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Transient receptor potential vanilloid 1 (\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1) ion channels and nerve growth factor (\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      ) in those cells are implicated in this modulatory effect and play a role in sensitizing pain\u2010related afferent pathways during inflammation. In this study, we investigated the interaction between\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1 channels in urothelial cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Urothelial cells from female\n                      <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>\n                      prague\u2010\n                      <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                      awley rat bladders were cultured to quantify membrane expression of\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1 channels and capsaicin\u2010induced\n                      <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n                      release in the presence of\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      alone or with\n                      <jats:styled-content style=\"fixed-case\">TrKA<\/jats:styled-content>\n                      or PI3K inhibitors. Pain scores from rats with cyclophosphamide (\n                      <jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>\n                      )\u2010induced bladder inflammation were assessed after treatment with a\n                      <jats:styled-content style=\"fixed-case\">TrkA<\/jats:styled-content>\n                      antagonist. Bladders (from control and\n                      <jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>\n                      rats) were collected and analysed for\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      content and\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1 channel expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Cultured cells responded to\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      with increased\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1 channel expression in the cell membrane and increased release of\n                      <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n                      . Both responses were blocked by either a\n                      <jats:styled-content style=\"fixed-case\">TrkA<\/jats:styled-content>\n                      antagonist or a\n                      <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>\n                      3K inhibitor. Treatment\n                      <jats:italic>in vivo<\/jats:italic>\n                      with the\n                      <jats:styled-content style=\"fixed-case\">TrkA<\/jats:styled-content>\n                      antagonist alleviated pain symptoms and reduced\n                      <jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>\n                      \u2010induced\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      overexpression in the mucosa. Furthermore, in urothelial cells from animals with bladder inflammation, expression of\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1 channels in the membrane was significantly increased.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      During bladder inflammation, increased production of\n                      <jats:styled-content style=\"fixed-case\">NGF<\/jats:styled-content>\n                      in urothelial cells induced increased expression and activity of\n                      <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>\n                      1 channels in the cell membrane. This effect was primarily mediated by the PI\n                      <jats:styled-content style=\"fixed-case\">3K<\/jats:styled-content>\n                      pathway.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.12958","type":"journal-article","created":{"date-parts":[[2014,10,8]],"date-time":"2014-10-08T22:37:44Z","timestamp":1412807864000},"page":"1691-1699","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Urinary bladder inflammation induces changes in urothelial nerve growth factor and\n                    <scp>TRPV<\/scp>\n                    1 channels"],"prefix":"10.1111","volume":"172","author":[{"given":"A","family":"Coelho","sequence":"first","affiliation":[{"name":"Department of Experimental Biology Faculty of Medicine University of Porto Porto Portugal"},{"name":"Institute for Molecular and Cell Biology (IBMC) University of Porto Porto Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A S","family":"Wolf\u2010Johnston","sequence":"additional","affiliation":[{"name":"Departmentof Urology Hospital S. 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