{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yin LM"],"funding":["Shanghai Talent Development Fund","National Natural Science Foundation of China","National Institutes of Health","Shanghai Key Research Program of Shanghai Municipal Commission of Health and Family Planning","Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning"],"pagination":["eaam8604"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6310021"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(427)"],"pubmed_abstract":["There is a clinical need for new bronchodilator drugs in asthma, because more than half of asthmatic patients do not receive adequate control with current available treatments. We report that inhibition of metallothionein-2 protein expression in lung tissues causes the increase of pulmonary resistance. Conversely, metallothionein-2 protein is more effective than β2-agonists in reducing pulmonary resistance in rodent asthma models, alleviating tension in tracheal spirals, and relaxing airway smooth muscle cells (ASMCs). Metallothionein-2 relaxes ASMCs via transgelin-2 (TG2) and induces dephosphorylation of myosin phosphatase target subunit 1 (MYPT1). We identify TSG12 as a nontoxic, specific TG2-agonist that relaxes ASMCs and reduces asthmatic pulmonary resistance. In vivo, TSG12 reduces pu"],"journal":["Science translational medicine"],"pubmed_title":["Transgelin-2 as a therapeutic target for asthmatic pulmonary resistance."],"pmcid":["PMC6310021"],"funding_grant_id":["JZ2016010","award299452","award357110","award299450","81273435","award356402","81774429","201610","R01-GM114180","ZY3-CCCX-3-3005","81473760","award350045","award357109","81574058","award299449","award299448"],"pubmed_authors":["Xu YD","Deng L","Wu YL","Li HY","Ge GB","Pang Y","Guan N","Ulloa L","Huang S","Chen Z","Wang WQ","Yang YQ","Yin LM","Duan TT","Liu JY","Peng LL","Han XJ","Zhu W","Wang Y","Xu Z"],"additional_accession":[]},"is_claimable":false,"name":"Transgelin-2 as a therapeutic target for asthmatic pulmonary resistance.","description":"There is a clinical need for new bronchodilator drugs in asthma, because more than half of asthmatic patients do not receive adequate control with current available treatments. We report that inhibition of metallothionein-2 protein expression in lung tissues causes the increase of pulmonary resistance. Conversely, metallothionein-2 protein is more effective than β2-agonists in reducing pulmonary resistance in rodent asthma models, alleviating tension in tracheal spirals, and relaxing airway smooth muscle cells (ASMCs). Metallothionein-2 relaxes ASMCs via transgelin-2 (TG2) and induces dephosphorylation of myosin phosphatase target subunit 1 (MYPT1). We identify TSG12 as a nontoxic, specific TG2-agonist that relaxes ASMCs and reduces asthmatic pulmonary resistance. In vivo, TSG12 reduces pu","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Feb","modification":"2025-04-21T21:36:51.374Z","creation":"2019-03-26T22:28:57Z"},"accession":"S-EPMC6310021","cross_references":{"pubmed":["29437149"],"doi":["10.1126/scitranslmed.aam8604"]}}