{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T10:43:18Z","timestamp":1789728198139,"version":"4.0.1"},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,4,4]],"date-time":"2014-04-04T00:00:00Z","timestamp":1396569600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004359","name":"Swedish Research Council","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100005301","name":"Swedish Dental Society","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100005301","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Swedish Patent Revenue fund"},{"name":"foundations of Crafoord, Magnus Bergvall, Lars Hierta, Sven and Lilly Thur\u00e9us"},{"name":"Greta and Johan Kock"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2015,2]]},"abstract":"\n Background and Objective<\/jats:title>\n \n High levels of the antimicrobial peptide,\n LL<\/jats:styled-content>\n \u201037, are detected in gingival crevicular fluid from patients with chronic periodontitis.\n LL<\/jats:styled-content>\n \u201037 not only shows antimicrobial activity but also affects host\u2010cell viability. The objective of the present study was to identify endogenous mechanisms that antagonize the detrimental effects of\n LL<\/jats:styled-content>\n \u201037 on osteoblast viability, focusing on the human peptide p33 expressed on the surface of various cell types.\n <\/jats:p>\n <\/jats:sec>\n \n Material and Methods<\/jats:title>\n \n Human osteoblast\u2010like\n MG<\/jats:styled-content>\n 63 cells and human h\n FOB<\/jats:styled-content>\n 1.19 osteoblasts were treated with or without\n LL<\/jats:styled-content>\n \u201037 in the presence or absence of p33. Recombinant human p33 was expressed in an\n \n E<\/jats:styled-content>\n scherichia coli\n <\/jats:italic>\n expression system. Lactate dehydrogenase (\n LDH<\/jats:styled-content>\n ) was assessed using an enzymatic spectrophotometric assay.\n DNA<\/jats:styled-content>\n synthesis was determined by measuring [\n 3<\/jats:sup>\n H<\/jats:styled-content>\n ]\u2010thymidine incorporation. Cell number was assessed by counting cells in a\n B<\/jats:styled-content>\n \u00fcrker chamber. Intracellular\n C<\/jats:styled-content>\n a\n 2+<\/jats:sup>\n was monitored by recording\n F<\/jats:styled-content>\n luo 4\u2010\n AM<\/jats:styled-content>\n fluorescence using a laser scanning confocal microscope. Cellular expression of p33 was determined by western blotting.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n LL<\/jats:styled-content>\n \u201037 caused a concentration\u2010dependent release of\n LDH<\/jats:styled-content>\n from human osteoblasts, showing a half\u2010maximal response value (\n EC<\/jats:styled-content>\n 50<\/jats:sub>\n ) of 4\u00a0\u03bc\n m<\/jats:sc>\n and a rapid and sustained rise in the intracellular\n C<\/jats:styled-content>\n a\n 2+<\/jats:sup>\n concentration of osteoblasts, suggesting that\n LL<\/jats:styled-content>\n \u201037 forms pores in the cell membrane. p33 (10\u00a0\u03bc\n m<\/jats:sc>\n ) inhibited the\n LL<\/jats:styled-content>\n \u201037\u2010induced\n LDH<\/jats:styled-content>\n release and\n LL<\/jats:styled-content>\n \u201037\u2010evoked rise in intracellular\n C<\/jats:styled-content>\n a\n 2+<\/jats:sup>\n concentration, suggesting that p33 prevents\n LL<\/jats:styled-content>\n \u201037\u2010induced permeabilization of the cell membrane. Moreover, p33 blocked\n LL<\/jats:styled-content>\n \u201037\u2010induced attenuation of osteoblast numbers. Also, mucin antagonized, at concentrations representative for nonstimulated whole saliva,\n LL<\/jats:styled-content>\n \u201037\u2010evoked\n LDH<\/jats:styled-content>\n release, whilst cationic endogenous polyamines had no impact on\n LL<\/jats:styled-content>\n \u201037\u2010induced\n LDH<\/jats:styled-content>\n release from osteoblasts.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n The endogenous peptide p33 prevents\n LL<\/jats:styled-content>\n \u201037\u2010induced reduction of human osteoblast viability. Importantly, this mechanism may protect the osteoblasts from\n LL<\/jats:styled-content>\n \u201037\u2010induced cell damage in patients suffering from chronic periodontitis associated with high levels of LL\u201037 locally.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/jre.12184","type":"journal-article","created":{"date-parts":[[2014,4,4]],"date-time":"2014-04-04T04:03:29Z","timestamp":1396584209000},"page":"80-88","source":"Crossref","is-referenced-by-count":13,"title":["Human endogenous peptide p33 inhibits detrimental effects of\n LL<\/scp>\n \u201037 on osteoblast viability"],"prefix":"10.1111","volume":"50","author":[{"given":"D.","family":"Svensson","sequence":"first","affiliation":[{"name":"Department of Experimental Medical Science Lund University Lund Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Westman","sequence":"additional","affiliation":[{"name":"Division of Infection Medicine Department of Clinical Sciences Lund University Lund 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