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| 1 | Focal adhesion protein Kindlin-2 regulates bone homeostasis in mice显示文摘Our recent studies demonstrate that the focal adhesion protein Kindlin-2 is critical for chondrogenesis and early skeletal development. Here, we show that deleting Kindlin-2 from osteoblasts using the 2.3-kb mouse Col1 a1-Cre transgene minimally impacts bone mass in mice, but deleting Kindlin-2 using the 10-kb mouse Dmp1-Cre transgene, which targets osteocytes and mature osteoblasts, results in striking osteopenia in mice. Kindlin-2 loss reduces the osteoblastic population but increases the osteoclastic and adipocytic populations in the bone microenvironment. Kindlin-2 loss upregulates sclerostin in osteocytes,downregulates β-catenin in osteoblasts, and inhibits osteoblast formation and differentiation in vitro and in vivo. Upregulation ofβ-catenin in the mutant cells reverses the osteopenia induced by Kindlin-2 deficiency. Kindlin-2 loss additionally increases the expression of RANKL in osteocytes and increases osteoclast formation and bone resorption. Kindlin-2 deletion in osteocytes promotes osteoclast formation in osteocyte/bone marrow monocyte cocultures, which is significantly blocked by an anti-RANKLneutralizing antibody. Finally, Kindlin-2 loss increases osteocyte apoptosis and impairs osteocyte spreading and dendrite formation.Thus, we demonstrate an important role of Kindlin-2 in the regulation of bone homeostasis and provide a potential target for the treatment of metabolic bone diseases. | Huiling Cao Qinnan Yan Dong Wang Yumei Lai Bo Zhou Qi Zhang Wenfei Jin Simin Lin Yiming Lei Liting Ma Yuxi Guo Yishu Wang Yilin Wang Xiaochun Bai Chuanju Liu Jian QFeng Chuanyue Wu Di Chen Xu Cao Guozhi Xiao | 2020 | Bone Research2020，8，1： | 8 |
| 2 | High power and stable P-doped yolk-shell structured Si@C anode simultaneously enhancing conductivity and Li^(+)diffusion kinetics显示文摘Silicon is a low price and high capacity ancxje material for lithium-ion batteries.The yolk-shell structure can effectively accommodate Si expansion to improve stability.However,the limited rate performance of Si anodes can't meet people's growing demand for high power density.Herein,the phosphorus-doped yolk-shell Si@C materials(P-doped Si@C)were prepared through carbon coating on P-doped Si/SiO_(x)matrix to obtain high power and stable devices.Therefore,the as-prepared P-doped Si@C electrodes delivered a rapid increase in Coulombic efficiency from 74.4%to 99.6%after only 6 cycles,high capacity retention of-95%over 800 cycles at 4 A·g^(-1),and great rate capability(510 mAh·g^(-1)at 35 A·g^(-1)).As a result,P-doped Si@C anodes paired with commercial activated carbon and LiFePO_(4)cathode to assemble lithium-ion capacitor(high power density of〜61,080 W·kg^(-1)at 20 A·g^(-1))and lithium-ion full cell(good rate performance with 68.3 mAh·g^(-1)at 5 C),respectively.This work can provide an effective way tofurther improve power density and stability for energy storage devices. | Ming Chen Qinnan Zhou Jiantao Zai Asma Iqbal TsegayeTadesse Tsega Boxu Dong Xuejiao Liu Yuchi Zhang Changyu Yan Liang Zhao Ali Nazakat SharelPeisan E CheeTongJohn Low Xuefeng Qian | 2021 | Nano Research2021，14，4： | 5 |
| 3 | Genetic Research and Utilization Reference of Saccharum spontaneum L.显示文摘[Objectives]The genetic characteristics of wild germplasm resources of Saccharum spontaneum L.were further investigated to provide a scientific theoretical basis for the improved hybridization of sugarcane varieties.[Methods]The first flowering date data of 112 wild resources were statistically analyzed by broad heritability for 3 consecutive years,and pollen quantity and yield were investigated to provide reference for hybridization.[Results]The broad heritability of the first flowering date of S.spontaneum was 0.079.The differences in the first flowering date between the S.spontaneum resources were in the range of 4-49 d,with an average of 13.65 d.The inter-annual changes within 20 d accounted for 90 %,and only 4.5% exceeded 30 d.The first flowering dates of some S.spontaneum resources were obviously postponed after being treated.[Conclusions]In the hybridization season,the hybridization plan must be adjusted according to the actual situation of the flowering period to make full use of it. | Jiale JI Qinnan WANG Yongsheng QIU Cheng FU Qiwei WU Houxiang HU Feng ZHOU Chuiming ZHANG Huanying XU Jing XIE | 2019 | Agricultural Biotechnology2019，8，3： | 1 |
| 4 | Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice显示文摘In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely understood.Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone.Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by PTH.Furthermore,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic pathway.Mechanistically,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone.Interestingly,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory loop.Finally,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice.Thus,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis. | Xuekun Fu Bo Zhou Qinnan Yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 0 |
| 5 | Past and recent advances in sugarcane cytogenetics显示文摘The Saccharum genus comprises species with large and variable chromosome numbers, leading to challenges in genomic studies and breeding improvement. Cytogenetics, including classical and molecular approaches, has played a central role in deciphering the genome structure, classification, and evolution of the genus Saccharum. The application of fluorescence in situ hybridization using oligonucleotide probes significantly improved our understanding of the complex genomes of Saccharum species. This paper reviews the application and progress of cytogenetic techniques in Saccharum. Future applications of cytogenetics are discussed, as they could benefit both genomic studies and breeding of sugarcane as well as other plants with complex genomes. | Kai Wang Hui Zhang Haris Khurshid Ayman Esh Caiwen Wu Qinnan Wang Nathalie Piperidis | 2023 | The Crop Journal2023，11，1： | 0 |
| 6 | Effect of Metformin on Lactate Metabolism in Normal Hepatocytes under High Glucose Stress in Vitro显示文摘To study the effect of metformin on lactate metabolism in hepatocytes in vitro under high glucose stress.Method:LO2 hepatocytes was cultured in vitro,hepatocytes were randomly divided into blank control group,25 mmol/L glucose solution,27 mmol/L glucose solution,29 mmol/L glucose solution,31 mmol/L glucose solution,33 mmol/L glucose solution,35 mmol/L glucose solution treatment group,after determining the optimal concentration as 31 mmol/L,use 30 mmol/L metformin solution,and then divided into blank control group,normal hepatocytes+the optimal concentration of glucose solution,normal hepatocytes+metformin solution,normal hepatocytes+.The optimal concentration of glucose solution normal hepatocytes+metformin solution,calculate the number of hepatocytes on cell count plate respectively in the 12 h,24 h,48 h,and use the lactic acid kit to determine the lactic acid value of the cell culture medium of normal liver cells+optimal concentration glucose solution and normal liver cells+optimal concentration glucose solution+metformin solution at 12 h,24 h,and 48 h,respectively.Results:There was no significant change in the lactic acid concentration but significant increase in the number of surviving hepatocytes in the high-glycemic control group compared with that in the high-glycemic control group without metformin.Conclusions:Metformin has no significant effect on lactic acid metabolism of hepatocytes under high glucose stress in vitro,and has a protective effect on hepatocytes under high glucose stress.Based on this,it is preliminarily believed that metformin is not the direct factor leading to diabetic lactic acidosis. | Jianhao Wu Qinnan Zhang Yubiao Yang Chunyue Wang Xindi Yue Zhilu Li Pingping Yan | 2021 | Journal of Advances in Medicine Science2021，4，2： | 0 |
| 7 | Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice显示文摘In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely understood.Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone.Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by PTH.Furthermore,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic pathway.Mechanistically,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone.Interestingly,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory loop.Finally,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice.Thus,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis. | Xuekun Fu Bo Zhou Qinnan Yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao | 2021 | Signal Transduction and Targeted Therapy2021，6，1： | 0 |
| 8 | Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice显示文摘The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint(TMJ) osteoarthritis(OA);however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4(Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore,Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis. | Yumei Lai Wei Zheng Minghao Qu Christopher C.Xiao Sheng Chen Qing Yao Weiyuan Gong Chu Tao Qinnan Yan Peijun Zhang Xiaohao Wu Guozhi Xiao | 2022 | International Journal of Oral Science2022，14，3： | 0 |
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