A mechanical design principle for tissue structure and function in the airway tree.
A mechanical design principle for tissue structure and function in the airway tree.
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DOI：
10.1371/journal.pcbi.1003083
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发表时间：
2013
影响因子：
4.3
通讯作者：
Suki B
中科院分区：
文献类型：
--
作者：
LaPrad AS;Lutchen KR;Suki B
每次呼吸时，动态变化的机械压力必须与肺细胞和软组织结构协调一致，以使空气有效地穿过气道树并在肺泡中进行气体交换。力学对细胞和组织功能的影响越来越明显，这就提出了一个问题：气道树如何在其机械环境中共存，以维持其分支结构中正常的细胞功能？我们为导气管树引入了一种新的机械设计原则，其中细胞水平的机械转导被驱动来协调气道壁结构变化，从而最好地维持首选的机械微环境。为了支持这一原则，我们报告了从健康牛肺中获得的一系列气道半径的体外半径-跨壁压力关系，并使用应变能函数和厚壁圆柱体描述对数据进行建模。从这个框架中，我们估计了整个气道树的周向应力和增量杨氏模量。我们的研究结果表明，传导气道始终在一种首选的机械稳态状态下运行，称为机械稳态，其特征是圆周应力和杨氏模量的范围很窄。通过气道壁尺寸和机械关系，整个树的所有气道都维持这种机械稳态。因此，整个气道树的气道壁内的细胞在呼吸过程中经历类似的振荡应变，比以前认为的要小得多。最后，我们讨论了在促进成熟所需的健康组织水平改变的同时，机械稳态的维持如何可能导致气道壁结构改变，从而导致慢性哮喘的潜在影响。每次呼吸时，肺部的机械压力都会发生变化，从而使空气有效地通过气道树并进行气体交换。这些压力变化也会影响细胞和组织的功能，这就提出了一个问题：气道树如何在其机械环境中共存，以维持其分支结构中正常的细胞功能？我们为导气管树引入了一种新的机械设计原则，其中机械转导，将细胞上的机械力转化为生化信号的过程，被驱动来协调组织水平的结构变化，从而最好地恢复首选的机械微环境；一个被称为机械内稳态的概念。我们报告了一系列气道尺寸的体外机械性能，并提出了一个描述数据的数学模型。我们的研究结果表明，气道确实始终在首选的机械稳态状态下运行。我们进一步描述了在促进成熟所必需的健康组织水平改变的同时，这种机械稳态如何无意中导致气道壁结构改变，从而导致慢性哮喘。
With every breath, the dynamically changing mechanical pressures must work in unison with the cells and soft tissue structures of the lung to permit air to efficiently traverse the airway tree and undergo gas exchange in the alveoli. The influence of mechanics on cell and tissue function is becoming apparent, raising the question: how does the airway tree co-exist within its mechanical environment to maintain normal cell function throughout its branching structure of diminishing dimensions? We introduce a new mechanical design principle for the conducting airway tree in which mechanotransduction at the level of cells is driven to orchestrate airway wall structural changes that can best maintain a preferred mechanical microenvironment. To support this principle, we report in vitro radius-transmural pressure relations for a range of airway radii obtained from healthy bovine lungs and model the data using a strain energy function together with a thick-walled cylinder description. From this framework, we estimate circumferential stresses and incremental Young's moduli throughout the airway tree. Our results indicate that the conducting airways consistently operate within a preferred mechanical homeostatic state, termed mechanical homeostasis, that is characterized by a narrow range of circumferential stresses and Young's moduli. This mechanical homeostatic state is maintained for all airways throughout the tree via airway wall dimensional and mechanical relationships. As a consequence, cells within the airway walls throughout the airway tree experience similar oscillatory strains during breathing that are much smaller than previously thought. Finally, we discuss the potential implications of how the maintenance of mechanical homeostasis, while facilitating healthy tissue-level alterations necessary for maturation, may lead to airway wall structural changes capable of chronic asthma. With every breath, mechanical pressures change in the lung and permit air to efficiently traverse the airway tree and undergo gas exchange. These pressure variations also influence cell and tissue function, raising the question: how does the airway tree co-exist within its mechanical environment to maintain normal cell function throughout its branching structure of diminishing dimensions? We introduce a new mechanical design principle for the conducting airway tree in which mechanotransduction, the process that converts mechanical forces on cells to biochemical signals, is driven to orchestrate tissue-level structural changes that can best restore a preferred mechanical microenvironment; a concept termed mechanical homeostasis. We report in vitro mechanical properties for a range of airway sizes and present a mathematical model that describes the data. Our results indicate that airways indeed consistently operate within a preferred mechanical homeostatic state. We further describe how this mechanical homeostasis while facilitating healthy tissue-level alterations necessary for maturation can inadvertently lead to airway wall structural changes capable of chronic asthma.
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影响因子：
3.3
作者：
LAMBERT, RK;WILSON, TA;RODARTE, JR
通讯作者：
RODARTE, JR
影响因子：
3.3
作者：
Noble, Peter B.;Jones, Robyn L.;McFawn, Peter K.
通讯作者：
McFawn, Peter K.
影响因子：
64.8
作者：
Mauroy, B;Filoche, M;Sapoval, B
通讯作者：
Sapoval, B
DOI：
10.1115/1.3138417
发表时间：
1983-01-01
影响因子：
1.7
作者：
CHUONG, CJ;FUNG, YC
通讯作者：
FUNG, YC
影响因子：
3.3
作者：
Brown, RH;Mitzner, W
通讯作者：
Mitzner, W