<scp>IGFBP</scp>5 enhances osteogenic differentiation potential of periodontal ligament stem cells and Wharton's jelly umbilical cord stem cells, <i>via</i> the <scp>JNK</scp> and <scp>MEK</scp>/Erk signalling pathways

Wang, Yuejun; Jia, Zhi; Xiao, Lin; Lian, Xiaomeng; Wang, Liping; Dong, Rui; Liu, Dayong

doi:10.1111/cpr.12284

Cited by 45 publications

(51 citation statements)

References 56 publications

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“…56 IGFBP5 enhances the osteogenic differentiation potentials of MSCs via the JNK and MEK/Erk signalling pathways. 16 Other studies have confirmed that PPAR-γ is a negative regulator of osteogenic differentiation. 59,60 For example, a study showed that enhanced PPAR-γ activity leads to bone loss, and reduced PPAR-γ activity causes bone mass to increase in animal models.…”

Section: Discussionmentioning

confidence: 95%

CB1 enhanced the osteo/dentinogenic differentiation ability of periodontal ligament stem cells via p38 MAPK and JNK in an inflammatory environment

et al. 2019

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Objectives Periodontitis is an inflammatory immune disease that causes periodontal tissue loss. Inflammatory immunity and bone metabolism are closely related to periodontitis. The cannabinoid receptor I (CB1) is an important constituent of the endocannabinoid system and participates in bone metabolism and inflammation tissue healing. It is unclear whether CB1 affects the mesenchymal stem cell (MSC) function involved in periodontal tissue regeneration. In this study, we revealed the role and mechanism of CB1 in the osteo/dentinogenic differentiation of periodontal ligament stem cells (PDLSCs) in an inflammatory environment. Materials and methods Alkaline phosphatase (ALP) activity, Alizarin Red staining, quantitative calcium analysis and osteo/dentinogenic markers were used to assess osteo/dentinogenic differentiation. Real‐time RT‐PCR and Western blotting were employed to detect gene expression. Results CB1 overexpression or CB1 agonist (10 µM R‐1 Meth) promoted the osteo/dentinogenic differentiation of PDLSCs. Deletion of CB1 or the application of CB1 antagonist (10 µM AM251) repressed the osteo/dentinogenic differentiation of PDLSCs. The activation of CB1 enhanced the TNF‐α‐ and INF‐γ‐impaired osteo/dentinogenic differentiation potential in PDLSCs. Moreover, CB1 activated p38 MAPK and JNK signalling and repressed PPAR‐γ and Erk1/2 signalling. Inhibition of JNK signalling could block CB1‐activated JNK and p38 MAPK signalling, while CB1 could activate p38 MAPK and JNK signalling, which was inhibited by TNF‐α and INF‐γ stimulation. Conclusions CB1 was able to enhance the osteo/dentinogenic differentiation ability of PDLSCs via p38 MAPK and JNK signalling in an inflammatory environment, which might be a potential target for periodontitis treatment.

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Section: Discussionmentioning

confidence: 95%

CB1 enhanced the osteo/dentinogenic differentiation ability of periodontal ligament stem cells via p38 MAPK and JNK in an inflammatory environment

et al. 2019

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“…It is widely accepted that the regulation of osteogenesis is a complex process which is associated with several signaling pathways. The MAPKs, a group of serine/threonine kinases, transmit signals from the cell membrane into the nucleus, exerting an important role in the regulation of cell differentiation (37). The MAPK family includes three distinctly-regulated groups: ERK1/2, JNK1/2 and p38 MAPKs (38)(39)(40)(41).…”

Section: Discussionmentioning

confidence: 99%

“…OSX, a zinc finger-containing transcription factor required for osteoblastic differentiation, is also essential for osteoblast differentiation and bone formation and acts as a downstream factor of RUNX2 in bone homoeostasis (44,45). It has been reported that the interaction domains in OSX and RUNX2 are phosphorylated by p38 and ERK MAPK (37). The physical interaction between OSX and RUNX2 and cooperative transcriptional effects can be disrupted by blocking p38 and ERK (46).…”

Section: Discussionmentioning

confidence: 99%

Gold nanoparticles promote osteogenic differentiation of human periodontal ligament stem cells via the p38 MAPK signaling pathway

Niu

Yuan

et al. 2017

Molecular Medicine Reports

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Gold nanoparticles (AuNPs) are a promising material for use in regenerative medicine due to their biocompatibility and easy functionalization with biomolecules including growth factors, DNA and peptides. In the present study, transmission electron microscopy indicated that the AuNPs were monodisperse and spherical in shape, with an estimated average diameter of 13 nm. And the cellular effects of AuNPs on the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) and the associated signaling pathways in cell differentiation were investigated based on histochemical analysis of alkaline phosphatase activity and mineralization, quantitative polymerase chain reaction, and western blotting. The results indicated that AuNPs enhanced the differentiation of hPDLSCs into osteoblasts, increasing their osteogenic transcriptional profile including alkaline phosphatase, osterix, collagen type I and runt‑related transcription factor 2 (RUNX2) and activating the p38 mitogen‑activated protein kinase (MAPK) signaling pathway. Furthermore, AuNPs increased the protein level of RUNX2, which is crucial for osteogenic differentiation. These results suggested that AuNPs stimulate the osteogenesis of hPDLSCs partially via activation of the p38 MAPK signaling pathway.

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“…Overexpression of IGFBP5 also was shown to enhance osteogenic differentiation in mesenchymal stem cells [59]. These observations resulted in increased phosphorylation of ERK1/2 and increased activity of the MAPK pathway, and predictably IGFBP5 knock down by shRNA reduced phosphorylation of ERK1/2 and subsequently downregulated the MAPK pathway [58][59][60]. Subsequently, our pathway analysis showed that the eight DE genes, including IGFBP5, were connected through the ERK/MAPK pathway.…”

Section: Discussionmentioning

confidence: 73%

Gene expression profiling of fibroblasts in a family with LMNA-related cardiomyopathy reveals molecular pathways implicated in disease pathogenesis

et al. 2020

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Background: Intermediate filament proteins that construct the nuclear lamina of a cell include the Lamin A/C proteins encoded by the LMNA gene, and are implicated in fundamental processes such as nuclear structure, gene expression, and signal transduction. LMNA mutations predominantly affect mesoderm-derived cell lineages in diseases collectively termed as laminopathies that include dilated cardiomyopathy with conduction defects, different forms of muscular dystrophies, and premature aging syndromes as Hutchinson-Gilford Progeria Syndrome. At present, our understanding of the molecular mechanisms regulating tissue-specific manifestations of laminopathies are still limited. Methods: To gain deeper insight into the molecular mechanism of a novel LMNA splice-site mutation (c.357-2A > G) in an affected family with cardiac disease, we conducted deep RNA sequencing and pathway analysis for nine fibroblast samples obtained from three patients with cardiomyopathy, three unaffected family members, and three unrelated, unaffected individuals. We validated our findings by quantitative PCR and protein studies. Results: We identified eight significantly differentially expressed genes between the mutant and non-mutant fibroblasts, that included downregulated insulin growth factor binding factor protein 5 (IGFBP5) in patient samples. Pathway analysis showed involvement of the ERK/MAPK signaling pathway consistent with previous studies. We found no significant differences in gene expression for Lamin A/C and B-type lamins between the groups. In mutant fibroblasts, RNA-seq confirmed that only the LMNA wild type allele predominately was expressed, and Western Blot showed normal Lamin A/C protein levels.

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IGFBP5 enhances osteogenic differentiation potential of periodontal ligament stem cells and Wharton's jelly umbilical cord stem cells, via the JNK and MEK/Erk signalling pathways

Abstract: Our results demonstrated that IGFBP5 promoted osteogenic differentiation potentials of PDLSCs and WJCMSCs via the JNK and MEK/Erk signalling pathways.

Cited by 45 publications

References 56 publications

CB1 enhanced the osteo/dentinogenic differentiation ability of periodontal ligament stem cells via p38 MAPK and JNK in an inflammatory environment

CB1 enhanced the osteo/dentinogenic differentiation ability of periodontal ligament stem cells via p38 MAPK and JNK in an inflammatory environment

Gold nanoparticles promote osteogenic differentiation of human periodontal ligament stem cells via the p38 MAPK signaling pathway

Gene expression profiling of fibroblasts in a family with LMNA-related cardiomyopathy reveals molecular pathways implicated in disease pathogenesis

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