{"id":365,"date":"2020-07-09T16:56:57","date_gmt":"2020-07-09T16:56:57","guid":{"rendered":"http:\/\/sites.rutgers.edu\/haesun-kim-lab\/?page_id=365"},"modified":"2022-08-31T16:16:53","modified_gmt":"2022-08-31T16:16:53","slug":"research","status":"publish","type":"page","link":"https:\/\/sites.rutgers.edu\/haesun-kim-lab\/research\/","title":{"rendered":"Research Projects"},"content":{"rendered":"<h5><strong>Research Projects<\/strong><\/h5>\n<p>One of the goals of my research program to define the mechanisms that underlie myelin abnormalities in the PNS.\u00a0 Using both cellular and animal models for peripheral neuropathies, we focus on understanding the genetic and intracellular signaling mechanisms that modulate Schwann cell myelination and myelin maintenance.\u00a0 Ultimately, we will use this information to design therapies to promote PNS recovery and function in diseases such as Charcot-Marie-Tooth (CMT) diseases, diabetic neuropathy and nerve trauma by promoting myelin repair and preventing myelin loss.\u00a0 We are also interested in elucidating the molecular mechanisms underlying myelin abnormalities associated with mild traumatic brain injury.\u00a0\u00a0Our extensive work on Schwann cells demonstrated an essential role for the external regulators such as growth factors and cell adhesion molecules in Schwann cell differentiation and myelination.\u00a0 We also demonstrated the importance of MAPK kinases in promoting Schwann cell plasticity, de-differentiation and myelin breakdown following PNS injury.\u00a0 We have considerable expertise in using both\u00a0<em>in vitro<\/em>\u00a0and\u00a0<em>in vivo<\/em>\u00a0genetic mouse models to study Schwann cell myelination.<\/p>\n<p><img decoding=\"async\" src=\"https:\/\/ncasapps.rutgers.edu\/webfm_send\/2946\" alt=\"\" \/><img decoding=\"async\" src=\"https:\/\/ncasapps.rutgers.edu\/webfm_send\/2947\" alt=\"\" \/>1.\u00a0<strong><em>Stemness of Schwann cell<\/em><\/strong><strong><em>:<\/em><\/strong>\u00a0Repair in the peripheral nervous system (PNS) depends upon the plasticity of the myelinating cells, Schwann cells, and their ability to dedifferentiate, direct axonal regrowth, re-myelinate and allow functional recovery. The ability of such an exquisitely specialized myelinating cell to revert to an immature de-differentiated cell that can direct repair is remarkable, making Schwann cells one of the very few regenerative cell types in our bodies.\u00a0 We are currently investigating the role of MiTF\/TFE transcription factors in promoting repair Schwann cell formation.\u00a0 For the project, we use both in vitro and in vivo modes of peripheral nerve injury models combined biochemical and genetic analyses.<\/p>\n<p>2.\u00a0<strong><em>Choline metabolism in regulation PNS myelination and repair:<\/em><\/strong>\u00a0Cells have a limited capacity to synthesize choline, thus cells depend on protein transporters to import choline.\u00a0 Choline is used to generate phospholipids, which are important components of myelin membrane.\u00a0 Choline is also metabolized to synthesize phosphotidylinositols which are important signaling lipids that regulate myelin formation.\u00a0 We have identified Choline-like-transporter 1 (CTL1) as a choline transporter in Schwann cells and generated Schwann cell-specific CTL1 knock-out mice.\u00a0 Using the in vivo tool, we are currently investigating the role of CTL1 and choline metabolism in regulating Schwann cell myelin formation and repair.<\/p>\n<p>3.<strong><em>\u00a0<\/em><\/strong><strong><em>Charcot-Marie-Tooth (CMT)<\/em><\/strong><strong><em>\u00a0disease:<\/em><\/strong>\u00a0CMT is the most common inherited demyelinating disorder affecting the peripheral nervous system (PNS).\u00a0 \u00a0CMT1A\u00a0 is caused by mutations on PMP22 that results in the protein accumulation in the ER.\u00a0 This triggers ER stress response which is believed to me one of the mechanisms that impair PNS myelin in CMT1A patients.\u00a0 \u00a0MiTF\/TFE transcription factors master regulators of lysosomal biogenesis and autophagy, a cellular function that removes unwanted proteins (cellular clearance).\u00a0 We are currently investigating the role of MiTF\/TFE proteins in CMT1A-related disease mechanisms in Schwann cells and myelin abnormalities.<\/p>\n<p>4.\u00a0<strong><em>Traumatic Brain Injury (TBI):\u00a0<\/em><\/strong>Chronic white matter atrophy or degeneration of myelinated axons is a common occurrence after repeated concussive injury, or mild TBI, which contributes to long-term functional deficits in the patients.\u00a0 This project focuses on elucidating the molecular mechanisms that contribute to myelin loss associated with mTBI.\u00a0 We are currently testing the hypothesis that mechanical injury disrupts normal axon-to-oligodendrocyte signaling necessary for maintaining myelin homeostasis in the brain.\u00a0 We use both\u00a0<em>in vitro<\/em>\u00a0myelinated axon stretch injury model and\u00a0<em>in vivo<\/em>\u00a0rodent mTBI models to elucidate the signaling mechanism associated with the myelin loss.<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<div class=\"page\" title=\"Page 1\">\n<div class=\"layoutArea\">\n<div class=\"column\">\n<p>&nbsp;<\/p>\n<\/div>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"<p>Research Projects One of the goals of my research program to define the mechanisms that underlie myelin abnormalities in the PNS.\u00a0 Using both cellular and animal models for peripheral neuropathies, &hellip; <a href=\"https:\/\/sites.rutgers.edu\/haesun-kim-lab\/research\/\" class=\"\">Read More<\/a><\/p>\n","protected":false},"author":21,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"template-custom.php","meta":{"_acf_changed":false,"footnotes":""},"class_list":["post-365","page","type-page","status-publish","hentry"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v23.5 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Research Projects - Dr. Haesun Kim&#039;s Lab<\/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:\/\/sites.rutgers.edu\/haesun-kim-lab\/research\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Research Projects - Dr. Haesun Kim&#039;s Lab\" \/>\n<meta property=\"og:description\" content=\"Research Projects One of the goals of my research program to define the mechanisms that underlie myelin abnormalities in the PNS.\u00a0 Using both cellular and animal models for peripheral neuropathies, &hellip; 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