{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:19:39Z","timestamp":1784557179378,"version":"3.55.0"},"reference-count":19,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,2,1]]},"abstract":"<jats:p>\n                    Basal ganglia calcification (BGC) is a common complication in hypoparathyroid patients, linked to hyperphosphatemia and altered vitamin-D and calcium homeostasis following conventional therapy. The pathogenesis of BGC in hypoparathyroidism is not clear. Recently, we developed an\n                    <jats:italic>ex vivo<\/jats:italic>\n                    model of BGC using rat-striatal cell culture in 10.0 mmol\/L of \u03b2-glycerophosphate (31.8 mg\/dL phosphate). However, the effect of 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D, calcium, and milder phosphate excess on BGC in hypoparathyroidism is not known. This study describes two modified\n                    <jats:italic>ex vivo<\/jats:italic>\n                    models investigating pathogenesis of BGC in \u2018drug-na\u00efve\u2019 and \u2018conventionally treated\u2019 hypoparathyroid state. The first modification involved striatal cells cultured in low concentration 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D (16.0 pg\/mL), ionized calcium(0.99 mmol\/L), hPTH\n                    <jats:sub>(1-34)<\/jats:sub>\n                    (6.0 pg\/mL), and 2.68 mmol\/L (8.3 mg\/dL) of phosphate akin to \u2018drug-na\u00efve\u2019 state for 24 days. In second modification, striatal cells were exposed to 46.0 pg\/mL of 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D, normal ionized calcium of 1.17 mmol\/L, and 2.20 mmol\/L (6.8 mg\/dL) of phosphate akin to \u2018conventionally treated\u2019 state. Striatal cell culture under \u2018drug-na\u00efve\u2019 state showed that even 16.0 pg\/mL of 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D enhanced the calcification. In \u2018conventionally treated\u2019 model, striatal cell calcification was enhanced in 54% cases over \u2018drug-na\u00efve\u2019 state. Calcification in \u2018conventionally treated\u2019 state further increased on increasing phosphate to 8.3 mg\/dL, suggesting importance of phosphatemic control in hypoparathyroid patients. Striatal cells in \u2018drug-na\u00efve\u2019 state showed increased mRNA expression of pro-osteogenic\n                    <jats:italic>Wnt3a<\/jats:italic>\n                    ,\n                    <jats:italic>Cd133,Vglut-1<\/jats:italic>\n                    -neuronal phosphate-transporters, calcium-ion channel-\n                    <jats:italic>Trvp2,Alp<\/jats:italic>\n                    , and\n                    <jats:italic>Collagen-1\u03b1<\/jats:italic>\n                    and decreased expression of\n                    <jats:italic>Ca-II<\/jats:italic>\n                    . These models suggest that in \u2018drug-na\u00efve\u2019 state, 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D along with moderately elevated phosphate increases the expression of pro-osteogenic molecules to induce BGC. Although normalization of calcium in \u2018conventionally treated\u2019 state increased the expression of\n                    <jats:italic>Opg, Osterix, Alp<\/jats:italic>\n                    , and\n                    <jats:italic>Cav2,<\/jats:italic>\n                    calcification increased only in a subset, akin to variation in progression of BGC in hypoparathyroid patients on conventional therapy.\n                  <\/jats:p>","DOI":"10.1530\/jme-22-0108","type":"journal-article","created":{"date-parts":[[2022,11,29]],"date-time":"2022-11-29T14:09:40Z","timestamp":1669730980000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":5,"title":["Effect of calcitriol and calcium on basal ganglia calcification in hypoparathyroidism: experimental models"],"prefix":"10.1530","volume":"70","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9909-4251","authenticated-orcid":true,"given":"Parmita","family":"Kar","sequence":"first","affiliation":[{"name":"Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3097-5074","authenticated-orcid":true,"given":"Ravinder","family":"Goswami","sequence":"additional","affiliation":[{"name":"Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"European Journal of Endocrinology","doi-asserted-by":"publisher","first-page":"895","DOI":"10.1530\/EJE-12-0946","article-title":"Neuropsychological dysfunction in idiopathic hypoparathyroidism and its relationship with intracranial calcification and serum total calcium","volume":"168","author":"Aggarwal","year":"2013","unstructured":"Aggarwal SKailash SSagar RTripathi MSreenivas VSharma RGupta NGoswami R2013Neuropsychological dysfunction in idiopathic hypoparathyroidism and its relationship with intracranial calcification and serum total calcium. 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