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10.1111/bpa.12362 http://scihub22266oqcxt.onion/10.1111/bpa.12362 C4967033!4967033 !26822507     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26822507 &cmd=llinks): Failed to open stream: HTTP request failed! 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SLC20A2 Deficiency in Mice Leads to Elevated Phosphate Levels in Cerbrospinal Fluid and Glymphatic Pathway-Associated Arteriolar Calcification, and Recapitulates Human Idiopathic Basal Ganglia Calcification |pdf=|usr=}}{{26822507 }} gab.com Text SLC20A2 Deficiency in Mice Leads to Elevated Phosphate Levels in Cerbrospinal Fluid and Glymphatic Pathway-Associated Arteriolar Calcification, and Recapitulates Human Idiopathic Basal Ganglia Calcification JO: Brain Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26822507 #FOAvip Idiopathic basal ganglia calcification is a brain calcification disorder that has been genetically linked to autosomal dominant mutations in the sodium-dependent phosphate co-transporter, SLC20A2. The mechanisms whereby deficiency of Slc20a2 leads to basal ganglion calcification are unknown. In the mouse brain, we found that Slc20a2 was expressed in tissues that produce and/or regulate cerebrospinal fluid, including choroid plexus, ependyma and arteriolar smooth muscle cells. Haploinsufficient Slc20a2 +/- mice developed age-dependent basal ganglia calcification that formed in glymphatic pathway-associated arterioles. Slc20a2 deficiency uncovered phosphate homeostasis dysregulation characterized by abnormally high cerebrospinal fluid phosphate levels and hydrocephalus, in addition to basal ganglia calcification. Slc20a2 siRNA knockdown in smooth muscle cells revealed increased susceptibility to high phosphate-induced calcification. These data suggested that loss of Slc20a2 led to dysregulated phosphate homeostasis and enhanced susceptibility of arteriolar smooth muscle cells to elevated phosphate-induced calcification. Together, dysregulated cerebrospinal fluid phosphate and enhanced smooth muscle cell susceptibility may predispose to glymphatic pathway-associated arteriolar calcification. Twit Text FOAVip SLC20A2 Deficiency in Mice Leads to Elevated Phosphate Levels in Cerbrospinal Fluid and Glymphatic Pathway-Associated Arteriolar Calcification, and Recapitulates Human Idiopathic Basal Ganglia Calcification ????Brain Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26822507 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26822507 #FOAvip English Wikipedia <ref>{{Cite pmid|26822507 }}</ref> SLC20A2 Deficiency in Mice Leads to Elevated Phosphate Levels in Cerbrospinal Fluid and Glymphatic Pathway-Associated Arteriolar Calcification, and Recapitulates Human Idiopathic Basal Ganglia Calcification #MMPMID26822507 Wallingford MC ; Chia JJ ; Leaf EM ; Borgeia S ; Chavkin NW ; Sawangmake C ; Marro K ; Cox TC ; Speer MY ; Giachelli CM Brain Pathol 2017[Jan]; 27 (1 ): 64-76 PMID26822507 show ga Idiopathic basal ganglia calcification is a brain calcification disorder that has been genetically linked to autosomal dominant mutations in the sodium-dependent phosphate co-transporter, SLC20A2. The mechanisms whereby deficiency of Slc20a2 leads to basal ganglion calcification are unknown. In the mouse brain, we found that Slc20a2 was expressed in tissues that produce and/or regulate cerebrospinal fluid, including choroid plexus, ependyma and arteriolar smooth muscle cells. Haploinsufficient Slc20a2 +/- mice developed age-dependent basal ganglia calcification that formed in glymphatic pathway-associated arterioles. Slc20a2 deficiency uncovered phosphate homeostasis dysregulation characterized by abnormally high cerebrospinal fluid phosphate levels and hydrocephalus, in addition to basal ganglia calcification. Slc20a2 siRNA knockdown in smooth muscle cells revealed increased susceptibility to high phosphate-induced calcification. These data suggested that loss of Slc20a2 led to dysregulated phosphate homeostasis and enhanced susceptibility of arteriolar smooth muscle cells to elevated phosphate-induced calcification. Together, dysregulated cerebrospinal fluid phosphate and enhanced smooth muscle cell susceptibility may predispose to glymphatic pathway-associated arteriolar calcification. |Animals [MESH] |Arterioles/*pathology [MESH] |Basal Ganglia Diseases/cerebrospinal fluid/*pathology [MESH] |Calcinosis/cerebrospinal fluid/*pathology [MESH] |Cataract/genetics [MESH] |Choroid Plexus/metabolism [MESH] |Ependyma/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Microphthalmos/genetics [MESH] |Models, Biological [MESH] |Muscle, Smooth, Vascular/metabolism/pathology [MESH] |Nerve Tissue Proteins/*deficiency/genetics/physiology [MESH] |Neurodegenerative Diseases/cerebrospinal fluid/*pathology [MESH] |Neuroimaging [MESH] |Phosphates/*cerebrospinal fluid/metabolism [MESH] |RNA Interference [MESH] |RNA, Small Interfering/genetics [MESH]SLC20A2 Deficiency in Mice Leads to Elevated Phosphate Levels in Cerbr(epmc).pdf DeepDyve Pubget Overpricing