{"id":292,"date":"2021-05-27T03:29:33","date_gmt":"2021-05-27T03:29:33","guid":{"rendered":"https:\/\/vinuni.edu.vn\/research\/?p=292"},"modified":"2022-09-05T03:31:03","modified_gmt":"2022-09-05T03:31:03","slug":"publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology","status":"publish","type":"post","link":"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/","title":{"rendered":"Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology"},"content":{"rendered":"<p>Abstract<\/p>\n<p>Hyperphosphatemia is the primary risk factor for vascular calcification, which is closely associated with cardiovascular morbidity and mortality. Recent evidence showed that oxidative stress by high inorganic phosphate (Pi) mediates calcific changes in vascular smooth muscle cells (VSMCs). However, intracellular signaling responsible for Pi-induced oxidative stress remains unclear. Here, we investigated molecular mechanisms of Pi-induced oxidative stress related with intracellular Ca2+\u00a0([Ca2+]i) disturbance, which is critical for calcification of VSMCs. VSMCs isolated from rat thoracic aorta or A7r5 cells were incubated with high Pi-containing medium. Extracellular signal-regulated kinase (ERK) and mammalian target of rapamycin were activated by high Pi that was required for vascular calcification. High Pi upregulated expressions of type III sodium-phosphate cotransporters PiT-1 and -2 and stimulated their trafficking to the plasma membrane. Interestingly, high Pi increased [Ca2+]i\u00a0exclusively dependent on extracellular Na+\u00a0and Ca2+\u00a0as well as PiT-1\/2 abundance. Furthermore, high-Pi induced plasma membrane depolarization mediated by PiT-1\/2. Pretreatment with verapamil, as a voltage-gated Ca2+\u00a0channel (VGCC) blocker, inhibited Pi-induced [Ca2+]i\u00a0elevation, oxidative stress, ERK activation, and osteogenic differentiation. These protective effects were reiterated by extracellular Ca2+-free condition, intracellular Ca2+\u00a0chelation, or suppression of oxidative stress. Mitochondrial superoxide scavenger also effectively abrogated ERK activation and osteogenic differentiation of VSMCs by high Pi. Taking all these together, we suggest that high Pi activates depolarization-triggered Ca2+\u00a0influx via VGCC, and subsequent [Ca2+]i\u00a0increase elicits oxidative stress and osteogenic differentiation. PiT-1\/2 mediates Pi-induced [Ca2+]i\u00a0overload and oxidative stress but in turn, PiT-1\/2 is upregulated by consequences of these alterations.<\/p>\n<p>Authors: Tuyet Thi Nguyen and other authors<\/p>\n<p>Read more about the article\u00a0<a href=\"https:\/\/journals.physiology.org\/doi\/abs\/10.1152\/ajpheart.00305.2020?af=R&amp;fbclid=IwAR2Hpyrfa-q7gp0Ta_GWtbcFJ8AvTZT3I8bAPCtb--5xWS5zyxiyQtW9t1k\">here<\/a><\/p>\n<p>Read more about the author\u2019s Tuyet Thi Nguyen publications\u00a0<a href=\"https:\/\/vinuni.edu.vn\/people\/nguyen-thi-tuyet-md-phd\/\">here<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Abstract Hyperphosphatemia is the primary risk factor for vascular calcification, which is closely associated with cardiovascular morbidity and mortality. Recent evidence showed that oxidative stress by high inorganic phosphate (Pi) mediates calcific changes in vascular smooth muscle cells (VSMCs). However, intracellular signaling responsible for Pi-induced oxidative stress remains unclear. Here, we investigated molecular mechanisms of [&hellip;]<\/p>\n","protected":false},"author":2,"featured_media":293,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[3],"tags":[38],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v19.6.1 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology - Vinuni Research Website<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology - Vinuni Research Website\" \/>\n<meta property=\"og:description\" content=\"Abstract Hyperphosphatemia is the primary risk factor for vascular calcification, which is closely associated with cardiovascular morbidity and mortality. Recent evidence showed that oxidative stress by high inorganic phosphate (Pi) mediates calcific changes in vascular smooth muscle cells (VSMCs). However, intracellular signaling responsible for Pi-induced oxidative stress remains unclear. Here, we investigated molecular mechanisms of [&hellip;]\" \/>\n<meta property=\"og:url\" content=\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/\" \/>\n<meta property=\"og:site_name\" content=\"Vinuni Research Website\" \/>\n<meta property=\"article:published_time\" content=\"2021-05-27T03:29:33+00:00\" \/>\n<meta property=\"article:modified_time\" content=\"2022-09-05T03:31:03+00:00\" \/>\n<meta property=\"og:image\" content=\"https:\/\/vinuni.edu.vn\/research\/wp-content\/uploads\/2022\/09\/pexels-photo-3952126-e1622107196761-660x410-1-e1662348644997.jpeg\" \/>\n\t<meta property=\"og:image:width\" content=\"600\" \/>\n\t<meta property=\"og:image:height\" content=\"389\" \/>\n\t<meta property=\"og:image:type\" content=\"image\/jpeg\" \/>\n<meta name=\"author\" content=\"phuong.ntn\" \/>\n<meta name=\"twitter:card\" content=\"summary_large_image\" \/>\n<meta name=\"twitter:label1\" content=\"Written by\" \/>\n\t<meta name=\"twitter:data1\" content=\"phuong.ntn\" \/>\n\t<meta name=\"twitter:label2\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data2\" content=\"2 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\/\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/\",\"url\":\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/\",\"name\":\"Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology - Vinuni Research Website\",\"isPartOf\":{\"@id\":\"https:\/\/vinuni.edu.vn\/research\/#website\"},\"datePublished\":\"2021-05-27T03:29:33+00:00\",\"dateModified\":\"2022-09-05T03:31:03+00:00\",\"author\":{\"@id\":\"https:\/\/vinuni.edu.vn\/research\/#\/schema\/person\/d19200a9f0488a2d6374d8641ee8c085\"},\"breadcrumb\":{\"@id\":\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/#breadcrumb\"},\"inLanguage\":\"en-US\",\"potentialAction\":[{\"@type\":\"ReadAction\",\"target\":[\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/\"]}]},{\"@type\":\"BreadcrumbList\",\"@id\":\"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/#breadcrumb\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology\"}]},{\"@type\":\"WebSite\",\"@id\":\"https:\/\/vinuni.edu.vn\/research\/#website\",\"url\":\"https:\/\/vinuni.edu.vn\/research\/\",\"name\":\"Vinuni Research Website\",\"description\":\"\",\"potentialAction\":[{\"@type\":\"SearchAction\",\"target\":{\"@type\":\"EntryPoint\",\"urlTemplate\":\"https:\/\/vinuni.edu.vn\/research\/?s={search_term_string}\"},\"query-input\":\"required name=search_term_string\"}],\"inLanguage\":\"en-US\"},{\"@type\":\"Person\",\"@id\":\"https:\/\/vinuni.edu.vn\/research\/#\/schema\/person\/d19200a9f0488a2d6374d8641ee8c085\",\"name\":\"phuong.ntn\",\"image\":{\"@type\":\"ImageObject\",\"inLanguage\":\"en-US\",\"@id\":\"https:\/\/vinuni.edu.vn\/research\/#\/schema\/person\/image\/\",\"url\":\"https:\/\/secure.gravatar.com\/avatar\/678312306781d0830679d2c1a8a112f1?s=96&d=mm&r=g\",\"contentUrl\":\"https:\/\/secure.gravatar.com\/avatar\/678312306781d0830679d2c1a8a112f1?s=96&d=mm&r=g\",\"caption\":\"phuong.ntn\"}}]}<\/script>\n<!-- \/ Yoast SEO plugin. -->","yoast_head_json":{"title":"Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology - Vinuni Research Website","robots":{"index":"index","follow":"follow","max-snippet":"max-snippet:-1","max-image-preview":"max-image-preview:large","max-video-preview":"max-video-preview:-1"},"canonical":"https:\/\/vinuni.edu.vn\/research\/publication-by-vinuniversity-college-of-health-sciences-lecture-in-american-journal-of-physiology\/","og_locale":"en_US","og_type":"article","og_title":"Publication by VinUniversity College Of Health Sciences\u2019 Lecture in American Journal of Physiology - Vinuni Research Website","og_description":"Abstract Hyperphosphatemia is the primary risk factor for vascular calcification, which is closely associated with cardiovascular morbidity and mortality. 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