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Induced Pluripotent Stem Cell‐Derived Neuroprogenitor Cells: A Model for Studying Cannabinoid Induced Cell Signaling
Author(s) -
Ryan Gabriella
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.07455
Subject(s) - induced pluripotent stem cell , chronic pain , cannabinoid , cannabinoid receptor , endocannabinoid system , neuroscience , synthetic cannabinoids , population , pharmacology , medicine , biology , receptor , embryonic stem cell , environmental health , biochemistry , gene , agonist
Chronic pain is a growing epidemic and public health issue that continue to affect the aging population in the US. Managing pain is particularly difficult with patients who suffer from cancer‐associated pain, neuropathic pain, as well as central pain states. These conditions are typically treated inadequately with opioids, antidepressants, and anticonvulsive drugs. There is growing evidence that cannabinoids natural products are beneficial for a range of clinical conditions, including pain and inflammations. The use of cannabinoids instead of highly regulated prescription drugs is fast approaching and the development of such cannabinoid drugs requires well planned medical trials as well as very stringent guidelines for contaminants such as heavy metals, pesticides, mycotoxins, etc. However, federal guidelines have not kept up with this emerging industry. Currently, each state is left to manage their own set of regulations, resulting in an industry that has great uncertainty and chaos as it attempts to satisfy the growing demand for its products. A low‐cost cellular model to study the neurological effects of cannabinoids is challenging. Here we show that Neuroprognitor cells (NPs) derived from induced pluripotent stem cells (iPSCs) can be used as a model for studying pathways associated with pain and cannabinoids. NPs derived from iPSCs can be differentiated into multiple lineages of neurons and glial cells. These cells have the Cannabinoid Receptor 1 (CB1) present which, when activated by cannabinoids, inhibits the inflammatory and pain stimulation of Cyclooxygenase 2 (COX2). We show expression and activation of CB1 in correlation to Cannabinoids treatment. Likewise we show how, in iPSC‐derived NPs Cannabinoid treatment leads to the inhibition of Cox‐2, therefore theoretically lessoning the potential for inflammation and pain. Support or Funding Information Omni International, Inc 935 Cobb Place Blvd Kennesaw Ga 30144