{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T16:48:01Z","timestamp":1773420481120,"version":"3.50.1"},"reference-count":51,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2014,2,19]],"date-time":"2014-02-19T00:00:00Z","timestamp":1392768000000},"content-version":"vor","delay-in-days":18,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000769","name":"University of Oxford","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000769","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2014,2]]},"abstract":"Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen responsible for physiological and pathological angiogenesis. Abnormal regulation ofVEGF<\/jats:styled-content>expression in anterior pituitary folliculostellate (FS<\/jats:styled-content>) cells has been implicated in pituitary tumour progression.FS<\/jats:styled-content>and endocrine cells expressVEGF<\/jats:styled-content>, which is considered to be secreted by the constitutive pathway. The present study investigated the mechanism ofVEGF<\/jats:styled-content>secretion in TtT\/GF<\/jats:styled-content>cells, a mouseFS<\/jats:styled-content>cell line. TtT\/GF<\/jats:styled-content>cells were shown to expressVEGF<\/jats:styled-content>164<\/jats:sub>, the most potent and bioavailable isoform ofVEGF<\/jats:styled-content>. Immunofluorescence and immunogold electron microscopy localisedVEGF<\/jats:styled-content>to the cytoplasm and small electron\u2010lucent vesicles.Pituitary adenylate cyclase\u2010activating polypeptide (PACAP)<\/jats:styled-content>, a well\u2010documented stimulant ofVEGF<\/jats:styled-content>secretion, caused a robust increase inVEGF<\/jats:styled-content>secretion over 24\u00a0h. Glyburide, anABCA<\/jats:styled-content>1 andKATP<\/jats:sub><\/jats:styled-content>channel blocker, also caused an increase inVEGF<\/jats:styled-content>secretion when applied alone, and amplified the response toPACAP<\/jats:styled-content>. OtherABCA<\/jats:styled-content>1 transport blockers did not affectVEGF<\/jats:styled-content>secretion. Exposure of TtT\/GF<\/jats:styled-content>cells to cycloheximide withPACAP<\/jats:styled-content>or glyburide inhibited the increased secretion ofVEGF<\/jats:styled-content>, consistent with control of secretion at the transcription level. TheSUR<\/jats:styled-content>2B\/Kir6.1 form ofKATP<\/jats:sub><\/jats:styled-content>channels was shown to be expressed by TtT\/GF<\/jats:styled-content>cells. Diazoxide, aKATP<\/jats:sub><\/jats:styled-content>activator, inhibitedPACAP<\/jats:styled-content>\u2010 andPACAP\u00a0<\/jats:styled-content>+\u00a0glyburide\u2010stimulatedVEGF<\/jats:styled-content>secretion but not that of glyburide alone. These data suggest thatKATP<\/jats:sub><\/jats:styled-content>channels are expressed byFS<\/jats:styled-content>cells and play a significant role in the control ofVEGF<\/jats:styled-content>secretion, and also that activation ofKATP<\/jats:sub><\/jats:styled-content>channels inhibits the secretion ofVEGF<\/jats:styled-content>at the level of transcription.<\/jats:p>","DOI":"10.1111\/jne.12117","type":"journal-article","created":{"date-parts":[[2013,10,31]],"date-time":"2013-10-31T16:35:54Z","timestamp":1383237354000},"page":"111-120","source":"Crossref","is-referenced-by-count":5,"title":["Vascular Endothelial Growth Factor Secretion from Pituitary Folliculostellate Cells: Role ofKATP<\/sub><\/scp>Channels"],"prefix":"10.1111","volume":"26","author":[{"given":"J.","family":"Budzik","sequence":"first","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford Oxford UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Omer","sequence":"additional","affiliation":[{"name":"Department of Physiology, Anatomy and Genetics University of Oxford Oxford UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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