Biophysical journal最新文献

筛选
英文 中文
Mammalian PIEZO channels rectify anionic currents. 哺乳动物的 PIEZO 通道可整流阴离子电流。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-14 DOI: 10.1016/j.bpj.2024.11.010
Tharaka D Wijerathne, Aashish Bhatt, Wenjuan Jiang, Yun L Luo, Jerome J Lacroix
{"title":"Mammalian PIEZO channels rectify anionic currents.","authors":"Tharaka D Wijerathne, Aashish Bhatt, Wenjuan Jiang, Yun L Luo, Jerome J Lacroix","doi":"10.1016/j.bpj.2024.11.010","DOIUrl":"10.1016/j.bpj.2024.11.010","url":null,"abstract":"<p><p>Under physiological conditions, mammalian PIEZO channels (PIEZO1 and PIEZO2) elicit transient currents mostly carried by monovalent and divalent cations. PIEZO1 is also known to permeate chloride ions, with a Cl<sup>-</sup>/Na<sup>+</sup> permeability ratio of about 0.2. Yet, little is known about how anions permeate PIEZO channels. Here, by separately measuring sodium and chloride currents using nonpermanent counterions, we show that both PIEZO1 and PIEZO2 rectify chloride currents outwardly, favoring entry of chloride ions at voltages above their reversal potential, whereas little to no rectification was observed for sodium currents. Interestingly, chloride currents elicited by 9K, an anion-selective PIEZO1 mutant harboring multiple positive residues along intracellular pore fenestrations, also rectify but in the inward direction. Molecular dynamics simulations reveal that the inward rectification of chloride currents in 9K correlates with the presence of a large positive electrostatic potential at intracellular pore fenestrations, suggesting that rectification can be tuned by the electrostatic polarity of the pore. These results demonstrate that the pore of mammalian PIEZO channels inherently rectifies chloride currents.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A continuum model of mechanosensation based on contractility kit assembly. 基于收缩套件组装的连续机械感觉模型
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-08 DOI: 10.1016/j.bpj.2024.10.020
David Dolgitzer, Alma I Plaza-Rodríguez, Miguel A Iglesias, Mark Allan C Jacob, Bethany A Todd, Douglas N Robinson, Pablo A Iglesias
{"title":"A continuum model of mechanosensation based on contractility kit assembly.","authors":"David Dolgitzer, Alma I Plaza-Rodríguez, Miguel A Iglesias, Mark Allan C Jacob, Bethany A Todd, Douglas N Robinson, Pablo A Iglesias","doi":"10.1016/j.bpj.2024.10.020","DOIUrl":"10.1016/j.bpj.2024.10.020","url":null,"abstract":"<p><p>The ability of cells to sense and respond to mechanical forces is crucial for navigating their environment and interacting with neighboring cells. Myosin II and cortexillin I form complexes known as contractility kits (CKs) in the cytosol, which facilitate a cytoskeletal response by accumulating locally at the site of inflicted stress. Here, we present a computational model for mechanoresponsiveness in Dictyostelium, analyzing the role of CKs within the mechanoresponsive mechanism grounded in experimentally measured parameters. Our model further elaborates on the established distributions and channeling of contractile proteins before and after mechanical force application. We rigorously validate our computational findings by comparing the responses of wild-type cells, null mutants, overexpression mutants, and cells deficient in CK formation to mechanical stresses. Parallel in vivo experiments measuring myosin II cortical distributions at equilibrium provide additional validation. Our results highlight the essential functions of CKs in cellular mechanosensitivity and suggest new insights into the regulatory dynamics of mechanoresponsiveness.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Physics of a super-fast viral jab. 超快速病毒注射的物理学原理
IF 4.3 3区 生物学
Biophysical journal Pub Date : 2024-11-07 DOI: 10.1016/j.bpj.2024.11.006
Alex Mogilner
{"title":"Physics of a super-fast viral jab.","authors":"Alex Mogilner","doi":"10.1016/j.bpj.2024.11.006","DOIUrl":"10.1016/j.bpj.2024.11.006","url":null,"abstract":"","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A comprehensive method to analyze single-cell vibrations. 分析单细胞振动的综合方法
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-06 DOI: 10.1016/j.bpj.2024.11.003
Ali Al-Khaz'Aly, Salim Ghandorah, Jared J Topham, Nasir Osman, Taye Louie, Farshad Farshidfar, Matthias Amrein
{"title":"A comprehensive method to analyze single-cell vibrations.","authors":"Ali Al-Khaz'Aly, Salim Ghandorah, Jared J Topham, Nasir Osman, Taye Louie, Farshad Farshidfar, Matthias Amrein","doi":"10.1016/j.bpj.2024.11.003","DOIUrl":"10.1016/j.bpj.2024.11.003","url":null,"abstract":"<p><p>All living cells vibrate depending on metabolism. It has been hypothesized that vibrations are unique for a given phenotype and thereby suitable to diagnose cancer type and stage and to pre-assess the effectiveness of pharmaceutical treatments in real time. However, cells exhibit highly variable vibrational signals, can be subject to environmental noise, and may be challenging to differentiate, having so far limited the phenomenon's applicability. Here, we combined the sensitive method of force spectroscopy using optical tweezers with comprehensive statistical analysis. After data acquisition, the signal was decomposed into its spectral components via fast Fourier transform. Peaks were parameterized and subjected to principal-component analysis to perform an unbiased multivariate statistical evaluation. This method, which we term cell vibrational profiling (CVP), systematically assesses cellular vibrations. To validate the CVP technique, we conducted experiments on five U251 glioblastoma cells, using 8- to 10-μm polystyrene beads as a control for comparison. We collected raw data using optical tweezers, segmenting into 150+ 5-s intervals. Each segment was converted into power spectra representing a frequency resolution of 10,000 Hz for both cells and controls. U251 glioblastoma cells exhibited significant vibrations at 402.6, 1254.6, 1909.0, 2169.4, and 3462.8 Hz (p < 0.0001). This method was further verified with principal-component analysis modeling, which revealed that, in cell-cell comparisons using the selected frequencies, overlap frequently occurred, and clustering was difficult to discern. In contrast, comparison between cell-bead models showed that clustering was easily distinguishable. Our paper establishes CVP as an unbiased, comprehensive technique to analyze cell vibrations. This technique effectively differentiates between cell types and evaluates cellular responses to therapeutic interventions. Notably, CVP is a versatile, cell-agnostic technique requiring minimal sample preparation and no labeling or external interference. By enabling definitive phenotypic assessments, CVP holds promise as a diagnostic tool and could significantly enhance the evaluation of pharmaceutical treatments.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Reversing the understanding of irreversibly sickled cells. 逆转对不可逆镰状细胞的理解。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-05 Epub Date: 2024-08-22 DOI: 10.1016/j.bpj.2024.08.013
Daniel B Kim-Shapiro
{"title":"Reversing the understanding of irreversibly sickled cells.","authors":"Daniel B Kim-Shapiro","doi":"10.1016/j.bpj.2024.08.013","DOIUrl":"10.1016/j.bpj.2024.08.013","url":null,"abstract":"","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":"3653-3654"},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Measuring PETase enzyme kinetics by single-molecule microscopy. 通过单分子显微镜测量 PETase 酶的动力学。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-05 Epub Date: 2024-09-19 DOI: 10.1016/j.bpj.2024.09.016
Yuwei Zhang, William O Hancock
{"title":"Measuring PETase enzyme kinetics by single-molecule microscopy.","authors":"Yuwei Zhang, William O Hancock","doi":"10.1016/j.bpj.2024.09.016","DOIUrl":"10.1016/j.bpj.2024.09.016","url":null,"abstract":"<p><p>Polyethylene terephthalate (PET) is one of the most widely produced man-made polymers and is a significant contributor to microplastics pollution. The environmental and human health impacts of microplastics pollution have motivated a concerted effort to develop microbe- and enzyme-based strategies to degrade PET and similar plastics. A PETase derived from the bacteria Ideonella sakaiensis was previously shown to enzymatically degrade PET, triggering multidisciplinary efforts to improve the robustness and activity of this and other PETases. However, because these enzymes only erode the surface of the insoluble PET substrate, it is difficult to measure standard kinetic parameters, such as k<sub>on</sub>, k<sub>off</sub>, and k<sub>cat</sub>, complicating interpretation of the activity of mutants using traditional enzyme kinetics frameworks. To address this challenge, we developed a single-molecule microscopy assay that quantifies the landing rate and binding duration of quantum dot-labeled PETase enzymes interacting with a surface-immobilized PET film. Wild-type PETase binding durations were well fit by a biexponential with a fast population having a 2.7 s time constant, interpreted as active binding events, and a slow population interpreted as nonspecific binding interactions that last tens of seconds. A previously described hyperactive mutant, S238F/W159H had both a faster apparent on-rate and a slower off-rate than wild-type PETase, potentially explaining its enhanced activity. Because this single-molecule approach provides a more detailed mechanistic picture of PETase enzymatic activity than standard bulk assays, it should aid future efforts to engineer more robust and active PETases to combat global microplastics pollution.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":"3669-3677"},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
EGFR does not directly interact with cortical actin: A SRRF'n'TIRF study. 表皮生长因子受体不直接与皮质肌动蛋白相互作用:SRRF'n'TIRF 研究。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-05 Epub Date: 2024-09-26 DOI: 10.1016/j.bpj.2024.09.022
Shambhavi Pandey, Thorsten Wohland
{"title":"EGFR does not directly interact with cortical actin: A SRRF'n'TIRF study.","authors":"Shambhavi Pandey, Thorsten Wohland","doi":"10.1016/j.bpj.2024.09.022","DOIUrl":"10.1016/j.bpj.2024.09.022","url":null,"abstract":"<p><p>The epidermal growth factor receptor (EGFR) governs pivotal signaling pathways in cell proliferation and survival, with mutations implicated in numerous cancers. The organization of EGFR on the plasma membrane (PM) is influenced by the lipids and the cortical actin (CA) cytoskeleton. Despite the presence of a putative actin-binding domain (ABD) spanning 13 residues, a direct interaction between EGFR and CA has not been definitively established. While disrupting the cytoskeleton can impact EGFR behavior, suggesting a connection, the influence of the static actin cytoskeleton has been found to be indirect. Here, we investigate the potential interaction between EGFR and CA, as well as the extent to which CA regulates EGFR's distribution on the PM using SRRF'n'TIRF, a spatiotemporal super-resolution microscopy technique that provides sub-100 nm resolution and ms-scale dynamics from the same data set. To label CA, we constructed PMT-mEGFP-F-tractin, which combines an inner leaflet targeting domain PMT, fluorescent probe mEGFP, and the actin-binding protein F-tractin. In addition to EGFR-mEGFP, we included two control constructs: 1) an ABD deletion mutant, EGFRΔ<sup>ABD</sup>-mEGFP serving as a negative control and 2) EGFR-mApple-F-tractin, where F-tractin is fused to the C-terminus of EGFR-mApple, serving as the positive control. We find that EGFR-mEGFP and EGFRΔ<sup>ABD</sup>-mEGFP show similar membrane dynamics, implying that EGFR-mEGFP dynamics and organization are independent of CA. EGFR dynamics show CA dependence when F-tractin is anchored to the cytoplasmic tail. Together, our results demonstrate that EGFR does not directly interact with the CA in its resting and activated state.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":"3736-3749"},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Electrophysical cardiac remodeling at the molecular level: Insights into ryanodine receptor activation and calcium-induced calcium release from a stochastic explicit-particle model. 分子水平上的电物理心脏重塑:从随机显式粒子模型深入了解瑞诺丁受体激活和钙诱导的钙释放。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-05 Epub Date: 2024-10-05 DOI: 10.1016/j.bpj.2024.09.029
Sophia P Hirakis, Thomas M Bartol, Ludovic Autin, Rommie E Amaro, Terrence J Sejnowski
{"title":"Electrophysical cardiac remodeling at the molecular level: Insights into ryanodine receptor activation and calcium-induced calcium release from a stochastic explicit-particle model.","authors":"Sophia P Hirakis, Thomas M Bartol, Ludovic Autin, Rommie E Amaro, Terrence J Sejnowski","doi":"10.1016/j.bpj.2024.09.029","DOIUrl":"10.1016/j.bpj.2024.09.029","url":null,"abstract":"<p><p>We present the first-ever, fully discrete, stochastic model of triggered cardiac Ca<sup>2+</sup> dynamics. Using anatomically accurate subcellular cardiac myocyte geometries, we simulate the molecular players involved in Ca<sup>2+</sup> handling using high-resolution stochastic and explicit-particle methods at the level of an individual cardiac dyadic junction. Integrating data from multiple experimental sources, the model not only replicates the findings of traditional in silico studies and complements in vitro experimental data but also reveals new insights into the molecular mechanisms driving cardiac dysfunction under stress and disease conditions. We improve upon older, nondiscrete models using the same realistic geometry by incorporating molecular mechanisms for spontaneous, as well as triggered calcium-induced calcium release (CICR). Action potentials are used to activate L-type calcium channels (LTCC), triggering CICR through ryanodine receptors (RyRs) on the surface of the sarcoplasmic reticulum. These improvements allow for the specific focus on the couplon: the structure-function relationship between LTCC and RyR. We investigate the electrophysical effects of normal and diseased action potentials on CICR and interrogate the effects of dyadic junction deformation through detubulation and orphaning of RyR. Our work demonstrates the importance of the electrophysical integrity of the calcium release unit on CICR fidelity, giving insights into the molecular basis of heart disease. Finally, we provide a unique, detailed, molecular view of the CICR process using advanced rendering techniques. This easy-to-use model comes complete with tutorials and the necessary software for use and analysis to maximize usability and reproducibility. Our work focuses on quantifying, qualifying, and visualizing the behavior of the molecular species that underlie the function and dysfunction of subcellular cardiomyocyte systems.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":"3812-3831"},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Elastic interactions compete with persistent cell motility to drive durotaxis. 弹性相互作用与持续的细胞运动相互竞争,推动了黑僵病的发生。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-05 Epub Date: 2024-09-26 DOI: 10.1016/j.bpj.2024.09.021
Subhaya Bose, Haiqin Wang, Xinpeng Xu, Arvind Gopinath, Kinjal Dasbiswas
{"title":"Elastic interactions compete with persistent cell motility to drive durotaxis.","authors":"Subhaya Bose, Haiqin Wang, Xinpeng Xu, Arvind Gopinath, Kinjal Dasbiswas","doi":"10.1016/j.bpj.2024.09.021","DOIUrl":"10.1016/j.bpj.2024.09.021","url":null,"abstract":"<p><p>Many animal cells that crawl on extracellular substrates exhibit durotaxis, i.e., directed migration toward stiffer substrate regions. This has implications in several biological processes including tissue development and tumor progression. Here, we introduce a phenomenological model for single-cell durotaxis that incorporates both elastic deformation-mediated cell-substrate interactions and the stochasticity of cell migration. Our model is motivated by a key observation in an early demonstration of durotaxis: a single, contractile cell at a sharp interface between a softer and a stiffer region of an elastic substrate reorients and migrates toward the stiffer region. We model migrating cells as self-propelling, persistently motile agents that exert contractile traction forces on their elastic substrate. The resulting substrate deformations induce elastic interactions with mechanical boundaries, captured by an elastic potential. The dynamics is determined by two crucial parameters: the strength of the cellular traction-induced boundary elastic interaction (A), and the persistence of cell motility (Pe). Elastic forces and torques resulting from the potential orient cells perpendicular (parallel) to the boundary and accumulate (deplete) them at the clamped (free) boundary. Thus, a clamped boundary induces an attractive potential that drives durotaxis, while a free boundary induces a repulsive potential that prevents antidurotaxis. By quantifying the steady-state position and orientation probability densities, we show how the extent of accumulation (depletion) depends on the strength of the elastic potential and motility. We compare and contrast crawling cells with biological microswimmers and other synthetic active particles, where accumulation at confining boundaries is well known. We define metrics quantifying boundary accumulation and durotaxis, and present a phase diagram that identifies three possible regimes: durotaxis, and adurotaxis with and without motility-induced accumulation at the boundary. Overall, our model predicts how durotaxis depends on cell contractility and motility, successfully explains some previous observations, and provides testable predictions to guide future experiments.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":"3721-3735"},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The dynamics of red blood cells traversing slits of mechanical heart valves under high shear. 高剪切力下红细胞穿过机械心脏瓣膜缝隙的动力学。
IF 3.2 3区 生物学
Biophysical journal Pub Date : 2024-11-05 Epub Date: 2024-09-26 DOI: 10.1016/j.bpj.2024.09.027
Kuilin Meng, Haosheng Chen, Yunfan Pan, Yongjian Li
{"title":"The dynamics of red blood cells traversing slits of mechanical heart valves under high shear.","authors":"Kuilin Meng, Haosheng Chen, Yunfan Pan, Yongjian Li","doi":"10.1016/j.bpj.2024.09.027","DOIUrl":"10.1016/j.bpj.2024.09.027","url":null,"abstract":"<p><p>Hemolysis, including subclinical hemolysis, is a potentially severe complications of mechanical heart valves (MHVs), which leads to shortened red blood cell (RBC) lifespan and hemolytic anemia. Serious hemolysis is usually associated with structural deterioration and regurgitation. However, the shear stress in MHVs' narrow leakage slits is much lower than the shear stress threshold causing hemolysis and the mechanisms in this context remain largely unclear. This study investigated the hemolysis mechanism of RBCs in cell-size slits under high shear rates by establishing in vitro microfluidic devices and a coarse-grained molecular dynamics (CGMD) model, considering both fluid and structural effects simultaneously. Microfluidic experiments and computational simulation revealed six distinct dynamic states of RBC traversal through MHVs' microscale slits under various shear rates and slit sizes. It elucidated that RBC dynamic states were influenced by not only by fluid forces but significantly by the compressive force of slit walls. The variation of the potential energy of the cell membrane indicated its stretching, deformation, and rupture during traversal, corresponding to the six dynamic states. The maximum forces exerted on membrane by water particles and slit walls directly determined membrane rupture, serving as a critical determinant. This analysis helps in understanding the contribution of the slit walls to membrane rupture and identifying the threshold force that leads to membrane rupture. The hemolysis mechanism of traversing microscale slits is revealed to effectively explain the occurrences of hemolysis and subclinical hemolysis.</p>","PeriodicalId":8922,"journal":{"name":"Biophysical journal","volume":" ","pages":"3780-3797"},"PeriodicalIF":3.2,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信