|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Mapping the immune microenvironment for mandibular alveolar bone homeostasis at single-cell resolution显示文摘Alveolar bone is the thickened ridge of jaw bone that supports teeth.It is subject to constant occlusal force and pathogens invasion,and is therefore under active bone remodeling and immunomodulation.Alveolar bone holds a distinct niche from long bone considering their different developmental origin and postnatal remodeling pattern.However,a systematic explanation of alveolar bone at single-cell level is still lacking.Here,we construct a single-cell atlas of mouse mandibular alveolar bone through single-cell RNA sequencing(scRNA-seq).A more active immune microenvironment is identified in alveolar bone,with a higher proportion of mature immune cells than in long bone.Among all immune cell populations,the monocyte/macrophage subpopulation most actively interacts with mesenchymal stem cells(MSCs)subpopulation.Alveolar bone monocytes/macrophages express a higher level of Oncostatin M(Osm)compared to long bone,which promotes osteogenic differentiation and inhibits adipogenic differentiation of MSCs.In summary,our study reveals a unique immune microenvironment of alveolar bone,which may provide a more precise immune-modulatory target for therapeutic treatment of oral diseases. | Weimin Lin Qiwen Li Danting Zhang Xiaohan Zhang Xingying Qi Qian Wang Yaqian Chen Caojie Liu Hanwen Li Shiwen Zhang Yuan Wang Bin Shao Li Zhang Quan Yuan | 2021 | Bone Research2021，9，1： | 6 |
| 2 | The association of cerebrospinal fluid pressure with optic nerve head and macular vessel density显示文摘The present study aims to investigate the effect of temporary cerebrospinal fluid pressure(CSFP) reduction on optic nerve head(ONH) and macular vessel density(VD) using optical coherence tomography angiography.Forty-four eyes of 44 adults with diagnostic lumbar puncture and CSFP reduction were recruited.Thirty-two eyes of 32 healthy volunteers were controls.ONH and macular VD images were evaluated differences between baseline and after CSFP reduction.The results showed that the mean CSFP decreased from(11.6±2.1) mm Hg to(8.2±3.4) mm Hg(P<0.001).VD in the macular regions decreased significantly after CSFP reduction in the study group(all P<0.05).The control group showed no significant changes in macular VD(all P>0.05).In the study group,decreased VD in the macular parainferior region was associated with CSFP reduction(R^(2)=0.192,P=0.003),the reduction of macular VD in parafoveal(R^(2)=0.098,P=0.018),parainferior(R^(2)=0.104,P=0.021),parasuperior(R^(2)=0.059,P=0.058),paranasal(R^(2)=0.057,P=0.042),paratemporal(R^(2)=0.079,P=0.026) was associated with mean ocular perfusion pressure decrease following CSFP reduction.ONH vessel density did not differ after CSFP reduction(all P>0.05).In conclusion,macular vessel density decreased in association with CSFP reduction.Retinal vessel density in the macular region is more sensitive than that in peripapillary region after CSFP reduction. | Xiangxiang Liu Mohamed M.Khodeiry Danting Lin Yunxiao Sun Qing Zhang Jiawei Wang Richard K.Lee Ningli Wang | 2022 | Science China(Life Sciences)2022，65，6： | 3 |
| 3 | Priming of NLRP3 inflammasome activation by Msn kinase MINK1 in macrophages显示文摘The nucleotide-binding domain,leucine-rich-repeat containing family,pyrin domain-containing 3(NLRP3)inflammasome is essential in inflammation and inflammatory disorders.Phosphorylation at various sites on NLRP3 differentially regulates inflammasome activation.The Ser725 phosphorylation site on NLRP3 is depicted in multiple inflammasome activation scenarios,but the importance and regulation of this site has not been clarified.The present study revealed that the phosphorylation of Ser725 was an essential step for the priming of the NLRP3 inflammasome in macrophages.We also showed that Ser725 was directly phosphorylated by misshapen(Msn)/NIK-related kinase 1(MINK1),depending on the direct interaction between MINK1 and the NLRP3 LRR domain.MINK1 deficiency reduced NLRP3 activation and suppressed inflammatory responses in mouse models of acute sepsis and peritonitis.Reactive oxygen species(ROS)upregulated the kinase activity of MINK1 and subsequently promoted inflammasome priming via NLRP3 Ser725 phosphorylation.Eliminating ROS suppressed NLRP3 activation and reduced sepsis and peritonitis symptoms in a MINK1-dependent manner.Altogether,our study reveals a direct regulation of the NLRP3 inflammasome by Msn family kinase MINK1 and suggests that modulation of MINK1 activity is a potential intervention strategy for inflammasomerelated diseases. | Kaixiang Zhu Xuexiao Jin Zhexu Chi Sheng Chen Songquan Wu Richard D.Sloan Xuai Lin Dante Neculai Di Wang Hu Hu Linrong Lu | 2021 | Cellular & Molecular Immunology2021，18，10： | 2 |
| 4 | PD0325901, an ERK inhibitor, enhances the efficacy of PD-1 inhibitor in non-small cell lung carcinoma显示文摘ERK pathway regulated the programmed death ligand-1(PD-L1)expression which was linked to the response of programmed death-1(PD-1)/PD-L1 blockade therapy.So it is deducible that ERK inhibitor could enhance the efficacy of PD-1 inhibitor in cancer immunotherapy.In this study,PD0325901,an oral potent ERK inhibitor,strongly enhanced the efficacy of PD-1 antibody in vitro and in vivo models in non-small cell lung carcinoma(NSCLC)cells.Mechanistically,PD0325901 or shRNA-ERK1/2 significantly downregulated the PD-L1 expression in NSCLC cells and increased the CD3+T cells infiltration and functions in tumor tissue.There was a positive correlation between the p-ERK1/2 expression and PD-L1 expression in patients with NSCLC.And the patients with low p-ERK1/2 expression were observed a high response rate of PD-1/PD-L1 blockage therapy.Our results demonstrate that PD0325901,an ERK inhibitor,can enhance the efficacy of PD-1 blockage against NSCLC in vitro and in vivo models.And the combination of ERK inhibitor such as PD0325901 and PD-1/PD-L1 blockage is a promising regimen and encouraged to be further confirmed in the treatment of patients with NSCLC. | Min Luo Yuhui Xia Fang Wang Hong Zhang Danting Su Chaoyue Su Chuan Yang Shaocong Wu Sainan An Suxia Lin Liwu Fu | 2021 | Acta Pharmaceutica Sinica B2021，11，10： | 1 |
| 5 | Magnesium promotes vascularization and osseointegration in diabetic states显示文摘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. | Linfeng Liu Feiyu Wang Wei Song Danting Zhang Weimin Lin Qi Yin Qian Wang Hanwen Li Quan Yuan Shiwen Zhang | 2024 | International Journal of Oral Science2024，16，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员