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| 1 | Transforming growth factor-β1-induced N-cadherin drives cell–cell communication through connexin43 in osteoblast lineage显示文摘Gap junction(GJ)has been indicated to have an intimate correlation with adhesion junction.However,the direct interaction between them partially remains elusive.In the current study,we aimed to elucidate the role of N-cadherin,one of the core components in adhesion junction,in mediating connexin 43,one of the functional constituents in gap junction,via transforming growth factor-β1(TGF-β1)induction in osteoblasts.We first elucidated the expressions of N-cadherin induced by TGF-β1 and also confirmed the upregulation of Cx43,and the enhancement of functional gap junctional intercellular communication(GJIC)triggered by TGF-β1 in both primary osteoblasts and MC3T3 cell line.Colocalization analysis and Co-IP experimentation showed that N-cadherin interacts with Cx43 at the site of cell–cell contact.Knockdown of N-cadherin by siRNA interference decreased the Cx43 expression and abolished the promoting effect of TGF-β1 on Cx43.Functional GJICs in living primary osteoblasts and MC3T3 cell line were also reduced.TGF-β1-induced increase in N-cadherin and Cx43 was via Smad3 activation,whereas knockdown of Smad3 signaling by using siRNA decreased the expressions of both N-cadherin and Cx43.Overall,these data indicate the direct interactions between N-cadherin and Cx43,and reveal the intervention of adhesion junction in functional gap junction in living osteoblasts. | Yueyi Yang Wenjing Liu JieYa Wei Yujia Cui Demao Zhang Jing Xie | 2021 | International Journal of Oral Science2021，13，2： | 4 |
| 2 | 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 |
| 3 | NUMB maintains bone mass by promoting degradation of PTEN and GLI1 via ubiquitination in osteoblasts显示文摘The adaptor protein NUMB is involved in asymmetric division and cell fate determination and recognized as an antagonist of Notch.Previous studies have proved that Notch activation in osteoblasts contributes to a high bone mass. In this study, however, an osteopenic phenotype was found in 9-week-old mice using osteoblastic specific Col1a1–2.3-Cre to ablate both Numb and its homologue Numbl. The trabecular bone mass decreased dramatically while the cortical bone mass was unaffected. Here, the Notch signal was not activated,while the tensin homologue deleted on human chromosome 10(PTEN), which dephosphorylates phosphatidylinositide 3-kinases, was elevated, attenuating protein kinase B(Akt). The ubiquitination assay revealed that NUMB may physiologically promote PTEN ubiquitination in the presence of neural precursor cell-expressed developmentally downregulated protein 4–1. In addition, the deficiency of Numb/Numbl also activated the Hedgehog pathway through GLI1. This process was found to improve the ratio of the receptor activator of nuclear factor-k B ligand to osteoprotegerin, which enhanced the differentiation of osteoclasts and bone resorption. In conclusion, this study provides an insight into new functons of NUMB and NUMBL on bone homeostasis. | Ling Ye Feng Lou Fanyuan Yu Demao Zhang Chenglin Wang Fanzi Wu Xin Li Yilin Ping Xiao Yang Jing Yang Dian Chen Bo Gao Dingming Huang Peng Liu | 2018 | Bone Research2018，6，4： | 3 |
| 4 | Osteoporosis-decreased extracellular matrix stiffness impairs connexin 43-mediated gap junction intercellular communication in osteocytes显示文摘Osteocytes are the main sensitive and responsive cells for mechanical stimuli in bone.The connexin family enables them to communicate with each other via forming functional gap junctions.However,how osteoporosis-impaired extracellular mechanical property modulates gap junction intercellular communication in osteocytes remains elusive.In this study,we established an ovariectomy(OVX)-induced osteoporosis mouse model in vivo and a polydimethylsiloxane(PDMS)-based cell culture substrate model in vitro to explore the influence of extracellular matrix(ECM)stiffness on cell-to-cell communication in osteocytes.Firstly,we established an OVX-induced osteoporosis mouse model by characterizing the changes in radiography,morphology and histochemistry of femurs.Our results showed that osteoporosis decreased the bone matrix stiffness together with the changes including the loss of osteocytes and the decrease of protein markers.Meanwhile,the dendritic process interconnection and channel-forming protein,Cx43,were reduced in osteoporosis mice.Next we mimicked ECM stiffness changes in vitro by using PDMS substrates at ratios 1:5 for normal stiffness and 1:45 for osteoporosis stiffness.Our results showed that the decreased ECM stiffness reduced the number of dendritic processes in a single cell and gap junctions between adjacent osteocytes.We further detected the decreased expression of Cx43,in the substrate with decreased stiffness.Finally,we found that gap junction-based intercellular communication was reduced in living osteocytes in the substrate with decreased stiffness.This study demonstrates the correlation between ECM mechanical property and cell-to-cell communication in osteocytes and might pave the way for further exploration of osteoporosis in terms of biomechanics. | Demao Zhang Xin Li Caixia Pi Linyi Cai Yang Liu Wei Du Wenbin Yang Jing Xie | 2020 | Acta Biochimica et Biophysica Sinica2020，52，5： | 3 |
| 5 | Compression tests of high strength steel channel columns with interaction between local and distortional buckling 显示文摘 | Demao Yang Hancock G J | 2004 | Journal of Structural Engineering ASCE2004，130，12： | 1 |
| 6 | Compression Tests of High Strength Steel Channel Columns with Interaction between Local and Distortional Buckling显示文摘 | Demao Yang and Gregory J Hancock | 2004 | Journal of Structural Engineering ASCE2004，130，12： | 1 |
| 7 | Compression Tests of High Strength Steel Channel Columns with Interaction Between Lo- cal and Distortional Buckling 显示文摘 | Yang Demao Hancock G J | 2004 | Journal of Structural Engi- neering2004，130，12： | 1 |
| 8 | Compression tests of high strength steel channel columns with interaction between local and distortional buckling显示文摘 | Yang Demao Hancock G J | 2004 | Journal of Structural Engineering2004，130，2： | 1 |
| 9 | Compression tests of high strength steel channel columns with interaction between local and distortional buckling显示文摘 | Yang Demao Hancock G J | 2004 | Journal of Structural Engineering2004，130，2： | 1 |
| 10 | Compression Tests of High Strength Steel Channel Columns with Interaction Between Local and Distortional Buckling显示文摘 | Yang Demao Hancock G J | 2004 | Journal of Structure Engineering2004，130，12： | 1 |
| 11 | Compression tests of high strength steel channel columns with interaction between local and distortional buckling显示文摘 | Yang Demao Hancock G J | 2004 | Journal of Structural Engineering2004，130，12： | 1 |
| 12 | Hancock Compression Tests of Cold-Re- duced High Strength Steel Sections: I-Long Columns 显示文摘 | Yang Demao Gregory J | 2004 | Journal of Structural Engineering2004，130，11： | 1 |
| 13 | 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 |
| 14 | Compression tests of high strength cold-formed steel channel columns with interaction between local and distortional buckling显示文摘 | Yang Demao Hancock G J | 2004 | Journal of Structural Engineering2004，130，12： | 1 |
| 15 | Annexin A5 derived from matrix vesicles protects against osteoporotic bone loss via mineralization显示文摘Matrix vesicles(MVs)have shown strong effects in diseases such as vascular ectopic calcification and pathological calcified osteoarthritis and in wound repair of the skeletal system due to their membranous vesicle characteristics and abundant calcium and phosphorus content.However,the role of MVs in the progression of osteoporosis is poorly understood.Here,we report that annexin A5,an important component of the matrix vesicle membrane,plays a vital role in bone matrix homeostasis in the deterioration of osteoporosis.We first identified annexin A5 from adherent MVs but not dissociative MVs of osteoblasts and found that it could be sharply decreased in the bone matrix during the occurrence of osteoporosis based on ovariectomized mice.We then confirmed its potential in mediating the mineralization of the precursor osteoblast lineage via its initial binding with collagen type I to achieve MV adhesion and the subsequent activation of cellular autophagy.Finally,we proved its protective role in resisting bone loss by applying it to osteoporotic mice.Taken together,these data revealed the importance of annexin A5,originating from adherent MVs of osteoblasts,in bone matrix remodeling of osteoporosis and provided a new strategy for the treatment and intervention of bone loss. | Guanyue Su Demao Zhang Tiantian Li Tong Pei Jie Yang Shasha Tu Sijun Liu Jie Ren Yaojia Zhang Mengmeng Duan Xinrui Yang Yang Shen Chenchen Zhou Jing Xie Xiaoheng Liu | 2023 | Bone Research2023，11，4： | 0 |
| 16 | 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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