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. 2020 Jun 10;11:384. doi: 10.3389/fneur.2020.00384

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Copyright © 2020 Yarlagadda, Ma and Doré.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Combination of various proposed mechanisms in endothelial cells for vitamin D prevention/mitigation of ischemic stroke. 1,25(OH)₂D₃ [or 25(OH)D₃D3, which is converted to of 1,25(OH)₂D₃ via 1-α-Hydroxylase] diffuses through the endothelial cell membrane, binds to vitamin D receptor (VDR), dimerizes with RXR, and translocates into the nucleus. The complex binds to VDRE for transcription of genes resulting in inhibition of renin-angiotensin and activation of SDF1a, VEGF, and NOS pathways for vasodilation and anti-inflammation; upregulation of IGF-1 (and thus neuroprotection of axon and dendrites and thrombolysis via plasminogen); expression of blood brain barrier (BBB) tight-junction proteins occludin and claudin-5; upregulation of nerve growth factor (NGF), which supports neuronal growth, maintenance, and survival.