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The mechanisms whereby deficiency of Slc20a2 leads to basal ganglion calcification are unknown. In the mouse brain, we found that <jats:italic>Slc20a2<\/jats:italic> was expressed in tissues that produce and\/or regulate cerebrospinal fluid, including choroid plexus, ependyma and arteriolar smooth muscle cells. Haploinsufficient <jats:italic>Slc20a2<\/jats:italic> +\/\u2212 mice developed age\u2010dependent basal ganglia calcification that formed in glymphatic pathway\u2010associated arterioles. <jats:italic>Slc20a2<\/jats:italic> deficiency uncovered phosphate homeostasis dysregulation characterized by abnormally high cerebrospinal fluid phosphate levels and hydrocephalus, in addition to basal ganglia calcification. <jats:italic>Slc20a2<\/jats:italic> siRNA knockdown in smooth muscle cells revealed increased susceptibility to high phosphate\u2010induced calcification. These data suggested that loss of <jats:italic>Slc20a2<\/jats:italic> led to dysregulated phosphate homeostasis and enhanced susceptibility of arteriolar smooth muscle cells to elevated phosphate\u2010induced calcification. Together, dysregulated cerebrospinal fluid phosphate and enhanced smooth muscle cell susceptibility may predispose to glymphatic pathway\u2010associated arteriolar calcification.<\/jats:p>","DOI":"10.1111\/bpa.12362","type":"journal-article","created":{"date-parts":[[2016,1,29]],"date-time":"2016-01-29T08:12:39Z","timestamp":1454055159000},"page":"64-76","source":"Crossref","is-referenced-by-count":88,"title":["SLC20A2 Deficiency in Mice Leads to Elevated Phosphate Levels in Cerbrospinal Fluid and Glymphatic Pathway\u2010Associated Arteriolar Calcification, and Recapitulates Human Idiopathic Basal Ganglia Calcification"],"prefix":"10.1111","volume":"27","author":[{"given":"Mary Catherine","family":"Wallingford","sequence":"first","affiliation":[{"name":"Department of Bioengineering University of Washington Seattle WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia Jun","family":"Chia","sequence":"additional","affiliation":[{"name":"Department of Bioengineering 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