{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T14:59:11Z","timestamp":1788447551432,"version":"build-2803163510"},"reference-count":0,"publisher":"SAGE Publications","issue":"1-4","license":[{"start":{"date-parts":[[2011,12,1]],"date-time":"2011-12-01T00:00:00Z","timestamp":1322697600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Clinical Hemorheology and Microcirculation"],"published-print":{"date-parts":[[2011,12]]},"abstract":"\n There are several reports demonstrating an involvement of bacterial toxins in the rigidity of red blood cells (RBC). The present study investigates the influence of E. coli F-583-Rd lipid A on RBC deformability under mechanical shear stress. Verapamil (Ca\n 2+<\/jats:sup>\n channel inhibitor), staurosporine (protein kinase inhibitor) and Y-27632 (rho-kinase inhibitor) were used to modify the effect of lipid A on RBC deformability. We also determined if E. coli F-583-Rd Lipid A could induce an increase of intracellular Ca\n 2+<\/jats:sup>\n concentration. For the deformation measurements RBC (10 adult donors) were incubated with E. coli F-583-Rd lipid A (100\u03bcg\/ml) and also co-incubated with either verapamil (10\n \u22127<\/jats:sup>\n mol\/l), staurosporine (10\n \u22127<\/jats:sup>\n mol\/l) or Y-27632 (10\n \u22127<\/jats:sup>\n mol\/l). The deformation of the RBC under different shear stresses (0.6\u201360 Pa) was measured by a shear stress diffractometer (Rheodyne SSD). Intracellular Ca\n 2+<\/jats:sup>\n was determinded by flow cytometry in RBC incubated with Lipid A and labeled with fluorescent Fluo-4\/AM which binds intracellular Ca\n 2+<\/jats:sup>\n with high affinity resulting in enhanced green fluorescence intensity. At increasing shear stresses Lipid A induced a significantly lower elongation. Co-incubation of the erythrocytes with verapamil or staurosporine inhibited lipid A induced decrease in elongation while Y-27632 had no effect. Verapamil, Staurosporine and Y-27632 did not influence the elongation response of the cells under control conditions. Lipid A induced a marked increase in fluorescence Fluo-4\/AM indicating increased intracellular Ca\n 2+<\/jats:sup>\n . These results suggest that E. coli F-583-Rd lipid A is able to influence red blood cell rigidity by a rapid and significant increase of intracellular Ca\n 2+<\/jats:sup>\n concentration. Verapamil and staurosporine abolished the decrease in deformability of Lipid A incubated RBC.\n <\/jats:p>","DOI":"10.3233\/ch-2011-1482","type":"journal-article","created":{"date-parts":[[2019,12,2]],"date-time":"2019-12-02T13:07:22Z","timestamp":1575292042000},"page":"315-322","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":8,"title":["Lipid A decreases human erythrocytes deformability by increasing intracellular Ca\n 2+<\/sup>\n : Effects of verapamil, staurosporine and the rho-kinase inhibitor Y-27632"],"prefix":"10.1177","volume":"49","author":[{"given":"P.","family":"Ruef","sequence":"first","affiliation":[{"name":"Clinic of Neonatology, Department of Pediatrics, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Ehrhard","sequence":"additional","affiliation":[{"name":"Clinic of Neonatology, Department of Pediatrics, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Frommhold","sequence":"additional","affiliation":[{"name":"Clinic of Neonatology, Department of Pediatrics, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Koch","sequence":"additional","affiliation":[{"name":"Clinic of Neonatology, Department of Pediatrics, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.","family":"Fritzsching","sequence":"additional","affiliation":[{"name":"Clinic of Neonatology, Department of Pediatrics, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Poeschl","sequence":"additional","affiliation":[{"name":"Clinic of Neonatology, Department of Pediatrics, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,2,26]]},"container-title":["Clinical Hemorheology and Microcirculation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/CH-2011-1482","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/CH-2011-1482","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T15:09:43Z","timestamp":1777388983000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.3233\/CH-2011-1482"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2011,12]]},"references-count":0,"journal-issue":{"issue":"1-4","published-print":{"date-parts":[[2011,12]]}},"alternative-id":["10.3233\/CH-2011-1482"],"URL":"https:\/\/doi.org\/10.3233\/ch-2011-1482","relation":{},"ISSN":["1386-0291","1875-8622"],"issn-type":[{"value":"1386-0291","type":"print"},{"value":"1875-8622","type":"electronic"}],"subject":[],"published":{"date-parts":[[2011,12]]}}}