scholarly journals Mir24-2-5p suppresses the osteogenic differentiation with Gnai3 inhibition presenting a direct target via inactivating JNK-p38 MAPK signaling axis

2021 ◽  
Vol 17 (15) ◽  
pp. 4238-4253
Author(s):  
Li Meng ◽  
Lichan Yuan ◽  
Jieli Ni ◽  
Mengru Fang ◽  
Shuyu Guo ◽  
...  
Keyword(s):  
Osteogenic Differentiation ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
Signaling Axis ◽  
Direct Target

Long non-coding RNA H19 acts as a microRNA-194 sponge to inhibit the apoptosis and promote the proliferation of hypertrophic scar fibroblasts

2021 ◽  
Author(s):  
Bo Liu ◽  
Lijuan Lin ◽  
Shengjin Yu ◽  
Rongjun Xia ◽  
Linlin Zheng
Keyword(s):  
P38 Mapk ◽  
Hypertrophic Scar ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Hypertrophic Scars ◽  
Downstream Effector ◽  
Non Coding Rna ◽  
Proliferation And Apoptosis ◽  
Signaling Axis ◽  
Underlying Mechanisms

The effects of long non-coding RNAs (lncRNAs) on the proliferation of hypertrophic scars have been described. However, the underlying mechanisms are not well characterized. The present study aimed to investigate the mechanisms of lncRNA H19 in hypertrophic scars. The effects of the lncRNA H19 on the proliferation and apoptosis of hypertrophic scar fibroblasts (HSFs) were analyzed using 5’-Ethynyl-2’-deoxyuridine staining, flow cytometry, and MTT. The results revealed H19 promoted the proliferation and inhibited the apoptosis in HSF. In addition, the binding associations between H19 and microRNA-194 (miR-194), and miR-194 and insulin-like growth factor-I receptor (IGF1R) were identified using bioinformatics screening and verified using dual-luciferase assays. Furthermore, the effects of the IGF1R knockdown on H19-induced HSF phenotypes and regulation over the p38 MAPK pathway were determined. Mechanistically, miR-194 was identified as the downstream effector of the H19-mediated phenotypes of HSFs through its ability to directly target IGF1R, thus modulating the p38 MAPK signaling pathway. In conclusion, the findings suggested that H19 may inhibit the apoptosis and promote the proliferation of HSFs through the miR-194/IGF1R/p38 MAPK signaling axis, thereby contributing to the progression of hypertrophic scars. These findings may provide novel targets for the treatment of hypertrophic scars.

scholarly journals Hypoxia Drives Breast Tumor Malignancy through a TET–TNFα–p38–MAPK Signaling Axis

2015 ◽  
Vol 75 (18) ◽  
pp. 3912-3924 ◽  
Author(s):  
Min-Zu Wu ◽  
Su-Feng Chen ◽  
Shin Nieh ◽  
Christopher Benner ◽  
Luo-Ping Ger ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Breast Tumor ◽  
Mapk Signaling ◽  
Signaling Axis

IL-1α regulates osteogenic differentiation and osteoclastic activity of dental follicle cells via JNK and p38 MAPK pathways

2020 ◽  
Author(s):  
mingmei meng ◽  
Yandi Chen ◽  
Xinlei Chen ◽  
Qiong Zhang ◽  
Weihua Guo ◽  
...  
Keyword(s):  
Osteogenic Differentiation ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
Tooth Eruption ◽  
Follicle Cells ◽  
Signal Pathways ◽  
Matrix Remodeling ◽  
Dental Follicle ◽  
Osteoclastic Activity ◽  
Specific Inhibitors

Abstract Background The expression of interleukin-1α (IL-1α) is increased in tooth with periapical lesion and the eruption of the permanent successor is accelerated in the presence of an infected deciduous tooth with abscess formation. Dental follicle (DF) plays a central role in tooth eruption through regulating alveolar bone resorption and formation. However, whether the increased IL-1α can disturb functions of DF and influence tooth eruption remains unknown. Herein, we studied the effect and possible mechanism of IL-1α on osteogenic differentiation, osteoclastic activity and matrix remodeling of the DF cells (DFCs). Methods Rat DFCs were treated with IL-1α. Quantitative real-time PCR and western blot were performed to analyze the expressions of osteogenesis, osteoclast formation and matrix remodeling related genes and proteins. DFC–bone marrow cell co-cultures, osteogenic differentiation and transwell matrigel invasion assay were used to determine the effect of IL-1α on DFCs further. Phosphorylation of JNK, ERK, p65 and p38 were evaluated in the IL-1α-treated group. Specific inhibitors of signal pathways were added to confirm their roles in this process. Results IL-1α decreased the expression of osteogenesis-related genes and proteins, and increased the expression of MMP9 and ratios of RANKL/OPG. DFCs cultured with IL-1α showed weaker osteogenic capacity, higher osteoclastogenic and invasive ability. Moreover, phosphorylation of JNK and p38 were up-regulated and pretreatment with specific inhibitors reversed the effect of IL-1α on DFCs. Conclusions IL-1α suppresses osteogenic differentiation, promotes osteoclastogenic ability and matrix remodeling of DFCs by activating JNK and p38 MAPK signaling pathways.

scholarly journals EphB4/ TNFR2/Erk/MAPK signaling pathway comprises a signaling axis to mediate the positive effect of TNF-α on osteogenic differentiation

2019 ◽  
Author(s):  
Yu Zhang ◽  
Chengzhe Yang ◽  
Shaohua Ge ◽  
Limei Wang ◽  
Jin Zhang ◽  
...  
Keyword(s):  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Precursor Cells ◽  
Mapk Signaling Pathway ◽  
Erk Mapk ◽  
Low Concentrations ◽  
Tnf Α ◽  
Signaling Axis ◽  
Positive Effect

Abstract Low concentrations of tumor necrosis factor-alpha and its receptor TNFR2 are both reported to promote osteogenic differentiation of osteoblast precursor cells. Moreover, low concentrations of TNF-α up-regulate the expression of EphB4. However, the molecular mechanisms underlying TNF-α-induced osteogenic differentiation and the roles of TNFR2 and EphB4 have not been fully elucidated. This study showed that with increase in ALP activity, mRNA and protein expression of Runx2, BSP and EphB4, TNFR2 expression was significantly promoted under 0.5 ng/ml TNF-α stimulation in osteoblast precursor cells MC3T3-E1. After TNFR2 was inhibited by gene knockdown with lentivirus-mediated shRNA interference or by a neutralizing antibody against TNFR2, the pro-osteogenic effect of TNF-α was partly reversed, but up-regulation of EphB4 by TNF-α kept unchanged. With EphB4 forward signaling suppressed by a potent inhibitor of EphB4 auto-phosphorylation, NVP-BHG712, TNF-α-enhanced expressions of TNFR2, BSP and Runx2 were significantly decreased. Further investigation into the signaling pathways revealed that TNF-α significantly augmented expression of p-JNK, p-Erk and p-p38, however, only p-Erk expression was significantly inhibited in TNFR2-knockdown cells. In addition, the Erk pathway inhibitor, U0126 (10μM), significantly inhibited the protein levels of Runx2 and BSP when compared with cells treated with TNF-α only. In conclusion, the EphB4, TNFR2 and Erk/MAPK signaling pathway comprise a signaling axis to mediate the positive effect of TNF-α on osteogenic differentiation.

Synergetic topography and chemistry cues guiding osteogenic differentiation in bone marrow stromal cells through ERK1/2 and p38 MAPK signaling pathway

2018 ◽  
Vol 6 (2) ◽  
pp. 418-430 ◽  
Author(s):  
Xinran Zhang ◽  
Haotian Li ◽  
Chucheng Lin ◽  
Congqin Ning ◽  
Kaili Lin
Keyword(s):  
Bone Marrow ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Mapk Signaling ◽  
Marrow Stromal Cells ◽  
Ion Doping ◽  
Mapk Signaling Pathways

Ordered micro-patterned topography and Sr ion doping in HAp synergistically enhance osteogenesis through ERK1/2 and p38 MAPK signaling pathways.

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