Hammersen F
Beitr Pathol. 1976 May;157(4):327-48. doi: 10.1016/s0005-8165(76)80049-2.
The rather old conception that endothelial cells possess an autonomous contractile capability has been reevaluated by several suthors during the past ten years on the basis of three different arguments of various validity: (1) After the topical application of inflammatory mediators tmajno et al. regularly found the endothelial nuclei furnished with numerous identations together with many interendothelial "gaps"; Both findings are assumed to be the morphological correlate of an endothelial shortening due to the contraction of the cells. While nuclear indentations seemed to be a rather weak argument to substantiate contractile capabilities, a mechanism other than contraction is outlined for the formation of "gaps"; (2) The second argument in favour of endothelial contractility is the occurrence of cytoplasmic filaments that occasionally form cross striated bundles and/or show a "thick" and "thin" variety. If all these data are assumed to be the morphological evidence for the contractile capability of cells then the conclusion: the more filaments the higher the contractile activity, must be valid. But when compiling those endothelia that are particularly rich in filaments this conclusion does not make sense, because e.g. the endothelium covering the venous valves is crowded with filaments yet an especially high "contractile activity" does not seem very probabble. On the other hand, the supposition that endothelial conttractility is entirely independent of the existence of cytoplasmic filaments leaves the question unanswered what then are the filaments for if not serving mechanical purposes. This line of reasoning is supported by both the localization of the filaments predominantly in those endothelia that have to sustain higher degrees of various mechanical stresses and the fact that filamentous structures significatnly increase in number under the influence of hypertension. (3) The final argument brought forward to substantiate endothelial contractility is the demonstration of actin and tropomyosin in the endothelium of various types of blood vessels that also occur under the influence of hypertension; tbut the significance of these findings as a proof for endothelial contractility is curtailed by the fact that the occurrence of actin alone is not conclusive for any contractile capabilities; Furthermore, a convincing demonstration of myosin in endothelial cells is still lacking and the "thick" filaments are believed to be noncontractile. Hence we suggest that the endothelial filaments together with the myoid proteins do not serve as a means for "contractility" in a true sense but simply act as a design to originate tensile strength.
在过去十年中，有几位作者基于三种不同但有效性各异的论据，对内皮细胞具有自主收缩能力这一相当陈旧的概念进行了重新评估：（1）在局部应用炎症介质后，Tmajno等人经常发现内皮细胞核有许多凹陷，以及许多内皮间“间隙”；这两个发现都被认为是细胞收缩导致内皮缩短的形态学相关表现。虽然核凹陷似乎是支持收缩能力的一个相当薄弱的论据，但对于“间隙”的形成提出了一种不同于收缩的机制；（2）支持内皮收缩性的第二个论据是细胞质细丝的存在，这些细丝偶尔会形成横纹束和/或呈现“粗”和“细”的不同形态。如果所有这些数据都被假定为细胞收缩能力的形态学证据，那么“细丝越多，收缩活性越高”这一结论必然成立。但在汇总那些细丝特别丰富的内皮细胞时，这个结论却不合理，因为例如覆盖静脉瓣膜的内皮细胞充满了细丝，但似乎并没有特别高的“收缩活性”。另一方面，假设内皮收缩性完全独立于细胞质细丝的存在，那么就留下了一个未解决的问题：如果这些细丝不是用于机械目的，那它们是干什么用的呢？这种推理思路得到了以下两方面的支持：细丝主要定位于那些必须承受更高程度各种机械应力的内皮细胞中，以及在高血压影响下丝状结构数量显著增加这一事实。（3）为证实内皮收缩性而提出的最后一个论据是，在各种类型血管的内皮中都证明了肌动蛋白和原肌球蛋白的存在，而且它们在高血压影响下也会出现；但这些发现作为内皮收缩性证据的意义因以下事实而受限：仅肌动蛋白的存在并不能确凿证明任何收缩能力；此外，在内皮细胞中仍缺乏令人信服的肌球蛋白证明，而且“粗”细丝被认为是无收缩性的。因此，我们认为内皮细丝连同类肌蛋白并非真正意义上用于“收缩”的手段，而仅仅是一种产生抗张强度的结构设计。
