Ehrlich H P, Rittenberg T
Section of Plastic and Reconstructive Surgery, Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA.
J Cell Physiol. 2000 Dec;185(3):432-9. doi: 10.1002/1097-4652(200012)185:3<432::AID-JCP14>3.0.CO;2-R.
The free-floating fibroblast-populated collagen lattice (FPCL) model introduced by Bell contains 0.5 x 10(5) cell/ml and here is defined as a moderate-density FPCL (MD-FPCL). One modification of the model is to increase the cell density by a factor of 10, where 5 x 10(5) cells/ml defines a high-density FPCL (HD-FPCL). The initial detection of HD-FPCL contraction is 2 h, whereas MD-FPCL is later, 6 h. A contracted HD-FPCL has a doughnut-like appearance, due to the high density of cells accumulating at the periphery. A contracted MD-FPCL is a flattened disc. The compacted collagen of MD-FPCL lattice exhibits a strong birefringence pattern due to organized collagen fiber bundles. In contracted HD-FPCL, a minimal birefringence develops, indicating minimal organization of collagen fiber bundles. MD-FPCL contraction was reduced with less than 10% serum; the disruption of microtubules, uncoupling of gap junctions, inhibition of tyrosine kinases, and addition of a blocking antibody to alpha2beta1 collagen integrin. Making HD-FPCL with only 1% serum or including the inhibitory agents had only minimal affect on lattice contraction. On the other hand, platelet-derived growth factor stimulated HD-FPCL contraction but had no influence on MD-FPCL contraction. It is suggested that the mechanism for HD-FPCL contraction is limited to the process of cells spreading. HD-FPCL contraction is independent of collagen organization, microtubules, gap junctions, alpha2beta1 integrin, and tyrosine phosphorylation. MD-FPCL contraction involves collagen organization and is optimized by the involvement of microtubules, gap junctions, alpha2beta1 integrin, and tyrosine phosphorylation. When studying cell physiology in a collagen matrix, cell-density influences need to be considered.
贝尔提出的游离漂浮成纤维细胞填充胶原晶格（FPCL）模型含有0.5×10⁵个细胞/毫升，在此被定义为中等密度FPCL（MD - FPCL）。该模型的一种改进是将细胞密度提高10倍，其中5×10⁵个细胞/毫升定义为高密度FPCL（HD - FPCL）。HD - FPCL收缩的初始检测时间为2小时，而MD - FPCL则较晚，为6小时。收缩后的HD - FPCL呈甜甜圈状外观，这是由于细胞在外围高密度聚集所致。收缩后的MD - FPCL是扁平圆盘状。MD - FPCL晶格压实的胶原由于有组织的胶原纤维束而呈现出强烈的双折射模式。在收缩的HD - FPCL中，仅产生最小程度的双折射，表明胶原纤维束的组织程度最低。血清含量低于10%时，MD - FPCL的收缩会减弱；微管的破坏、间隙连接的解偶联、酪氨酸激酶的抑制以及添加针对α2β1胶原整合素的阻断抗体也会导致其收缩减弱。用仅含1%血清制作HD - FPCL或加入抑制剂对晶格收缩仅有极小的影响。另一方面，血小板衍生生长因子刺激HD - FPCL收缩，但对MD - FPCL收缩没有影响。有人提出，HD - FPCL收缩的机制仅限于细胞铺展过程。HD - FPCL收缩独立于胶原组织、微管、间隙连接、α2β1整合素和酪氨酸磷酸化。MD - FPCL收缩涉及胶原组织，并且通过微管、间隙连接、α2β1整合素和酪氨酸磷酸化的参与而得到优化。在研究胶原基质中的细胞生理学时，需要考虑细胞密度的影响。
