Microglia participate in central nervous system (CNS) development and homeostasis and are often implicated in modulating disease processes. However, less is known about the role of microglia in the biology of the neurovascular unit (NVU). In particular, data are scant on whether microglia are involved in CNS vascular pathology. In this study, we use a mouse model of primary familial brain calcification, Pdgfb^ret/ret, to investigate the role of microglia in calcification of the NVU. We report that microglia enclosing vessel calcifications, coined calcification-associated microglia, display a distinct activation phenotype. Pharmacological ablation of microglia with the CSF1R inhibitor PLX5622 leads to aggravated vessel calcification. Mechanistically, we show that microglia require functional TREM2 for controlling vascular calcification. Our results demonstrate that microglial activity in the setting of pathological vascular calcification is beneficial. In addition, we identify a previously unrecognized function of microglia in halting the expansion of vascular calcification.

小胶质细胞参与中枢神经系统（CNS）的发育和体内平衡，并且通常参与调节疾病过程。然而，人们对小胶质细胞在神经血管单元（NVU）生物学中的作用知之甚少。特别是，关于小胶质细胞是否参与中枢神经系统血管病理学的数据很少。在本研究中，我们使用原发性家族性脑钙化小鼠模型Pdgfb ^ret/ret来研究小胶质细胞在 NVU 钙化中的作用。我们报告说，包围血管钙化的小胶质细胞，即钙化相关的小胶质细胞，表现出独特的激活表型。使用 CSF1R 抑制剂 PLX5622 对小胶质细胞进行药物消融会导致血管钙化加剧。从机制上讲，我们表明小胶质细胞需要功能性 TREM2 来控制血管钙化。我们的结果表明，小胶质细胞活性在病理性血管钙化的情况下是有益的。此外，我们还发现了小胶质细胞在阻止血管钙化扩张方面以前未被认识的功能。