<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dragunas G</submitter><funding>NHLBI NIH HHS</funding><funding>Fundação de Amparo à Pesquisa do Estado de São Paulo</funding><funding>National Institutes of Health</funding><pagination>7703-7717</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7302963</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>34(6)</volume><pubmed_abstract>Parasympathetic neurons in the airways control bronchomotor tone. Increased activity of cholinergic neurons are mediators of airway hyperresponsiveness (AHR) in asthma, however, mechanisms are not elucidated. We describe remodeling of the cholinergic neuronal network in asthmatic airways driven by brain-derived neurotrophic factor (BDNF) and Tropomyosin receptor kinase B (TrkB). Human bronchial biopsies were stained for cholinergic marker vesicular acetylcholine transporter (VAChT). Human lung gene expression and single nucleotide polymorphisms (SNP) in neuroplasticity-related genes were compared between asthma and healthy patients. Wild-type (WT) and mutated TrkB knock-in mice (Ntrk2tm1Ddg/J) with impaired BDNF signaling were chronically exposed to ovalbumin (OVA). Neuronal VAChT staining</pubmed_abstract><journal>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</journal><pubmed_title>Cholinergic neuroplasticity in asthma driven by TrkB signaling.</pubmed_title><pmcid>PMC7302963</pmcid><funding_grant_id>R01 HL088029</funding_grant_id><funding_grant_id>2018/18762‐8</funding_grant_id><funding_grant_id>NIHR01HL088029</funding_grant_id><pubmed_authors>Ditz B</pubmed_authors><pubmed_authors>Bos ST</pubmed_authors><pubmed_authors>Nijboer S</pubmed_authors><pubmed_authors>Vonk JM</pubmed_authors><pubmed_authors>Munhoz CD</pubmed_authors><pubmed_authors>van Asselt J</pubmed_authors><pubmed_authors>Vohlidalova E</pubmed_authors><pubmed_authors>Kistemaker LEM</pubmed_authors><pubmed_authors>Vermeulen CJ</pubmed_authors><pubmed_authors>Prakash YS</pubmed_authors><pubmed_authors>Dragunas G</pubmed_authors><pubmed_authors>Gosens R</pubmed_authors><pubmed_authors>Woest ME</pubmed_authors><pubmed_authors>de Groot AP</pubmed_authors><pubmed_authors>Ten Hacken NHT</pubmed_authors><pubmed_authors>Koppelman GH</pubmed_authors><pubmed_authors>van den Berge M</pubmed_authors><pubmed_authors>Timens W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cholinergic neuroplasticity in asthma driven by TrkB signaling.</name><description>Parasympathetic neurons in the airways control bronchomotor tone. Increased activity of cholinergic neurons are mediators of airway hyperresponsiveness (AHR) in asthma, however, mechanisms are not elucidated. We describe remodeling of the cholinergic neuronal network in asthmatic airways driven by brain-derived neurotrophic factor (BDNF) and Tropomyosin receptor kinase B (TrkB). Human bronchial biopsies were stained for cholinergic marker vesicular acetylcholine transporter (VAChT). Human lung gene expression and single nucleotide polymorphisms (SNP) in neuroplasticity-related genes were compared between asthma and healthy patients. Wild-type (WT) and mutated TrkB knock-in mice (Ntrk2tm1Ddg/J) with impaired BDNF signaling were chronically exposed to ovalbumin (OVA). Neuronal VAChT staining</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jun</publication><modification>2026-04-18T01:10:52.959Z</modification><creation>2020-09-30T07:02:08Z</creation></dates><accession>S-EPMC7302963</accession><cross_references><pubmed>32277855</pubmed><doi>10.1096/fj.202000170R</doi></cross_references></HashMap>