The role of oncostatin M regulates osteoblastic differentiation of dental pulp stem cells through STAT3 pathway

Feng, Xiaoxing; Shen, Shuling; Cao, Peipei; Zhu, Linhe; Zhang, Ye; Zheng, Ke; Feng, Guoliang; Zhang, Dongmei

doi:10.1007/s10616-016-9995-9

Cited by 17 publications

(14 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The activation of STAT3 signaling has been reported to enhance the osteogenic differentiation of precursor cells and bone defect healing [19, 32]. Gao et al had reported that hypoxia enhances STAT3 signaling in synovial fibroblasts [33].…”

Section: Discussionmentioning

confidence: 99%

Cellular hypoxia promotes osteogenic differentiation of mesenchymal stem cells and bone defect healing via STAT3 signaling

Wan

et al. 2019

Cell Mol Biol Lett

View full text Add to dashboard Cite

BackgroundHypoxia in the vicinity of bone defects triggers the osteogenic differentiation of precursor cells and promotes healing. The activation of STAT3 signaling in mesenchymal stem cells (MSCs) has similarly been reported to mediate bone regeneration. However, the interaction between hypoxia and STAT3 signaling in the osteogenic differentiation of precursor cells during bone defect healing is still unknown.MethodsIn this study, we assessed the impact of different durations of CoCl2-induced cellular hypoxia on the osteogenic differentiation of MSCs. Role of STAT3 signaling on hypoxia induced osteogenic differentiation was analyzed both in vitro and in vivo. The interaction between cellular hypoxia and STAT3 signaling in vivo was investigated in a mouse femoral bone defect model.ResultsThe peak osteogenic differentiation and expression of vascular endothelial growth factor (VEGF) occurred after 3 days of hypoxia. Inhibiting STAT3 reversed this effect. Hypoxia enhanced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and STAT3 phosphorylation in MSCs. Histology and μ-CT results showed that CoCl2 treatment enhanced bone defect healing. Inhibiting STAT3 reduced this effect. Immunohistochemistry results showed that CoCl2 treatment enhanced Hif-1α, ALP and pSTAT3 expression in cells present in the bone defect area and that inhibiting STAT3 reduced this effect.ConclusionsThe in vitro study revealed that the duration of hypoxia is crucial for osteogenic differentiation of precursor cells. The results from both the in vitro and in vivo studies show the role of STAT3 signaling in hypoxia-induced osteogenic differentiation of precursor cells and bone defect healing.

show abstract

Section: Discussionmentioning

confidence: 99%

Cellular hypoxia promotes osteogenic differentiation of mesenchymal stem cells and bone defect healing via STAT3 signaling

Wan

et al. 2019

Cell Mol Biol Lett

View full text Add to dashboard Cite

show abstract

“…Several studies have reported that OSM can activate osteogenesis through activation of STAT3. 25,26 In addition, BMP2 is a well-known growth factor that promotes osteogenesis, and has been used in clinical applications. 27 BMP2 promotes osteogenic differentiation mainly through the Smad1/5/9 signal pathway.…”

mentioning

confidence: 99%

Immunomodulatory properties of graphene oxide for osteogenesis and angiogenesis

Xue

Chen

Zhong

et al. 2018

IJN

View full text Add to dashboard Cite

BackgroundThe osteo-immunomodulatory properties of biomaterials play an important role in the outcomes of bone regeneration. Graphene oxide (GO) has been widely applied in many research fields due to its unique properties. However, the immunomodulatory properties of GO as a biomaterial for bone tissue engineering are still unclear.Materials and methodsIn this study, we evaluated the Inflammatory response of RAW264.7 cells influenced by GO. Then the osteogenic differentiation of BMSCs, and angiogenic differentiation of human umbilical vein endothelial cells (HUVECs) by stimulation with GO/RAW 264.7-conditioned culture medium were accessed. We also further investi gated the possible mechanisms underlying the osteo- and angio-immunomodulatory effects of GO.ResultsOur results showed that GO stimulates the secretion of oncostatin M, tumor necrosis factor alpha and other factors through the nuclear factor-κB pathway. GO/RAW264.7-conditioned medium promoted the osteogenic differentiation of BMSCs, stimulated upregulation of the HUVECs of vascular-related receptors, and promoted their tube formation in vitro.ConclusionIn conclusion, our research shows that GO, as a biomaterial, can induce the formation of a beneficial osteo-immunomodulatory environment and is a promising biomaterial for bone tissue engineering.

show abstract

“…IL-21 activates multiple signaling pathways, including the Janus kinase 1 and 3-signal transducer and activator of transcription (STAT3) pathway, the MAPK pathway, and the PI3K/AKT signalling pathway 25 through its receptor. Some studies have shown that members of the IL-6 family (IL-6, OSM) regulate osteoblastic differentiation of dental-pulp stem cells, human bone-marrow mesenchymal stem cells, and vascular smooth-muscle cells through the STAT3 pathway 11 , 26 . STAT3 plays an essential role in heart protection 27 .…”

Section: Discussionmentioning

confidence: 99%

IL-21 promotes osteoblastic differentiation of human valvular interstitial cells through the JAK3/STAT3 pathway

Liu¹,

Wang²,

Shi³

et al. 2020

Int. J. Med. Sci.

View full text Add to dashboard Cite

Objectives : This study amied to whether IL-21 promotes osteoblast transdifferentiation of cultured human Valvular interstitial cells (VICs). Methods : We first confirmed that IL-21 alters gene expression between CAVD aortic valve tissue and normal samples by immunohistochemistry, qPCR, and western blotting. VICs were cultured and treated with IL-21. Gene and protein expression levels of the osteoblastic markers ALP and Runx2, which can be blocked by specific JAK3 inhibitors and/or siRNA of STAT3, were measured. Results: IL-21 expression was upregulated in calcified aortic valves and promotes osteogenic differentiation of human VICs. IL-21 accelerated VIC calcification through the JAK3/STAT3 pathway. Conclusion: Our data suggest that IL-21 is a key factor in valve calcification and a promising candidate for targeted therapeutics for CAVD.

show abstract

The role of oncostatin M regulates osteoblastic differentiation of dental pulp stem cells through STAT3 pathway

Cited by 17 publications

References 35 publications

Cellular hypoxia promotes osteogenic differentiation of mesenchymal stem cells and bone defect healing via STAT3 signaling

Cellular hypoxia promotes osteogenic differentiation of mesenchymal stem cells and bone defect healing via STAT3 signaling

Immunomodulatory properties of graphene oxide for osteogenesis and angiogenesis

IL-21 promotes osteoblastic differentiation of human valvular interstitial cells through the JAK3/STAT3 pathway

Contact Info

Product

Resources

About