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| 1 | Runxl protects against the pathological progression of osteoarthritis显示文摘Runt-related transcription factor-1(Runxl)is required for chondrocyte-to-osteoblast lineage commitment by enhancing both chondrogenesis and osteogenesis during vertebrate development.However,the potential role of Runxl in joint diseases is not well known.In the current study,we aimed to explore the role of Runxl in osteoarthritis induced by anterior cruciate ligament transaction(ACLT)surgery.We showed that chondrocyte-specific Runxl knockout(Runx1f/fCol2a1-Cre)aggravated cartilage destruction by accelerating the loss of proteoglycan and collagen II in early osteoarthritis.Moreover,we observed thinning and ossification of the growth plate,a decrease in chondrocyte proliferative capacity and the loss of bone matrix around the growth plate in late osteoarthritis.We overexpressed Runxl by adeno-associated virus(AAV)in articular cartilage and identified its protective effect by slowing the destruction of osteoarthritis in cartilage in early osteoarthritis and alleviating the pathological progression of growth plate cartilage in late osteoarthritis.ChIP-seq analysis identified new targets that interacted with Runxl in cartilage pathology,and we confirmed the direct interactions of these factors with Runxl by ChIP-qPCR.This study helps us to understand the function of Runxl in osteoarthritis and provides new clues for targeted osteoarthritis therapy. | Chenchen Zhou Yujia Cui Yueyi Yang Daimo Guo Demao Zhang Yi Fan Xiaobing Li Jing Zou Jing Xie | 2021 | Bone Research2021，9，4： | 4 |
| 2 | Disturbed bone remodelling activity varies in different stages of experimental, gradually progressive apical periodontitis in rats显示文摘Bone remodelling keeps going through the lifespan of human by bone formation and bone resorption.In the craniofacial region,mandibles act as the main force for biting and chewing,and also become susceptible to a common bone-loss disease,namely,apical periodontitis,once infected dental pulp is not treated timely,during which bone resorption occurs from the apical foramen to the apical bone area.Although conventional root canal treatment(RCT)can remove the most of the infection,chronical apical periodontitis due to incomplete removal of dental pulp and subsequent microleakage will become refractory and more challenging,and this process has scarcely been specifically studied as a bone remodelling issue in rat models.Therefore,to study chronical and refractory apical periodontitis owing to incomplete cleaning of infected dental pulp and microleackage in vivo,we establish a modified rat model of gradually progressive apical periodontitis by sealing residual necrotic dental pulp and introducing limited saliva,which simulates gradually progressive apical periodontitis,as observed in the clinical treatment of chronical and refractory apical periodontitis.We show that bone-loss is inevitable and progressive in this case of apical periodontitis,which confirms again that complete and sound root canal treatment is crucial to halt the progression of chronical and refractory apical periodontitis and promote bone formation.Interestingly,bone remodelling was enhanced at the initial stage of apical periodontitis in this model while reduced with a high osteoblast number afterwards,as shown by the time course study of the modified model.Suggesting that the pathological apical microenvironment reserve its hard tissue formation ability to some degree but in a disturbed manner.Hopefully,our findings can provide insights for future bone regenerative treatment for apical periodontitisassociated bone loss. | Ruoshi Xu Daimo Guo Xuedong Zhou Jianxun Sun Yachuan Zhou Yi Fan Xin Zhou Mian Wan Wei Du Liwei Zheng | 2019 | International Journal of Oral Science2019，11，4： | 1 |
| 3 | PDGF-AA promotes cell-to-cell communication in osteocytes through PI3K/Akt signaling pathway显示文摘Osteocytes are the main sensitive cells in bone remodeling due to their potent functional cell processes from the mineralized bone matrix to the bone surface&the bone marrow.Neighboring osteocytes communicate with each other by these cell processes to achieve molecular exchange through gap junction channels.Platelet-derived growth factor-AA(PDGF-AA)has been reported to enhance bone tissue remodeling by promoting cell proliferation,migration,&autocrine secretion in osteoid cell linage.However,the effect of PDGF-AA on intercellular communication between osteocytes is still unclear.In the present study,we elucidated that PDGF-AA could enhance the formation of dendritic processes of osteocytes&the gap junctional intercellular communication by promoting the expression of connexin43(Cx43).This modulation process was mainly dependent on the activation of phosphorylation of Akt protein by phosphatidylinositol 3-kinase(PI3K)/Akt(also known as protein kinase B,PKB)signaling.Inhibition of PI3K/Akt signaling decreased the Cx43 expression induced by PDGF-AA.These results establish a bridge between PDGF-AA&cell–cell communication in osteocytes,which could help us understand the molecular exchange between bone cells and fracture healing. | Yang Liu Mengmeng Duan Daimo Guo Shiyi Kan Li Zhang Munire Aili Demao Zhang Wei Du Jing Xie | 2021 | Acta Biochimica et Biophysica Sinica2021，53，12： | 1 |
| 4 | Microenvironmental stiffness mediates cytoskeleton re-organization in chondrocytes through laminin-FAK mechanotransduction显示文摘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. | Chenchen Zhou Mengmeng Duan Daimo Guo Xinmei Du Demao Zhang Jing Xie | 2022 | International Journal of Oral Science2022，14，2： | 0 |
| 5 | Osteoblasts induce glucose-derived ATP perturbations in chondrocytes through noncontact communication显示文摘Cartilage and subchondral bone communicate with each other through material and signal exchanges.However,direct evidence provided by experimental studies on their interactions is insufficient.In the present study,we establish a noncontact co-culture model with a transwell chamber to explore the energetic perturbations in chondrocytes influenced by osteoblasts.Our results indicate that osteoblasts induce more ATP generation in chondrocytes through an energetic shift characterized by enhanced glycolysis and impaired mitochondrial tricarboxylic acid cycle.Enhanced glycolysis is shown by an increase of secreted lactate and the upregulation of glycolytic enzymes,including glucose-6-phosphate isomerase(Gpi),liver type ATP-dependent 6-phosphofructokinase(Pfkl),fructose-bisphosphate aldolase C(Aldoc),glyceraldehyde-3-phosphate dehydrogenase(Gapdh),triosephosphate isomerase(Tpi1),and phosphoglycerate kinase 1(Pgk1).Impaired mitochondrial tricarboxylic acid cycle is characterized by the downregulation of cytoplasmic aspartate aminotransferase(Got1)and mitochondrial citrate synthase(Cs).Osteoblasts induce the activation of Akt and P38 signaling to mediate ATP perturbations in chondrocytes.This study may deepen our understanding of the maintenance of metabolic homeostasis in the bone-cartilage unit. | Jieya Wei Yueyi Yang Daimo Guo Siqun Xu Hongcan Huang Demao Zhang Jing Xie Xuedong Zhou | 2022 | Acta Biochimica et Biophysica Sinica2022，54，5： | 0 |
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