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Filename: controllers/Detail.php
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Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 249
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
Line: 316
Function: require_once
Severity: Warning
Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 249
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: models/Detail_model.php
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Function: insertAPISummary
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The quest for surfaces able to interface cells and modulate their functionality has raised, in recent years, the development of biomaterials endowed with nanocues capable of mimicking the natural extracellular matrix (ECM), especially for tissue regeneration purposes. In this context, carbon nanotubes (CNTs) are optimal candidates, showing dimensions and a morphology comparable to fibril ECM constituents. Moreover, when immobilized onto surfaces, they demonstrated outstanding cytocompatibility and ease of chemical modification with ad hoc functionalities. In this study, we interface porcine aortic valve interstitial cells (pVICs) to multi-walled carbon nanotube (MWNT) carpets, investigating the impact of surface nano-morphology on cell properties. The results obtained indicate that CNTs significantly affect cell behavior in terms of cell morphology, cytoskeleton organization, and mechanical properties. We discovered that CNT carpets appear to maintain interfaced pVICs in a sort of "quiescent state", hampering cell activation into a myofibroblasts-like phenotype morphology, a cellular evolution prodromal to Calcific Aortic Valve Disease (CAVD) and characterized by valve interstitial tissue stiffening. We found that this phenomenon is linked to CNTs' ability to alter cell tensional homeostasis, interacting with cell plasma membranes, stabilizing focal adhesions and enabling a better strain distribution within cells. Our discovery contributes to shedding new light on the ECM contribution in modulating cell behavior and will open the door to new criteria for designing nanostructured scaffolds to drive cell functionality for tissue engineering applications.
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http://dx.doi.org/10.3390/nano11102724 | DOI Listing |
BMC Med
December 2024
Present Address: State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 167A Beilishi Road, Beijing, Xi Cheng District, 100037, China.
Background: Functional mitral regurgitation (MR) is a common form of mitral valve dysfunction that often persists even after surgical intervention, requiring reoperation in some cases. To advance our understanding of the pathogenesis of functional MR, it is crucial to characterize the cellular composition of the mitral valve leaflet and identify molecular changes in each cell subtype within the mitral valves of MR patients. Therefore, we aimed to comprehensively examine the cellular and molecular components of mitral valves in patients with MR.
View Article and Find Full Text PDFZhonghua Xin Xue Guan Bing Za Zhi
December 2024
Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiaotong University School of Medicine, Shanghai200030, China.
Cardiovasc Res
December 2024
Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 510260, China.
Aims: Calcific aortic valve disease (CAVD) is a common heart valve disease with significant clinical consequences. The mechanisms that drive the pathogenesis of CAVD remain to be fully elucidated. N6-methyladenosine (m6A), the most prevalent RNA epigenetic regulator, has recently been implicated in cardiovascular disease, but its role in CAVD has yet to be investigated.
View Article and Find Full Text PDFAsian J Surg
November 2024
Department of Emergency, The First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan Province, China. Electronic address:
medRxiv
November 2024
Basic Science and Engineering (BASE) Initiative, Stanford Children's Health, Betty Irene Moore Children's Heart Center, Stanford, CA, USA.
Congenital heart defects (CHD) arise in part due to inherited genetic variants that alter genes and noncoding regulatory elements in the human genome. These variants are thought to act during fetal development to influence the formation of different heart structures. However, identifying the genes, pathways, and cell types that mediate these effects has been challenging due to the immense diversity of cell types involved in heart development as well as the superimposed complexities of interpreting noncoding sequences.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!