<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Wang S</submitter><pubmed_abstract>Parathyroid hormone is the main endocrine regulator of extracellular calcium and phosphorus levels. Secondary hyperparathyroidism-induced endothelial dysfunction may be related to calcium homeostasis disorders. Here, we investigated the effects of parathyroid hormone on human umbilical vein endothelial cells (HUVECs) and characterized the involvement of store-operated Ca&lt;sup>2+&lt;/sup> entry (SOCE) and the nuclear factor of activated T cells (NFAT) signaling pathway. We used immunoblot experiments to find that parathyroid hormone significantly enhanced the expression of the Orai1 channel, a type of channel mediating SOCE, SOCE activity, and Orai1-mediated proliferation of HUVECs but did not increase Orai2 and Orai3. RNA-seq was utilized to identify 1,655 differentially expressed genes (823 u</pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>844671</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8965836</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Parathyroid Hormone Promotes Human Umbilical Vein Endothelial Cell Migration and Proliferation Through Orai1-Mediated Calcium Signaling.</pubmed_title><pmcid>PMC8965836</pmcid><pubmed_authors>Xu L</pubmed_authors><pubmed_authors>Fang Y</pubmed_authors><pubmed_authors>Wu K</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Lin Z</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Shen B</pubmed_authors><pubmed_authors>Shen H</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Parathyroid Hormone Promotes Human Umbilical Vein Endothelial Cell Migration and Proliferation Through Orai1-Mediated Calcium Signaling.</name><description>Parathyroid hormone is the main endocrine regulator of extracellular calcium and phosphorus levels. Secondary hyperparathyroidism-induced endothelial dysfunction may be related to calcium homeostasis disorders. Here, we investigated the effects of parathyroid hormone on human umbilical vein endothelial cells (HUVECs) and characterized the involvement of store-operated Ca&lt;sup>2+&lt;/sup> entry (SOCE) and the nuclear factor of activated T cells (NFAT) signaling pathway. We used immunoblot experiments to find that parathyroid hormone significantly enhanced the expression of the Orai1 channel, a type of channel mediating SOCE, SOCE activity, and Orai1-mediated proliferation of HUVECs but did not increase Orai2 and Orai3. RNA-seq was utilized to identify 1,655 differentially expressed genes (823 u</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-04-08T17:45:38.773Z</modification><creation>2025-02-19T01:54:45.862Z</creation></dates><accession>S-EPMC8965836</accession><cross_references><pubmed>35369318</pubmed><doi>10.3389/fcvm.2022.844671</doi></cross_references></HashMap>