Strain-induced collagen denaturation is rate dependent in failure of cerebral arteries
Strain-induced collagen denaturation is rate dependent in failure of cerebral arteries
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应变诱导的胶原变性与脑动脉衰竭的速率相关
DOI：
10.1016/j.actbio.2023.04.032
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发表时间：
2023
影响因子：
9.7
通讯作者：
Monson, Kenneth L.
中科院分区：
文献类型：
--
作者：
Anderl, William J.;Pearson, Noah;Converse, Matthew I.;Yu, S. Michael;Monson, Kenneth L.
虽然软组织通常受到机械负荷的损伤，但这种损伤在微观结构水平上的表现尚未完全了解。具体而言，虽然率诱导硬化已被观察到在脑动脉，相关的变化，高速率负荷后的微观结构损伤模式在很大程度上是不确定的。在这项研究中，我们在0.01和>150 s-1时拉伸猪大脑中动脉，使其轴向和周向失效，然后使用胶原杂交肽（CHP）探测变性原胶原。我们发现，胶原纤维对齐的负载方向经历了较少的变性后，失败的测试在高比低的利率。其他人已经证明了软组织衰竭期间原胶原蛋白变性的相似速率依赖性，但这是第一项使用CHP量化这种行为并报告脑动脉的研究。这些发现可能对创伤性脑损伤和颅内球囊血管成形术具有重要意义。我们还观察到可能的原胶原蛋白变性的血管层主要由纤维横向排列的负载轴。据我们所知，这是第一次观察到的胶原变性由于横向加载，但需要进一步的研究来证实这一finding.Statement的意义以前的工作表明，胶原杂交肽（CHP）可以用来识别胶原分子的展开和变性在机械超载的软组织，包括脑动脉。但是实验还没有探索与创伤性脑损伤相关的胶原蛋白损伤率。在这项工作中，我们量化了高速率和低速率下脑动脉拉伸失败的胶原蛋白损伤。我们发现，胶原蛋白分子在高速率下比在低速率下受损更少，这表明胶原蛋白分子或胶原蛋白超结构的其他元素的损伤机制是速率依赖性的。这项工作意味着动脉在高比率下失败，例如在创伤性脑损伤中，将具有与动脉在低比率下失败不同的分子水平损伤模式。因此，未来可能会扩大对损伤特征的更好理解，以更好地告知胶原蛋白损伤的临床相关病例，如血管成形术和损伤愈合。
While soft tissues are commonly damaged by mechanical loading, the manifestation of this damage at the microstructural level is not fully understood. Specifically, while rate-induced stiffening has been previously observed in cerebral arteries, associated changes in microstructural damage patterns following high-rate loading are largely undefined. In this study, we stretched porcine middle cerebral arteries to failure at 0.01 and >150 s−1, both axially and circumferentially, followed by probing for denatured tropocollagen using collagen hybridizing peptide (CHP). We found that collagen fibrils aligned with the loading direction experienced less denaturation following failure tests at high than low rates. Others have demonstrated similar rate dependence in tropocollagen denaturation during soft tissue failure, but this is the first study to quantify this behavior using CHP and to report it for cerebral arteries. These findings may have significant implications for traumatic brain injury and intracranial balloon angioplasty. We additionally observed possible tropocollagen denaturation in vessel layers primarily composed of fibrils transversely aligned to the loading axis. To our knowledge, this is the first observation of collagen denaturation due to transverse loading, but further research is needed to confirm this finding.Statement of significancePrevious work shows that collagen hybridizing peptide (CHP) can be used to identify collagen molecule unfolding and denaturation in mechanically overloaded soft tissues, including the cerebral arteries. But experiments have not explored collagen damage at rates relevant to traumatic brain injury. In this work, we quantified collagen damage in cerebral arteries stretched to failure at both high and low rates. We found that the collagen molecule is less damaged at high than at low rates, suggesting that damage mechanisms of either the collagen molecule or other elements of the collagen superstructure are rate dependent. This work implies that arteries failed at high rates, such as in traumatic brain injury, will have different molecular-level damage patterns than arteries failed at low rates. Consequently, improved understanding of damage characteristics may be expanded in the future to better inform clinically relevant cases of collagen damage such as angioplasty and injury healing.