PROTEOLYTIC ACTIVITY OF SPECIALIZED SURFACE PROTRUSIONS FORMED AT ROSETTE CONTACT SITES OF TRANSFORMED-CELLS
PROTEOLYTIC ACTIVITY OF SPECIALIZED SURFACE PROTRUSIONS FORMED AT ROSETTE CONTACT SITES OF TRANSFORMED-CELLS
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DOI：
10.1002/jez.1402510206
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发表时间：
1989-08-01
影响因子：
--
通讯作者：
CHEN, WT
中科院分区：
文献类型：
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作者：
CHEN, WT
运动细胞前缘的表面突起与周围的细胞外基质（ECM）接触，是其运动和侵袭的主要动力。如干涉反射显微镜（TEM）所示，由劳斯肉瘤病毒（RSV-CEF）转化的鸡胚胎成纤维细胞在平面基质上形成专门的膜玫瑰花状接触部位。正常细胞缺乏这种活性。这些玫瑰花结接触比其他粘连部位（如局灶性和密切接触）更不稳定。超微结构的研究表明，roeps是网站的膜突起从腹侧细胞表面接触的基质。这些突起充满了微丝的网状结构，含有pp 60 srconcogene产物、肌动蛋白、黏着斑蛋白和α-辅肌动蛋白。然而，与焦点接触不同，在roadly这些蛋白质相互作用，以延长高度能动的膜。玫瑰花结具有降解ECM成分的生物学活性，表现为：（1）在玫瑰花结接触部位，而非局灶性和密切接触部位，纤维连接蛋白基质局部降解;（2）在玫瑰花结接触部位，而非局灶性和密切接触部位，推定的抗蛋白酶抗体定位;（3）透射电子显微镜（TEM）观察到纤连蛋白基质在扩张活性部位的局部破坏。此外，玫瑰花结接触的形成对离子载体莫能菌素和蛋白水解酶抑制剂不敏感，而玫瑰花结接触处的局部纤连蛋白降解被金属蛋白酶抑制剂1，10-菲咯啉和NP-20抑制。我认为RSV转化细胞中玫瑰花结接触的这些膜突起是专门的结构实体-侵入伪足-参与ECM的局部降解。
Surface protrusions at the leading edge of a moving cell that make contact with the surrounding extracellular matrix (ECM) are its main motor for locomotion and invasion. Chicken embryonic fibroblasts transformed by Rous sarcoma virus (RSV‐CEF) form specialized membrane rosette‐shaped contact sites on planar substrata as shown by interference reflection microscopy (IRM). Such activity is lacking in normal cells. These rosette contacts are more labile than other adhesion sites, such as focal and close contacts. Ultrastructural studies demonstrate that rosettes are sites at which membrane protrusions from the ventral cell surface contact the substratum. These protrusions are filled with meshworks of microfilaments and contain the pp60srconcogene product, actin, vinculin, and α‐actinin. However, unlike focal contacts, at the rosettes these proteins interact to extend a highly motile membrane. Rosettes have the biological activity of degrading ECM components, as demonstrated by (1) local degradation of fibronectin substrata at sites of rosette contacts, but not focal and close contacts; (2) localization of putative antiprotease antibody at sites of rosette contacts, but not at focal an close contacts; and (3) local disruption of fibronectin matrix at sites of protrusive activity seen by transmission electron microscopy (TEM). In addition, formation of the rosette contact is insensitive to the ionophore monensin, and to inhibitors of proteolytic enzymes, while local fibronectin degradation at rosette contacts is inhibited by inhibitors of metalloproteases, 1,10‐phenanthroline and NP‐20. I consider these membrane protrusions of the rosette contacts in RSV‐transformed cells specialized structural entities—invadopodia—that are involved in the local degradation of the ECM.