生物谷Bioon.com 訊 8月6日,，重慶大學生物工程學院鄧林紅教授實驗室與美國哈佛大學合作實驗室在PLoS ONE上發(fā)表論文，揭示機械拉伸引發(fā)細胞流態(tài)化響應的內(nèi)在機制,。
該合作研究是鄧林紅教授與哈佛大學合作者繼2007年在Nature上發(fā)表有關機械拉伸引起細胞流態(tài)化響應論文后的進一步深化,。（Xavier Trepat,Linhong Deng et al.Universal physical responses to stretch in the living cell.Nature. doi:10.1038/nature05824）。2007年發(fā)表在Nature上的論文首次提出了活細胞在收到短暫機械牽張之后會迅速軟化并向流體狀態(tài)轉(zhuǎn)化,，隨后又逐漸恢復到拉伸前的狀態(tài),。這一現(xiàn)象在各種細胞和生化環(huán)境下具有普遍性，因此對于理解細胞的物理行為和相關生理病理現(xiàn)象具有十分重要的意義,。但該現(xiàn)象的內(nèi)在機制仍然沒有得到完全的揭示,。
該文章第一作者陳誠等利用細胞牽張力顯微測量技術，磁微粒扭轉(zhuǎn)細胞流變測量技術等細胞力學領域先進技術動態(tài)觀測了人體膀胱平滑肌細胞在受到短暫的機械牽張后,，其細胞硬度,、細胞牽張力、以及細胞骨架形態(tài)的變化,。實驗結(jié)果表明,，膀胱平滑肌細胞在受到短暫牽張之后迅速"液化"，然后緩慢的"再固化",，逐漸恢復到拉伸前的狀態(tài),。更為重要的是，由于短暫拉伸持續(xù)的時間非常短，細胞發(fā)生的所有物理相應過程并不是通過細胞內(nèi)部的生物化學信號通路調(diào)控的,，而是通過細胞骨架的纖維型肌動蛋白（F-actin）的迅速分解和緩慢再重組來實現(xiàn)和調(diào)控的,。
論文不僅采用人體內(nèi)另一種同樣收到機械牽張力的影響的膀胱平滑肌細胞進一步證實了細胞在受到短暫拉伸后迅速發(fā)生流態(tài)化與緩慢恢復的普遍性，并且找出首次觀測到了F-actin在其中扮演的關鍵作用,，部分揭示了此現(xiàn)象的內(nèi)在物理調(diào)控機制,。
隨著現(xiàn)代細胞生物學和細胞動力學的共同發(fā)展，機械力和物理環(huán)境如何對細胞結(jié)構和功能發(fā)生影響并決定許多重大生命活動過程的謎團正在被逐步打開,。因此,，在對細胞進行傳統(tǒng)的生物分析和化學分析的同時，系統(tǒng)地研究細胞的物理環(huán)境和受力情況以及相應的細胞行為規(guī)律,，將對更準確,、更深入地理解細胞的運作機制、為細胞生理學和病理學的研究提供新的啟發(fā)和思路,。（生物谷Bioon.com）
生物谷推薦英文摘要：
PLoS ONE doi:10.1371/journal.pone.0012035
Fluidization and Resolidification of the Human Bladder Smooth Muscle Cell in Response to Transient Stretch
Cheng Chen1,2#, Ramaswamy Krishnan2#, Enhua Zhou2, Aruna Ramachandran3, Dhananjay Tambe2, Kavitha Rajendran2, Rosalyn M. Adam3, Linhong Deng1,2*, Jeffrey J. Fredberg2
1 Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing, China, 2 Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, United States of America, 3 Urological Diseases Research Center, Department of Urology, Children's Hospital Boston and Department of Surgery, Harvard Medical School, Boston, Massachusetts, United States of America
Abstract
Background：Cells resident in certain hollow organs are subjected routinely to large transient stretches, including every adherent cell resident in lungs, heart, great vessels, gut, and bladder. We have shown recently that in response to a transient stretch the adherent eukaryotic cell promptly fluidizes and then gradually resolidifies, but mechanism is not yet understood.
Principal Findings：In the isolated human bladder smooth muscle cell, here we applied a 10% transient stretch while measuring cell traction forces, elastic modulus, F-actin imaging and the F-actin/G-actin ratio. Immediately after a transient stretch, F-actin levels and cell stiffness were lower by about 50%, and traction forces were lower by about 70%, both indicative of prompt fluidization. Within 5min, F-actin levels recovered completely, cell stiffness recovered by about 90%, and traction forces recovered by about 60%, all indicative of resolidification. The extent of the fluidization response was uninfluenced by a variety of signaling inhibitors, and, surprisingly, was localized to the unstretch phase of the stretch-unstretch maneuver in a manner suggestive of cytoskeletal catch bonds. When we applied an "unstretch-restretch" (transient compression), rather than a "stretch-unstretch" (transient stretch), the cell did not fluidize and the actin network did not depolymerize.
Conclusions：Taken together, these results implicate extremely rapid actin disassembly in the fluidization response, and slow actin reassembly in the resolidification response. In the bladder smooth muscle cell, the fluidization response to transient stretch occurs not through signaling pathways, but rather through release of increased tensile forces that drive acute disassociation of actin.
