Cell type-specific evaluation of ADGRG1/GPR56 function in developmental central nervous system myelination.,Glia

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Cell type-specific evaluation of ADGRG1/GPR56 function in developmental central nervous system myelination.
Glia ( IF 5.4 ) Pub Date : 2020-09-09 , DOI: 10.1002/glia.23906
Brian Chiou ₁ , Chuang Gao _{2,

3} , Stefanie Giera _{2,

4} , Christopher J Folts _{2,

5} , Priya Kishore ₁ , Diankun Yu ₁ , Hayeon C Oak _{1,

2} , Rongcai Jiang ₃ , Xianhua Piao _{1,

2,

6,

7}

Affiliation

Myelination of axons in the central nervous system (CNS) is a concerted effort between many cell types, resulting in significant cross‐talk and communication among cells. Adhesion G protein‐coupled receptor ADGRG1 (GPR56) is expressed in all major glial cells and regulates a wide variety of physiological processes by mediating cell–cell and cell–matrix communications. Previous literature has demonstrated the requirement of ADGRG1 in oligodendrocyte precursor cells (OPCs) during developmental myelination. However, it is unknown if ADGRG1 is responsible for myelin formation in a cell‐type‐specific manner. To that end, here we profiled myelin status in response to deletion of Adgrg1 specifically in OPCs, microglia, astrocytes, and neurons. Interestingly, we find that knocking out Adgrg1 in OPCs significantly decreases OPC proliferation and reduced number of myelinated axons. However, deleting Adgrg1 in microglia, astrocytes, and neurons does not impact developmental myelination. These data support an autonomous functional role for Adgrg1 in OPCs related to myelination.

中文翻译：

ADGRG1/GPR56 在发育中枢神经系统髓鞘形成中功能的细胞类型特异性评估。

中枢神经系统 (CNS) 中轴突的髓鞘形成是许多细胞类型之间的协同努力，导致细胞之间显着的串扰和交流。粘附 G 蛋白偶联受体 ADGRG1 (GPR56) 在所有主要的神经胶质细胞中表达，并通过介导细胞-细胞和细胞-基质通讯来调节多种生理过程。以前的文献已经证明在发育髓鞘形成过程中少突胶质前体细胞 (OPCs) 中需要 ADGRG1。然而，尚不清楚 ADGRG1 是否以细胞类型特异性方式负责髓鞘形成。为此，我们在这里分析了髓鞘状态以响应Adgrg1的缺失，特别是在 OPC、小胶质细胞、星形胶质细胞和神经元中。有趣的是，我们发现敲除Adgrg1在 OPCs 中显着降低 OPC 增殖并减少有髓轴突的数量。然而，删除小胶质细胞、星形胶质细胞和神经元中的Adgrg1不会影响发育髓鞘形成。这些数据支持Adgrg1在与髓鞘形成相关的 OPCs 中的自主功能作用。

更新日期：2020-09-09

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