A genetic tool for the longitudinal study of a subset of post-inflammatory reactive astrocytes

被引:6
作者
Agnew-Svoboda, William [1 ,2 ]
Ubina, Teresa [1 ,2 ]
Figueroa, Zoe [1 ,3 ]
Wong, Yiu-Cheung [2 ,5 ]
Vizcarra, Edward A. [3 ,4 ]
Roebini, Bryan [2 ]
Wilson, Emma H. [1 ,3 ,4 ]
Fiacco, Todd A. [1 ,2 ,4 ]
Riccomagno, Martin M. [1 ,2 ,4 ]
机构
[1] Univ Calif Riverside, Neurosci Grad Program, Riverside, CA 92521 USA
[2] Univ Calif Riverside, Dept Mol Cell & Syst Biol, Riverside, CA 92521 USA
[3] Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA
[4] Univ Calif Riverside, Biomed Sci Grad Program, Riverside, CA 92521 USA
[5] Stanford Univ, Dept Dev Biol, Dev Biol Program, Stanford, CA 94305 USA
来源
CELL REPORTS METHODS | 2022年 / 2卷 / 08期
基金
美国国家卫生研究院;
关键词
HIGHLY-EFFICIENT; MOUSE LINES; CELLS; INHIBITION; INJECTION; MICE; CRE;
D O I
10.1016/j.crmeth.2022.100276
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Astrocytes are vital support cells that ensure proper brain function. In brain disease, astrocytes reprogram into a reactive state that alters many of their cellular roles. A long-standing question in the field is whether downregulation of reactive astrocyte (RA) markers during resolution of inflammation is because these astrocytes revert back to a non-reactive state or die and are replaced. This has proven difficult to answer mainly because existing genetic tools cannot distinguish between healthy versus RAs. Here we describe the generation of an inducible genetic tool that can be used to specifically target and label a subset of RAs. Longitudinal analysis of an acute inflammation model using this tool revealed that the previously observed downregulation of RA markers after inflammation is likely due to changes in gene expression and not because of cell death. Our findings suggest that cellular changes associated with astrogliosis after acute inflammation are largely reversible.
引用
收藏
页数:17
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