2014年1月16日 訊 /生物谷BIOON/ --紅細胞在機體中可以隨意變換形狀，其或許是所有類型細胞中最具有延展性的了，近日，來自賓夕法尼亞大學等處的研究人員通過研究發現，當機體血塊形成過程中紅細胞被壓縮後會形成一種新的幾何學結構，相關研究成果刊登於國際雜誌Blood上。
儘管研究人員在17世紀中期首次觀察到了紅細胞的形態，然而這項研究描述了此前科學家並未見到過的一種紅細胞形態，這就為了解紅細胞的潛在功能提供了一定思路。
文章中，研究者發現，紅細胞可以被壓縮成多面緊密包裹的多面體結構；通常當組織損傷後，血塊需要形成合適硬度來阻止血液流動，一旦血塊形成，血小板上的肌動蛋白和肌球蛋白就會開啟收縮過程從而促使血塊收縮到原來尺寸的三分之一，這是阻止流血發生的一個重要階段，而且這也可以降低對血管的損傷。
目前研究者並不清楚在收縮過程中收縮的凝塊的結構以及紅細胞在其中的作用，研究者Weisel表示，我們發現收縮的血塊可以產生一種明顯的結構，而在血塊外部存在一種纖維蛋白的網狀結構以及會發生血小板聚集。
當血凝開始後研究者就可以觀察到血塊的形態學結構，研究者表示，這項研究對於臨床上具有重要意義，臨床醫生們需要注射血栓溶解劑比如tPA來快速打碎阻斷血流的血栓和凝塊，常見的例子就是治療心臟病過程中，或者是中風。隨著時間延長，血栓慢慢產生抗性，這也就是為何進行早期的幹預措施非常重要了，當然血塊的收縮或許是一個潛在的幹預靶點來幫助抑制患者疾病的發生。（生物谷Bioon.com）
Clot contraction: compression of erythrocytes into tightly packed polyhedra and redistribution of platelets and fibrin
Douglas B. Cines1, Tatiana Lebedeva1, Chandrasekaran Nagaswami2, Vincent Hayes3, Walter Massefski4, Rustem I. Litvinov2, Lubica Rauova5, Thomas J. Lowery4, and John W. Weisel2,*
Contraction of blood clots is necessary for hemostasis, wound healing and to restore flow past obstructive thrombi, but little has been known about the structure of contracted clots or the role of erythrocytes in contraction. We found that contracted blood clots develop a remarkable structure, with a meshwork of fibrin and platelet aggregates on the exterior of the clot and a close-packed, tessellated array of compressed polyhedral erythrocytes within. The same results were obtained after initiation of clotting with various activators and also with clots from reconstituted human blood and mouse blood. Such close-packed arrays of polyhedral erythrocytes, or polyhedrocytes, were also observed in human arterial thrombi taken from patients. The mechanical nature of this shape change was confirmed by polyhedrocyte formation from the forces of centrifugation of blood without clotting. Platelets (with their cytoskeletal motility proteins) and fibrin(ogen) (as the substrate bridging platelets for contraction) are required to generate the forces necessary to segregate platelets/fibrin from erythrocytes and to compress erythrocytes into a tightly packed array. These results demonstrate how contracted clots form an impermeable barrier important for hemostasis and wound healing and help explain how fibrinolysis is greatly retarded as clots contract.