiting tissue or cell growth when it is used as an anti-inflammatory therapy. However, the influence of meloxicam on bovine endometrial regeneration has not been reported. This study was to research the effect of meloxicam (0.5 and 5 μM) on the proliferation of primary bovine endometrial epithelial cells (BEECs) stimulated by Escherichia coli lipopolysaccharide. The cell viability, cell cycle, and cell proliferation were evaluated by Cell Counting Kit-8, flow cytometry, and cell scratch test, respectively. The mRNA transcriptions of prostaglandin-endoperoxide synthase 1 (PTGS1) and PTGS2, Toll-like receptor 4, and proliferation factors were detected using quantitative reverse-transcription polymerase chain reaction. The activations of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and Wnt/β-catenin pathways were determined using western blot and immunofluorescence. As a result, co-treatment of meloxicam and lipopolysaccharide inhibited (P < 0.05) the cell cycle progression and reduced (P < 0.05) the cell healing rate and the mRNA level of proliferation factors as compared with the cells treated with lipopolysaccharide alone. Meloxicam decreased (P < 0.05) the lipopolysaccharide-induced PTGS2 gene expression. Neither lipopolysaccharide nor meloxicam changed PTGS1 mRNA abundance (P > 0.05). Meloxicam inhibited (P < 0.05) the lipopolysaccharide-activated Wnt/β-catenin pathway by reducing (P < 0.05) the protein levels of β-catenin, c-Myc, cyclin D1, and glycogen synthase kinase-3β and prevented the lipopolysaccharide-induced β-catenin from entering the nucleus. Meloxicam suppressed (P < 0.05) the phosphorylation of PI3K and AKT. In conclusion, meloxicam alone did not influence the cell cycle progression or the cell proliferation in BEEC but caused cell cycle arrest and inhibited cell proliferation in lipopolysaccharide-stimulated BEEC. This inhibitory effect of meloxicam was probably mediated by Wnt/β-catenin and PI3K/AKT pathways.

Dataset Information

P75NTR-/- mice exhibit an alveolar bone loss phenotype and inhibited PI3K/Akt/?-catenin pathway.

Publications

p75NTR<sup>-/-</sup> mice exhibit an alveolar bone loss phenotype and inhibited PI3K/Akt/β-catenin pathway.

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