Nr4a2(Nurr1)is well known to be vital for midbrain dopaminergic neurons.Recent single-cell RNA analyses reveal that Nr4a2 is expressed in lateral cerebral regions,within neurons named L4/L5/L6 IT Car3.These neurons ha...Nr4a2(Nurr1)is well known to be vital for midbrain dopaminergic neurons.Recent single-cell RNA analyses reveal that Nr4a2 is expressed in lateral cerebral regions,within neurons named L4/L5/L6 IT Car3.These neurons have attracted intense attention for the molecular mechanisms underlying their development and functions.We classified Car3 neurons into neocortical(Ncx-Car3),claustral(CLA-Car3),and dorsal endopiriform nucleus(dEn-Car3)subpopulations,focusing on the characterization of Ncx-Car3 neurons.These neurons exhibit distinct birthdates and migratory morphologies compared to CLA-and dEn-Car3 neurons,but share a common transcriptomic profile when Nr4a2 is deleted at the embryonic stage or in adulthood.Notably,Nr4a2 misexpression ectopically induces Car3-enriched genes in vivo.Mice lacking Nr4a2 in Car3 ensembles during the embryonic stage or in adulthood display hyperactivity and reduced anxiety-like behaviors.Therefore,our results demonstrate that Nr4a2 is a key factor in regulating the development and functional maintenance of the forebrain Car3 neurons.展开更多
Objective To explore the role of coxsackievirus and adenovirus receptor（CAR） in cardiotoxicity infected by coxsackieviras B3. Methods A toxic cellular model was established in vitro by adding myocarditic coxsackievi...Objective To explore the role of coxsackievirus and adenovirus receptor（CAR） in cardiotoxicity infected by coxsackieviras B3. Methods A toxic cellular model was established in vitro by adding myocarditic coxsackievirus B3 （CVB3m） into the culture of neonatal mouse cardiomyocytes. 48 h later, the cardiomyocytes were divided into control, CVB3m, and CAR antibody ＋ CVB3m groups. CVB3m-mediated myocytopathic effect of above three groups was observed after further culturing for 48h. At the same time, the cardiomyocytes＇ viability of above three groups was assessed by MTT assay. Results The degree of cytopathic effect（CPE） of CAR antibody ＋ CVB3m group was significantly lower than CVB3m group （ P 〈 0. 01 ） and there was a significant increase in cell viability in CAR antibody ＋ CVB3m group compared with CVB3m group（ P 〈 0. 01 ）. No significant difference was found between CAR antibody ＋ CVB3m group and control group. Conclusion CAR antibody possesses a protective effect on CVB3m infected cardiomyoctyes, which indicates that CAR may play an important role in mediating cardiotoxicity infected by CVB3m.展开更多
基金STI2030-Major Projects(2022ZD0204900)Natural Science Foundation of Shanghai(22ZR1466300,23ZR1413500)+6 种基金National Natural Science Foundation of China(82401384,32271072)Collaborative Innovation Program of Shanghai Municipal Health Commission(2020CXJQ01)Shanghai Sailing Program of the Shanghai Municipal Science and Technology Program(23YF1407500)Shanghai Blue Cross Brain Hospital Co.,LtdShanghai Tongji University Education Development FoundationShanghai Municipal Science and Technology Major Project(2018SHZDZX01)Zhangjiang(ZJ)Lab。
文摘Nr4a2(Nurr1)is well known to be vital for midbrain dopaminergic neurons.Recent single-cell RNA analyses reveal that Nr4a2 is expressed in lateral cerebral regions,within neurons named L4/L5/L6 IT Car3.These neurons have attracted intense attention for the molecular mechanisms underlying their development and functions.We classified Car3 neurons into neocortical(Ncx-Car3),claustral(CLA-Car3),and dorsal endopiriform nucleus(dEn-Car3)subpopulations,focusing on the characterization of Ncx-Car3 neurons.These neurons exhibit distinct birthdates and migratory morphologies compared to CLA-and dEn-Car3 neurons,but share a common transcriptomic profile when Nr4a2 is deleted at the embryonic stage or in adulthood.Notably,Nr4a2 misexpression ectopically induces Car3-enriched genes in vivo.Mice lacking Nr4a2 in Car3 ensembles during the embryonic stage or in adulthood display hyperactivity and reduced anxiety-like behaviors.Therefore,our results demonstrate that Nr4a2 is a key factor in regulating the development and functional maintenance of the forebrain Car3 neurons.
文摘Objective To explore the role of coxsackievirus and adenovirus receptor（CAR） in cardiotoxicity infected by coxsackieviras B3. Methods A toxic cellular model was established in vitro by adding myocarditic coxsackievirus B3 （CVB3m） into the culture of neonatal mouse cardiomyocytes. 48 h later, the cardiomyocytes were divided into control, CVB3m, and CAR antibody ＋ CVB3m groups. CVB3m-mediated myocytopathic effect of above three groups was observed after further culturing for 48h. At the same time, the cardiomyocytes＇ viability of above three groups was assessed by MTT assay. Results The degree of cytopathic effect（CPE） of CAR antibody ＋ CVB3m group was significantly lower than CVB3m group （ P 〈 0. 01 ） and there was a significant increase in cell viability in CAR antibody ＋ CVB3m group compared with CVB3m group（ P 〈 0. 01 ）. No significant difference was found between CAR antibody ＋ CVB3m group and control group. Conclusion CAR antibody possesses a protective effect on CVB3m infected cardiomyoctyes, which indicates that CAR may play an important role in mediating cardiotoxicity infected by CVB3m.
