胶原原纤维片段转位在早期内源性肌腱修复中起作用的证据。
Evidence that translocation of collagen fibril segments plays a role in early intrinsic tendon repair.
机构信息
Hershey, Pa. From the Division of Plastic Surgery, The Pennsylvania State University, College of Medicine.
出版信息
Plast Reconstr Surg. 2012 Feb;129(2):300e-306e. doi: 10.1097/PRS.0b013e31823aeb5a.
BACKGROUND
Severed tendon repair advances with either a scar through extrinsic repair or regeneration through intrinsic repair. The authors examined whether intrinsic tendon repair reintroduces embryonic fibrillogenesis, whereby preformed collagen fibril segments are incorporated into growing collagen fibers at wound edges.
METHODS
Isolated tendons from 10-day-old chicken embryos were suspended in 1 mg/ml of the antibiotic gentamicin for 90 days, which released fibril segments that were fluorescently tagged with rhodamine. Tendons isolated from 14-day-old chicken embryos were wounded to half their diameter and then maintained as explants in stationary organ culture. Fluorescent-tagged fibril segments were introduced to wounded tendon explants in the presence of high concentrations of neomycin, an antibiotic; cycloheximide, a protein synthesis inhibitor; cytochalasin D, a disruptor of microfilaments; and colchicine, a disruptor of microtubules. At 24 hours, explants were viewed by means of fluorescent microscopy.
RESULTS
Untreated, wounded tendon explants showed the translocation of fluorescent-tagged fibril segments from the explant surface to accumulation at wound edges. In the presence of high concentrations of neomycin, cytochalasin D, or colchicine, fluorescent-tagged fibril segments failed to accumulate at wound edges and were retained on the explant surface. Inhibition of protein synthesis by cycloheximide did not alter the accumulation of fluorescent-tagged fibril segments at wound edges.
CONCLUSIONS
Inhibiting fluorescent-tagged fibril segment accumulation by antibiotics is consistent with their role in releasing fibril segments. Experimental findings show fibril segment translocation and accumulation at wound edges involves microfilaments and microtubules, but not protein synthesis. The experiments support the hypothesis that intrinsic tendon repair advances through the incorporation of fibril segments at wound edges.
背景
肌腱断裂的修复方式有两种，一种是通过外在修复形成疤痕，另一种是通过内在修复实现再生。作者研究了内在肌腱修复是否会重新引入胚胎原纤维发生，即在伤口边缘将预先形成的胶原原纤维段整合到正在生长的胶原纤维中。
方法
将 10 日龄鸡胚的分离肌腱在 1mg/ml 的抗生素庆大霉素中孵育 90 天，释放出用罗丹明标记的荧光原纤维段。将 14 日龄鸡胚的分离肌腱切断至其直径的一半，并作为组织块在静态器官培养中维持。在高浓度新霉素（一种抗生素）、细胞松弛素 D（一种破坏微丝的物质）和秋水仙素（一种破坏微管的物质）存在的情况下，将荧光标记的原纤维段引入受伤的肌腱组织块中。24 小时后，通过荧光显微镜观察组织块。
结果
未处理的、受伤的肌腱组织块显示荧光标记的原纤维段从组织块表面转移到伤口边缘的聚集。在高浓度新霉素、细胞松弛素 D 或秋水仙素存在的情况下，荧光标记的原纤维段未能在伤口边缘聚集，而是保留在组织块表面。用细胞松弛素 D 抑制蛋白质合成并不改变荧光标记的原纤维段在伤口边缘的聚集。
结论
抗生素抑制荧光标记的原纤维段聚集与其释放原纤维段的作用一致。实验结果表明，原纤维段的转移和在伤口边缘的聚集涉及微丝和微管，但不涉及蛋白质合成。这些实验支持内在肌腱修复是通过在伤口边缘整合原纤维段来推进的假设。
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