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AFF4 regulates osteogenic differentiation of human dental follicle cells

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International Journal of oral Science 2020年第4期12卷 287-297页

作者： Qingyue Xiao Yuning Zhang Xingying Qi Yaqian Chen Rui Sheng Ruoshi Xu Quan Yuan Chenchen Zhou State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&West China Hospital of Stomatology Sichuan UniversityChengduChina state key laboratory of oral diseases&national clinical research center for oral diseases&Department of Cariology and Endodontology West China Hospital of StomatologySichuan UniversityChengduChina state key laboratory of oral diseases&national clinical research center for oral diseases&Department of oral Implantology West China Hospital of StomatologySichuan UniversityChengduChina state key laboratory of oral diseases&national clinical research center for oral diseases&Department of Pediatric Dentistry West China Hospital of StomatologySichuan UniversityChengduChina

As a member of the AFF(AF4/FMR2)family,AFF4 is a transcription elongation factor that is a component of the super elongation complex.AFF4 serves as a scaffolding protein that connects transcription factors and promotes gene transcription through elongation and chromatin remodelling.Here,we investigated the effect of AFF4 on human dental follicle cells(DFCs)in osteogenic differentiation.In this study,we found that small interfering RNA-mediated depletion of AFF4 resulted in decreased alkaline phosphatase(ALP)activity and impaired mineralization.In addition,the expression of osteogenic-related genes(DLX5,SP7,RUNX2 and BGLAP)was significantly downregulated.In contrast,lentivirus-mediated overexpression of AFF4 significantly enhanced the osteogenic potential of human DFCs.Mechanistically,we found that both the mRNA and protein levels of ALKBH1,a critical regulator of epigenetics,changed in accordance with AFF4 expression levels.Overexpression of ALKBH1 in AFF4-depleted DFCs partially rescued the impairment of osteogenic differentiation.Our data indicated that AFF4 promoted the osteogenic differentiation of DFCs by upregulating the transcription of ALKBH1.

关键词： impaired impairment alkaline

circ_0003204 regulates the osteogenic differentiation of human adipose-derived stem cells via miR-370-3p/HDAC4 axis

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International Journal of oral Science 2022年第3期14卷 360-370页

作者： Liyuan Yu Kai Xia Jing Zhou Zhiai Hu Xing Yin Chenchen Zhou Shujuan Zou Jun Liu state key laboratory of oral diseases&national clinical research center for oral diseases&Department of Orthodontics West China Hospital of StomatologySichuan UniversityChengduChina Department of stomatology Kunming Yan’an hospitalKunmingChina state key laboratory of oral diseases&national clinical research center for oral diseases&Department of Pediatric Dentistry West China Hospital of StomatologySichuan UniversityChengduChina

Human adipose-derived stem cells(hASCs)are a promising cell type for bone tissue regeneration.Circular RNAs(circRNAs)have been shown to play a critical role in regulating various cell differentiation and involve in mesenchymal stem cell osteogenesis.However,how circRNAs regulate hASCs in osteogenesis is still unclear.Herein,we found circ_0003204 was significantly downregulated during osteogenic differentiation of hASCs.Knockdown of circ_0003204 by si RNA or overexpression by lentivirus confirmed circ_0003204 could negatively regulate the osteogenic differentiation of hASCs.We performed dual-luciferase reporting assay and rescue experiments to verify circ_0003204 regulated osteogenic differentiation via sponging miR-370-3p.We predicted and confirmed that miR-370-3p had targets in the 3′-UTR of HDAC4 m RNA.The following rescue experiments indicated that circ_0003204 regulated the osteogenic differentiation of hASCs via miR-370-3p/HDAC4 axis.Subsequent in vivo experiments showed the silencing of circ_0003204 increased the bone formation and promoted the expression of osteogenic-related proteins in a mouse bone defect model,while overexpression of circ_0003204 inhibited bone defect repair.Our findings indicated that circ_0003204 might be a promising target to promote the efficacy of hASCs in repairing bone defects.

关键词： regulates the osteogenic differentiation of human adipose-derived stem cells via miR-370-3p/HDAC4 axis miR

PTHrP promotes subchondral bone formation in TMJ-OA

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International Journal of oral Science 2022年第4期14卷 489-496页

作者： Jun Zhang Caixia Pi Chen Cui Yang Zhou Bo Liu Juan Liu Xin Xu Xuedong Zhou Liwei Zheng State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&West China Hospital of Stomatology Sichuan UniversityChengduChina Yunnan key laboratory of stomatology KunmingChina Department of Affiliated Stomatological HospitalKunming Medical UniversityKunmingChina

PTH-related peptide(PTHr P) improves the bone marrow micro-environment to activate the bone-remodelling, but the coordinated regulation of PTHr P and transforming growth factor-β(TGFβ) signalling in TMJ-OA remains incompletely understood. We used disordered occlusion to establish model animals that recapitulate the ordinary clinical aetiology of TMJ-OA. Immunohistochemical and histological analyses revealed condylar fibrocartilage degeneration in model animals following disordered occlusion. TMJ-OA model animals administered intermittent PTHr P(i PTH) exhibited significantly decreased condylar cartilage degeneration. Micro-CT,histomorphometry, and western Blot analyses disclosed that i PTH promoted subchondral bone formation in the TMJ-OA model animals. In addition, i PTH increased the number of osterix(OSX)-positive cells and osteocalcin(OCN)-positive cells in the subchondral bone marrow cavity. However, the number of osteoclasts was also increased by i PTH, indicating that subchondral bone volume increase was mainly due to the i PTH-mediated increase in the bone-formation ability of condylar subchondral bone.In vitro, PTHr P treatment increased condylar subchondral bone marrow-derived mesenchymal stem cell(SMSC) osteoblastic differentiation potential and upregulated the gene and protein expression of key regulators of osteogenesis. Furthermore, we found that PTHr P-PTH1R signalling inhibits TGFβ signalling during osteoblastic differentiation. Collectively, these data suggested that i PTH improves OA lesions by enhancing osteoblastic differentiation in subchondral bone and suppressing aberrant active TGFβsignalling. These findings indicated that PTHr P, which targets the TGFβ signalling pathway, may be an effective biological reagent to prevent and treat TMJ-OA in the clinic.

关键词： TMJ degeneration occlusion

Aberrant NF-κB activation in odontoblasts orchestrates inflammatory matrix degradation and mineral resorption

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International Journal of oral Science 2022年第1期14卷 80-90页

作者： Fanyuan Yu Fengli Huo Feifei Li Yanqin Zuo Chenglin Wang Ling Ye state key laboratory of oral diseases&national clinical research center for oral diseases West China Hospital of StomatologySichuan UniversityChengduChina Department of Endodontics West China Stomatology HospitalSichuan UniversityChengduChina

Inflammation-associated proteinase functions are key determinants of inflammatory stromal tissues deconstruction.As a specialized inflammatory pathological process,dental internal resorption(IR)includes both soft and hard tissues deconstruction within the dentin-pulp complex,which has been one of the main reasons for inflammatory tooth loss.Mechanisms of inflammatory matrix degradation and tissue resorption in IR are largely unclear.In this study,we used a combination of Cre-loxP reporter,flow cytometry,cell transplantation,and enzyme activities assay to mechanistically investigate the role of regenerative cells,odontoblasts(ODs),in inflammatory mineral resorption and matrices degradation.We report that inflamed ODs have strong capabilities of matrix degradation and tissue resorption.Traditionally,ODs are regarded as hard-tissue regenerative cells;however,our data unexpectedly present ODs as a crucial population that participates in IR-associated tissue deconstruction.Specifically,we uncovered that nuclear factor-kappa b(NF-κB)signaling orchestrated Tumor necrosis factorα(TNF-α)-induced matrix metalloproteinases(Mmps)and Cathepsin K(Ctsk)functions in ODs to enhance matrix degradation and tissue resorption.Furthermore,TNF-αincreases Rankl/Opg ratio in ODs via NF-κB signaling by impairing Opg expression but increasing Rankl level,which utterly makes ODs cell line 17IIA11(A11)become Trap^(+) and Ctsk^(+) multinucleated cells to perform resorptive actions.Blocking of NF-κB signaling significantly rescues matrix degradation and resorptive functions of inflamed ODs via repressing vital inflammatory proteinases Mmps and Ctsk.Utterly,via utilizing NF-κB specific small molecule inhibitors we satisfactorily attenuated inflammatory ODs-associated human dental IR in vivo.Our data reveal the underlying mechanisms of inflammatory matrix degradation and resorption via proteinase activities in IR-related pathological conditions.

关键词： inflammatory matrix utilizing

Microenvironmental stiffness mediates cytoskeleton re-organization in chondrocytes through laminin-FAK mechanotransduction

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International Journal of oral Science 2022年第2期14卷 182-191页

作者： Chenchen Zhou Mengmeng Duan Daimo Guo Xinmei Du Demao Zhang Jing Xie state key laboratory of oral diseases&national clinical research center for oral diseases West China Hospital of StomatologySichuan UniversityChengduChina Department of Cariology and Endodontics West China Hospital of StomatologySichuan UniversityChengduChina

Microenvironmental biophysical factors play a fundamental role in controlling cell behaviors including cell morphology,proliferation,adhesion and differentiation,and even determining the cell fate.Cells are able to actively sense the surrounding mechanical microenvironment and change their cellular morphology to adapt to it.Although cell morphological changes have been considered to be the first and most important step in the interaction between cells and their mechanical microenvironment,their regulatory network is not completely clear.In the current study,we generated silicon-based elastomer polydimethylsiloxane(PDMS)substrates with stiff(15:1,PDMS elastomer vs.curing agent)and soft(45:1)stiffnesses,which showed the Young’s moduli of~450 k Pa and 46 kPa,respectively,and elucidated a new path in cytoskeleton re-organization in chondrocytes in response to changed substrate stiffnesses by characterizing the axis shift from the secreted extracellular protein lamininβ1,focal adhesion complex protein FAK to microfilament bundling.We first showed the cellular cytoskeleton changes in chondrocytes by characterizing the cell spreading area and cellular synapses.We then found the changes of secreted extracellular linkage protein,lamininβ1,and focal adhesion complex protein,FAK,in chondrocytes in response to different substrate stiffnesses.These two proteins were shown to be directly interacted by Co-IP and colocalization.We next showed that impact of FAK on the cytoskeleton organization by showing the changes of microfilament bundles and found the potential intermediate regulators.Taking together,this modulation axis of lamininβ1-FAK-microfilament could enlarge our understanding about the interdependence among mechanosensing,mechanotransduction,and cytoskeleton re-organization.

关键词： laminin mec stiffness

Magnesium promotes vascularization and osseointegration in diabetic states

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International Journal of oral Science 2024年第1期16卷 122-133页

作者： Linfeng Liu Feiyu Wang Wei Song Danting Zhang Weimin Lin Qi Yin Qian Wang Hanwen Li Quan Yuan Shiwen Zhang state key laboratory of oral diseases&national center for stomatology&national clinical research center for oral diseases&west china hospital of stomatology Sichuan UniversityChengduChina state key laboratory of oral diseases&national center for stomatology&national clinical research center for oral diseases&Department of oral Implantology West China Hospital of StomatologySichuan UniversityChengduChina

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg^(2+)promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated thealveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg^(2+)promoted the degradation of Kelch-like ECH-associated protein 1 (Keap1) and the nucleation of nuclear factor erythroid 2-related factor 2 (Nrf2) by up-regulating the expression of sestrin 2 (SESN2) in endothelial cells,thus reducing theelevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg^(2+)promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondria metabolism.

关键词： healing diabetic impaired

Hippo-YAP/TAZ signaling in osteogenesis and macrophage polarization:Therapeutic implications in bone defect repair

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Genes & diseases 2023年第6期10卷 2528-2539页

作者： Haochen Wang Hui Yu Tianyu Huang Bin Wang Lin Xiang state key laboratory of oral diseases&national clinical research center for oral diseases West China Hospital of StomatologySichuan UniversityChengduSichuan 610041China Department of oral Implantology West China Hospital of StomatologySichuan UniversityChengduSichuan 610041China

Bone defects caused by diseases or surgery are a common clinical problem.researchers are devoted to finding biological mechanisms that accelerate bone defect repair,which is a complex and continuous process controlled by many factors.As members of transcriptional costimulatory molecules,Yes-associated protein(YAP)and transcriptional co-activator with PDZ-binding motif(TAZ)play an important regulatory role in osteogenesis,and they affect cell function by regulating the expression of osteogenic genes in osteogenesis-related cells.Macrophages are an important group of cells whose function is regulated by YAP/TAZ.Currently,the relationship between YAP/TAZ and macrophage polarization has attracted increasing attention.In bone tissue,YAP/TAZ can realize diverse osteogenic regulation by mediating macrophage polarization.Macrophages polarize into M1 and M2 phenotypes under different stimuli.M1 macrophages dominate the inflammatory response by releasing a number of inflammatory mediators in the early phase of bone defect repair,while massive aggregation of M2 macrophages is beneficial for inflammation resolution and tissue repair,as they secrete many anti-inflammatory and osteogenesis-related cytokines.The mechanism of YAP/TAZ-mediated macrophage polarization during osteogenesis warrants further study and it is likely to be a promising strategy for bone defect repair.In this article,we review the effect of Hippo-YAP/TAZ signaling and macrophage polarization on bone defect repair,and highlight the regulation of macrophage polarization by YAP/TAZ.

关键词： Bone defect repair Hippo-YAP/TAZ signaling Inflammation Macrophage polarization Osteogenesis

PKD3 promotes metastasis and growth of oral squamous cell carcinoma through positive feedback regulation with PD-L1 and activation of ERK-STAT1/3-EMT signalling

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International Journal of oral Science 2021年第1期13卷 79-88页

作者： Bomiao Cui Jiao Chen Min Luo Yiying Liu Hongli Chen Die Lü Liwei Wang Yingzhu Kang Yun Feng Libin Huang Ping Zhang State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&West China Hospital of Stomatology Sichuan UniversityChengduChina Department of Gastroenterology West China HospitalSichuan UniversityChengduChina

oral squamous cell carcinoma(OSCC)has a high incidence of metastasis.Tumour immunotherapy targeting PD-L1 or PD-1 has been revolutionary;however,only a few patients with OSCC respond to this treatment.Therefore,it is essential to gain insights into the molecular mechanisms underlying the growth and metastasis of OSCC.In this study,we analysed the expression levels of protein kinase D3(PKD3)and PD-L1 and their correlation with the expression of mesenchymal and epithelial markers.We found that the expression of PKD3 and PD-L1 in OSCC cells and tissues was significantly increased,which correlated positively with that of mesenchymal markers but negatively with that of epithelial markers.Silencing PKD3 significantly inhibited the growth,metastasis and invasion of OSCC cells,while its overexpression promoted these processes.Our further analyses revealed that there was positive feedback regulation between PKD3 and PD-L1,which could drive EMT of OSCC cells via the ERK/STAT1/3 pathway,thereby promoting tumour growth and metastasis.Furthermore,silencing PKD3 significantly inhibited the expression of PD-L1,and lymph node metastasis of OSCC was investigated with a mouse footpad xenograft model.Thus,our findings provide a theoretical basis for targeting PKD3 as an alternative method to block EMT for regulating PD-L1 expression and inhibiting OSCC growth and metastasis.

关键词： metastasis inhibited squamous

Mini suture anchor: An effective device for reduction and fixation of displaced temporomandibular joint disc with intracapsular condylar fracture

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Chinese Journal of Traumatology 2022年第1期25卷 49-53页

作者： Shubhechha Shakya Kai-De Li Dou Huang Zuo-Qiang Liu Zhi-Ru Liu Lei Liu state key laboratory of oral diseases&national clinical research center for oral diseases&Department of oral and Maxillofacial Surgery West China Hospital of StomatologySichuan UniversityChengdu610041China

Purpose::The main aim is to provide clinical reference for the application of mini suture anchor in the reduction and fixation of displaced temporomandibular joint(TMJ)disc with intracapsular condylar fracture.Methods::From October 2018 to October 2019,21 patients(31 sides)with intracapsular condylar fractures and articular disc displacement from west china hospital of stomatology,Sichuan University were included.The selection criteria were:(1)mandibular condylar fractures accompanied by displacement of the TMJ disc,confirmed by clinical examination,CT scan and other auxiliary examinations;(2)indication for surgical treatment;(3)no surgical contraindications;(4)no previous history of surgery in the operative area;(5)no facial nerve injury before the surgery;(6)informed consent to participate in the research program and(7)complete data.Patients without surgical treatment were excluded.The employed patients were followed up at 1,3,6 and 12 months after operation.Outcomes were assessed by success rate of operation,TMJ function and radiological examination results at 3 months after operation.Data were expressed as number and percent and analyzed using SPSS 19.0.Results::All the surgical procedures were completed successfully and all the articular discs were firmly attached to the condyles.The articular disc sufficiently covered the condylar head after the fixation.The fixation remained stable when the mandible was moved in each direction by the surgeons.No complications occurred.The functions of the TMJ were well-recovered postoperatively in most cases.CT scan revealed that the screws were completely embedded in the bone without loosening or displacement.Conclusion::Mini suture anchor can provide satisfactory stabilization for the reduced articular disc and also promote the recovery of TMJ functions.

关键词： Intracapsular condylar fracture Displacement of temporomandibular joint disc Disc reduction Disc fixation Mini suture anchor