FAK and BMP-9 synergistically trigger osteogenic differentiation and bone formation of adipose derived stem cells through enhancing Wnt-β-catenin signaling

Yuan, Cheng; Gou, Xiaoli; Deng, Jing; Dong, Zhibao; Ye, Peng; Hu, Zhenming

doi:10.1016/j.biopha.2018.04.185

Cited by 28 publications

(26 citation statements)

References 21 publications

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“…In vitro studies have shown that FAK can promote cell mineralization in the modulation of osteogenic and odontogenic differentiation [9]. In addition, Yuan et al [11] demonstrated that FAK and BMP-9 could cross-talk on Wnt signal pathway and promote ADSCs osteogenesis. The current study found that BMP9 could obviously promote the cell proliferation, migration and osteogenic differentiation of SMSCs in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Besides, FAK is also known as a signal adaptor, which could cross-talk with multiple signal transduction pathways in mediating cellular apoptosis, cell mobility and differentiation [8][9][10]. A previous survey demonstrated that FAK could promote osteogenesis of ADSCs via Wnt/b-catenin signal [11]. The function of FAK in osteogenic process of MSCs needs further investigation.…”

Section: Introductionmentioning

confidence: 99%

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FAK mediates BMP9-induced osteogenic differentiation via Wnt and MAPK signaling pathway in synovial mesenchymal stem cells

Zheng

Sun

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objective: Focal adhesion kinase (FAK) has critical functions in proliferation and differentiation of many cell types, however, the role of FAK on BMP9-induced osteogenic differentiation in SMSCs has not been characted. The purpose of current study is to explore the mechanism of FAK on the BMP9induced osteogenesis of SMSCs in vitro and in vivo. Methods: The optimal dose of BMP9 was determined by incubation in different BMP9 concentrations, then cells were transfected with siRNA-induced FAK knockdown in BMP9-induced osteogenesis. Cell proliferation, migration, the osteogenic capacity, and the underlying mechanism were further detected in vitro. Imaging and pathological examination were conducted to observe the bone formation in vivo. Results: Our findings suggested that BMP9 could obviously promote FAK phosphorylation in osteogenic conditions. In contrast, FAK knockdown significantly decreased the cell proliferation, migration, the osteogenic capacity of SMSCs. To be specific, FAK knockdown could markedly inhibit the Wnt and MAPK signal pathway of SMSCs induced by BMP9. Besides, FAK knockdown could also effectively inhibit BMP-9-induced bone formation in vivo. Conclusion: FAK plays a pivotal role in promoting BMP9-induced osteogenesis of SMSCs, which is probably via activating Wnt and MAPK pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

FAK mediates BMP9-induced osteogenic differentiation via Wnt and MAPK signaling pathway in synovial mesenchymal stem cells

Zheng

Sun

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Its importance in physiology and disease was quickly recognised and a host of cellular and in vivo studies have since placed FAK as a key player of cellular processes which in some form usually require controlled cell motility. As such, FAK is required for various aspects during development [3][4][5][6] as well as tissue regeneration and wound healing [7][8][9][10]. The importance of FAK in cell motility is also reflected in disease where FAK plays major roles in tumour invasion and metastasis [11].…”

Section: Introductionmentioning

confidence: 99%

FAK Structure and Regulation by Membrane Interactions and Force in Focal Adhesions

2020

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Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase with key roles in the regulation of cell adhesion migration, proliferation and survival. In cancer FAK is a major driver of invasion and metastasis and its upregulation is associated with poor patient prognosis. FAK is autoinhibited in the cytosol, but activated upon localisation into a protein complex, known as focal adhesion complex. This complex forms upon cell adhesion to the extracellular matrix (ECM) at the cytoplasmic side of the plasma membrane at sites of ECM attachment. FAK is anchored to the complex via multiple sites, including direct interactions with specific membrane lipids and connector proteins that attach focal adhesions to the actin cytoskeleton. In migrating cells, the contraction of actomyosin stress fibres attached to the focal adhesion complex apply a force to the complex, which is likely transmitted to the FAK protein, causing stretching of the FAK molecule. In this review we discuss the current knowledge of the FAK structure and how specific structural features are involved in the regulation of FAK signalling. We focus on two major regulatory mechanisms known to contribute to FAK activation, namely interactions with membrane lipids and stretching forces applied to FAK, and discuss how they might induce structural changes that facilitate FAK activation.

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“…In the migration of retinal pigment epithelial cells, FAK regulates cell transformation and migration by tyrosine phosphorylation [9]. FAK could participate in BMP-9 induced ADSCs osteogenesis via the Wnt signaling pathway [10]. Among the many membrane receptors that can mediate the communication between the ECM and migrating cells, the integrin mediated focal adhesion (FA) is one of the most important [11].…”

Section: Introductionmentioning

confidence: 99%

Platelet endothelial aggregation receptor-1 regulates bovine muscle satellite cell migration and differentiation via integrin beta-1 and focal adhesion kinase

Pang

Zhang

Zhao

et al. 2019

Cell Adhesion & Migration

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PEAR1 is highly expressed at bovine MDSC differentiation. However, its biological function remains unclear. Western blotting results showed that PEAR1 increased between day 0 and day 2 of cell differentiation and decreased from day 3. Moreover, scratch test showed that wound healing rate increased after PEAR1 overexpression and decreased upon its suppression. Meanwhile, we found that, upon PEAR1 induction, both the expression of the focal adhesion-associated and MyoG, and the myotube fusion rate increased. However, when PEAR1 was suppressed, opposite results were obtained. Immunoprecipitation revealed an association between PEAR1 and ITGB1. Notably, inhibition of FAK and ITGB1 repressed cell differentiation. In conclusion, our study indicated that PEAR1 is involved in the regulation of bovine MDSC migration and differentiation.

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FAK and BMP-9 synergistically trigger osteogenic differentiation and bone formation of adipose derived stem cells through enhancing Wnt-β-catenin signaling

Cited by 28 publications

References 21 publications

FAK mediates BMP9-induced osteogenic differentiation via Wnt and MAPK signaling pathway in synovial mesenchymal stem cells

FAK mediates BMP9-induced osteogenic differentiation via Wnt and MAPK signaling pathway in synovial mesenchymal stem cells

FAK Structure and Regulation by Membrane Interactions and Force in Focal Adhesions

Platelet endothelial aggregation receptor-1 regulates bovine muscle satellite cell migration and differentiation via integrin beta-1 and focal adhesion kinase

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