{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T07:24:21Z","timestamp":1790148261979,"version":"4.0.1"},"reference-count":57,"publisher":"American Diabetes Association","issue":"2","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2008,2,1]]},"abstract":"<jats:p>OBJECTIVE\u2014 Aggregation of human amylin (hA) into \u03b2-sheet\u2013containing oligomers is linked to islet \u03b2-cell dysfunction and the pathogenesis of type 2 diabetes. Here, we investigated possible contributions of Fas-associated death-receptor signaling to the mechanism of hA-evoked \u03b2-cell apoptosis.<\/jats:p>\n                  <jats:p>RESEARCH DESIGN AND METHODS\u2014 We measured responses to hA in isolated mouse islets and two insulinoma cell lines, wherein we measured Fas\/Fas ligand (FasL) and Fas-associated death domain (FADD) expression by quantitative RT-PCR, Western blotting, and immunofluorescence staining. We used two anti-Fas\/FasL blocking antibodies and the Fas\/FasL antagonist Kp7\u20136 to probe roles of Fas interactions in the regulation of apoptosis in hA-treated \u03b2-cells and measured Kp7\u20136\u2013mediated effects on \u03b2-sheet formation and aggregation using circular dichroism and thioflavin-T binding.<\/jats:p>\n                  <jats:p>RESULTS\u2014 hA treatment stimulated Fas and FADD expression in \u03b2-cells. Both blocking antibodies suppressed hA-evoked apoptosis but did not modify its aggregation. Therefore, Fas receptor interactions played a critical role in induction of this pathway. Interestingly, hA-evoked \u03b2-cell apoptosis was suppressed and rescued by Kp7\u20136, which also impaired hA \u03b2-sheet formation.<\/jats:p>\n                  <jats:p>CONCLUSIONS\u2014 This is the first report linking hA-evoked induction and activation of Fas and FADD to \u03b2-cell apoptosis. We have identified a Fas\/FasL antagonist, Kp7\u20136, as a potent inhibitor of hA aggregation and related \u03b2-cell death. These results also support an interaction between hA and Fas on the surface of apoptotic \u03b2-cells. Increased expression and activation of Fas in \u03b2-cells could constitute a molecular event common to the pathogenesis of both type 1 and type 2 diabetes, although the mode of pathway activation may differ between these common forms of diabetes.<\/jats:p>","DOI":"10.2337\/db07-0849","type":"journal-article","created":{"date-parts":[[2007,10,31]],"date-time":"2007-10-31T20:54:28Z","timestamp":1193864068000},"page":"348-356","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":60,"title":["Fas-Associated Death Receptor Signaling Evoked by Human Amylin in Islet \u03b2-Cells"],"prefix":"10.2337","volume":"57","author":[{"given":"Shaoping","family":"Zhang","sequence":"first","affiliation":[{"name":"School of Biological Sciences, Faculty of Science, University of Auckland, Auckland, New Zealand"},{"name":"Maurice Wilkins Centre for Molecular BioDiscovery, University of Auckland, Auckland, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Liu","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, Faculty of Science, University of Auckland, Auckland, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Yu","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, Faculty of Science, University of Auckland, Auckland, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Garth J.S.","family":"Cooper","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, Faculty of Science, University of Auckland, Auckland, New Zealand"},{"name":"Maurice Wilkins Centre for Molecular BioDiscovery, University of Auckland, Auckland, New Zealand"},{"name":"Medical Research Council Immunochemistry Unit, Department of Biochemistry, University of Oxford, Oxford, U.K"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","reference":[{"key":"2022031207591594500_R1","doi-asserted-by":"crossref","unstructured":"Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC: \u03b2-Cell deficit and increased \u03b2-cell apoptosis in humans with type 2 diabetes. 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