Jansa Rado, Sustar Vid, Frank Mojca, Susanj Petra, Bester Janez, Mancek-Keber Mateja, Krzan Mojca, Iglic Ales
Department of Gastroenterology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Blood Cells Mol Dis. 2008 Jul-Aug;41(1):124-32. doi: 10.1016/j.bcmd.2008.01.009. Epub 2008 Apr 1.
It was recently shown that the plasma protein-mediated attractive interaction between phospholipid membranes could in the budding process cause adhesion of the bud to the mother membrane [J. Urbanija, N. Tomsic, M. Lokar, A. Ambrozic, S. Cucnik, M. Kanduser, B. Rozman, A. Iglic, V. Kralj-Iglic, Coalescence of phospholipid membranes as a possible origin of anticoagulant effect of serum proteins, Chem. Phys. Lipids 150 (2007) 49-57]. Since in the in vivo conditions the budding of cell membranes leads to the release of microvesicles into the circulation, a hypothesis was put forward that the ability of plasma to cause adhesion between membranes supresses the microvesiculation process. In the present work, this hypothesis was tested in a population of 19 patients with gastrointestinal diseases. The number of microvesicles in peripheral blood of patients was determined by flow cytometry while the ability of plasma to cause adhesion between membranes was determined by adding patient's plasma to the suspension of giant phospholipid vesicles created by electroformation method, and measuring the average effective angle of contact between the adhered vesicles. Statistically significant negative correlations between the number of microvesicles and the average effective angle of contact (Pearson coefficient -0.50, p=0.031) and between the number of microvesicles per number of platelets and the average effective angle of contact (Pearson coefficient -0.64, p=0.003) were found, which is in favor of the above hypothesis. Patients with gastrointestinal cancer had larger number of microvesicles (difference 140%, statistical significance 0.033) and smaller average effective angle of contact (difference 20%, statistical significance 0.013) compared to patients with other gastrointestinal diseases.
最近的研究表明,血浆蛋白介导的磷脂膜之间的吸引相互作用在出芽过程中可能导致芽与母膜的粘附[J. Urbanija, N. Tomsic, M. Lokar, A. Ambrozic, S. Cucnik, M. Kanduser, B. Rozman, A. Iglic, V. Kralj-Iglic, 磷脂膜的聚结作为血清蛋白抗凝作用的可能起源,《化学与物理脂质》150 (2007) 49 - 57]。由于在体内条件下细胞膜的出芽会导致微泡释放到循环中,因此提出了一个假设,即血浆引起膜间粘附的能力会抑制微泡形成过程。在本研究中,在19例胃肠道疾病患者群体中对这一假设进行了检验。通过流式细胞术测定患者外周血中的微泡数量,同时通过将患者血浆加入电形成法制备的巨型磷脂囊泡悬浮液中,并测量粘附囊泡之间的平均有效接触角,来测定血浆引起膜间粘附的能力。发现微泡数量与平均有效接触角之间(Pearson系数 -0.50,p = 0.031)以及每血小板微泡数量与平均有效接触角之间(Pearson系数 -0.64,p = 0.003)存在统计学上显著的负相关,这支持了上述假设。与其他胃肠道疾病患者相比,胃肠道癌症患者的微泡数量更多(差异140%,统计学显著性0.033),平均有效接触角更小(差异20%,统计学显著性0.013)。