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  1. Article ; Online: Striving toward hyperthermia-free analgesia

    Tingting Li / Man-Kyo Chung

    The Journal of Clinical Investigation, Vol 133, Iss

    lessons from loss-of-function mutations of human TRPV1

    2023  Volume 3

    Abstract: Transient receptor potential vanilloid 1 (TRPV1), a receptor for capsaicin and noxious heat, has been one of the most compelling targets for analgesics. However, systemic inhibition of TRPV1 is an impractical approach as a pain killer, since systemic ... ...

    Abstract Transient receptor potential vanilloid 1 (TRPV1), a receptor for capsaicin and noxious heat, has been one of the most compelling targets for analgesics. However, systemic inhibition of TRPV1 is an impractical approach as a pain killer, since systemic antagonism induces hyperthermia. Two articles in this issue of the JCI report phenotypes from separate, rare missense mutations of human TRPV1. He, Zambelli, and colleagues investigated TRPV1K710N, which showed reduced functionality, while Katz, Zaguri, and co-authors reported on TRPV1N331K, which led to a complete functional knockout. The findings provide insights that will improve our understanding of the endogenous functions of TRPV1 in humans and may facilitate a rational TRPV1-targeting approach to achieve hyperthermia-free analgesia.
    Keywords Medicine ; R
    Language English
    Publishing date 2023-02-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: A virtual case-based learning module for pain in dentistry.

    Chung, Man-Kyo

    Journal of dental education

    2021  Volume 85 Suppl 3, Page(s) 1928–1929

    MeSH term(s) Dentistry ; Education, Dental ; Humans ; Learning ; Pain
    Language English
    Publishing date 2021-02-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 410579-5
    ISSN 1930-7837 ; 0022-0337
    ISSN (online) 1930-7837
    ISSN 0022-0337
    DOI 10.1002/jdd.12567
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  3. Article ; Online: Striving toward hyperthermia-free analgesia: lessons from loss-of-function mutations of human TRPV1.

    Li, Tingting / Chung, Man-Kyo

    The Journal of clinical investigation

    2023  Volume 133, Issue 3

    Abstract: Transient receptor potential vanilloid 1 (TRPV1), a receptor for capsaicin and noxious heat, has been one of the most compelling targets for analgesics. However, systemic inhibition of TRPV1 is an impractical approach as a pain killer, since systemic ... ...

    Abstract Transient receptor potential vanilloid 1 (TRPV1), a receptor for capsaicin and noxious heat, has been one of the most compelling targets for analgesics. However, systemic inhibition of TRPV1 is an impractical approach as a pain killer, since systemic antagonism induces hyperthermia. Two articles in this issue of the JCI report phenotypes from separate, rare missense mutations of human TRPV1. He, Zambelli, and colleagues investigated TRPV1K710N, which showed reduced functionality, while Katz, Zaguri, and co-authors reported on TRPV1N331K, which led to a complete functional knockout. The findings provide insights that will improve our understanding of the endogenous functions of TRPV1 in humans and may facilitate a rational TRPV1-targeting approach to achieve hyperthermia-free analgesia.
    MeSH term(s) Humans ; Body Temperature ; TRPV Cation Channels/genetics ; Fever ; Pain/genetics ; Analgesia ; Capsaicin/pharmacology ; Mutation
    Chemical Substances TRPV Cation Channels ; Capsaicin (S07O44R1ZM) ; TRPV1 protein, human
    Language English
    Publishing date 2023-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI167338
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  4. Article ; Online: Piezo1 and Piezo2 collectively regulate jawbone development.

    Nie, Xuguang / Abbasi, Yasaman / Chung, Man-Kyo

    Development (Cambridge, England)

    2024  

    Abstract: Piezo1 and Piezo2 are novel mechanosensory ion channels that transduce mechanical stimuli from the environment into intracellular biochemical signals in various tissues and organ systems. Here, we showed that Piezo1 and Piezo2 displayed a robust ... ...

    Abstract Piezo1 and Piezo2 are novel mechanosensory ion channels that transduce mechanical stimuli from the environment into intracellular biochemical signals in various tissues and organ systems. Here, we showed that Piezo1 and Piezo2 displayed a robust expression during jawbone development. Deletion of Piezo1 in neural crest cells caused jawbone malformations in a small but significant number of mice. We further demonstrated that disruption of Piezo1 and Piezo2 in neural crest cells caused more striking defects in jawbone development than any single knockout, suggesting essential but partially redundant roles of Piezo1 and Piezo2. In addition, we observed defects in other neural crest derivatives such as malformation of the vascular smooth muscle in double knockout mice. Moreover, TUNEL examinations revealed excessive cell death in osteogenic cells of the maxillary and mandibular arches of the double knockout mice, suggesting that Piezo1 and Piezo2 together regulate cell survival during jawbone development. We further demonstrated that Yoda1, a Piezo1 agonist, promotes mineralization in the mandibular arches. Altogether, these data firmly establish that Piezo channels play important roles in regulating jawbone formation and maintenance.
    Language English
    Publishing date 2024-04-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.202386
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  5. Article ; Online: Nociceptor mechanisms underlying pain and bone remodeling via orthodontic forces: toward no pain, big gain.

    Wang, Sheng / Ko, Ching-Chang / Chung, Man-Kyo

    Frontiers in pain research (Lausanne, Switzerland)

    2024  Volume 5, Page(s) 1365194

    Abstract: Orthodontic forces are strongly associated with pain, the primary complaint among patients wearing orthodontic braces. Compared to other side effects of orthodontic treatment, orthodontic pain is often overlooked, with limited clinical management. ... ...

    Abstract Orthodontic forces are strongly associated with pain, the primary complaint among patients wearing orthodontic braces. Compared to other side effects of orthodontic treatment, orthodontic pain is often overlooked, with limited clinical management. Orthodontic forces lead to inflammatory responses in the periodontium, which triggers bone remodeling and eventually induces tooth movement. Mechanical forces and subsequent inflammation in the periodontium activate and sensitize periodontal nociceptors and produce orthodontic pain. Nociceptive afferents expressing transient receptor potential vanilloid subtype 1 (TRPV1) play central roles in transducing nociceptive signals, leading to transcriptional changes in the trigeminal ganglia. Nociceptive molecules, such as TRPV1, transient receptor potential ankyrin subtype 1, acid-sensing ion channel 3, and the P2X3 receptor, are believed to mediate orthodontic pain. Neuropeptides such as calcitonin gene-related peptides and substance P can also regulate orthodontic pain. While periodontal nociceptors transmit nociceptive signals to the brain, they are also known to modulate alveolar bone remodeling in periodontitis. Therefore, periodontal nociceptors and nociceptive molecules may contribute to the modulation of orthodontic tooth movement, which currently remains undetermined. Future studies are needed to better understand the fundamental mechanisms underlying neuroskeletal interactions in orthodontics to improve orthodontic treatment by developing novel methods to reduce pain and accelerate orthodontic tooth movement-thereby achieving "big gains with no pain" in clinical orthodontics.
    Language English
    Publishing date 2024-02-22
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 2673-561X
    ISSN (online) 2673-561X
    DOI 10.3389/fpain.2024.1365194
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  6. Article ; Online: Piezo channels for skeletal development and homeostasis: Insights from mouse genetic models.

    Nie, Xuguang / Chung, Man-Kyo

    Differentiation; research in biological diversity

    2022  Volume 126, Page(s) 10–15

    Abstract: Piezo1 and Piezo2 are recently discovered mechanosensory ion channels. Piezo channels transduce mechanical stimulation into cellular signaling in a variety of tissues and organ systems. The functional roles of Piezo1 and Piezo2 have been revealed in both ...

    Abstract Piezo1 and Piezo2 are recently discovered mechanosensory ion channels. Piezo channels transduce mechanical stimulation into cellular signaling in a variety of tissues and organ systems. The functional roles of Piezo1 and Piezo2 have been revealed in both developmental and physiological scenarios by using mouse genetic models. Mechanotransduction by Piezo1 channels regulates osteoblast/osteocyte activity and, thus, strengthens the skeleton enabling it to adapt to a wide range of mechanical loadings. Deletion of the Piezo1 gene in the developing skeleton causes bone malformations that lead to spontaneous bone fractures, while inactivity of Piezo1 in adulthood results in osteoporosis. Furthermore, Piezo2 channels in sensory neurons might provide another route of skeletal regulation. Piezo channels also regulate the proliferation and differentiation of various types of stem cells. PIEZO1 and PIEZO2 mutations and channel malfunctions have been implicated in an increasing number of human diseases, and PIEZO channels are currently emerging as potential targets for disease treatment. This review summarizes the important findings of Piezo channels for skeletal development and homeostasis using the mouse genetic model system.
    MeSH term(s) Adult ; Animals ; Homeostasis/genetics ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Mechanotransduction, Cellular/genetics ; Mice ; Models, Genetic
    Chemical Substances Ion Channels ; PIEZO1 protein, human ; Piezo1 protein, mouse
    Language English
    Publishing date 2022-07-03
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 184540-8
    ISSN 1432-0436 ; 0301-4681
    ISSN (online) 1432-0436
    ISSN 0301-4681
    DOI 10.1016/j.diff.2022.06.001
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  7. Article: Elucidation of neuronal activity in mouse models of TMJ injury by

    Son, Hyeonwi / Shannonhouse, John / Zhang, Yan / Gomez, Ruben / Chung, Man-Kyo / Kim, Yu Shin

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Patients with temporomandibular disorders (TMD) typically experience facial pain and discomfort or tenderness in the temporomandibular joint (TMJ), causing disability in daily life. Unfortunately, existing treatments for TMD are not always effective, ... ...

    Abstract Patients with temporomandibular disorders (TMD) typically experience facial pain and discomfort or tenderness in the temporomandibular joint (TMJ), causing disability in daily life. Unfortunately, existing treatments for TMD are not always effective, creating a need for more advanced, mechanism-based therapies. In this study, we used
    Language English
    Publishing date 2024-01-16
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.16.575919
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  8. Article ; Online: Creeping attachment following free gingival grafts around dental implants exhibiting mucosal recession with a lack of keratinised mucosa: A case series.

    Oh, Se-Lim / Chung, Man-Kyo

    International journal of oral implantology (Berlin, Germany)

    2021  Volume 13, Issue 4, Page(s) 401–409

    MeSH term(s) Dental Implantation, Endosseous ; Dental Implants ; Gingiva/surgery ; Humans ; Mucous Membrane ; Oral Surgical Procedures
    Chemical Substances Dental Implants
    Language English
    Publishing date 2021-01-22
    Publishing country Germany
    Document type Case Reports ; Journal Article
    ZDB-ID 2968002-5
    ISSN 2631-6439 ; 2631-6420
    ISSN (online) 2631-6439
    ISSN 2631-6420
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  9. Article: Intermittent Hypoxia Interferes with Autocrine Effects of GABA on Insulin Secretion in Postnatal Rodents-Implications for Pediatric Obstructive Sleep Apnea.

    Pae, Eung-Kwon / Chung, Man-Kyo / Harper, Ronald M

    Children (Basel, Switzerland)

    2022  Volume 9, Issue 9

    Abstract: Gamma-amino butyric acid (GABA) is well known to help elevate pancreatic β cell vitality and insulin levels in blood. GABA works via a coupling with GABA receptors; thus, the concentration of ... ...

    Abstract Gamma-amino butyric acid (GABA) is well known to help elevate pancreatic β cell vitality and insulin levels in blood. GABA works via a coupling with GABA receptors; thus, the concentration of GABA
    Language English
    Publishing date 2022-08-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2732685-8
    ISSN 2227-9067
    ISSN 2227-9067
    DOI 10.3390/children9091305
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  10. Article ; Online: Peripheral glutamate receptor and transient receptor potential channel mechanisms of craniofacial muscle pain.

    Chung, Man-Kyo / Ro, Jin Y

    Molecular pain

    2020  Volume 16, Page(s) 1744806920914204

    MeSH term(s) Animals ; Facial Pain/metabolism ; Facial Pain/physiopathology ; Humans ; Inflammation ; Ligands ; Myalgia/metabolism ; Neurons, Afferent/metabolism ; Nociception ; Phosphorylation ; Protein Kinase C/metabolism ; Receptors, Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Signal Transduction ; TRPA1 Cation Channel/metabolism ; TRPV Cation Channels/metabolism
    Chemical Substances Ligands ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate ; TRPA1 Cation Channel ; TRPA1 protein, human ; TRPV Cation Channels ; TRPV1 protein, human ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2020-03-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2174252-2
    ISSN 1744-8069 ; 1744-8069
    ISSN (online) 1744-8069
    ISSN 1744-8069
    DOI 10.1177/1744806920914204
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