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Cells
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Cardiovascular Disease and Vascular Engineering
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Cardiovascular Disease and Vascular Engineering

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (15 September 2023) | Viewed by 20288

Special Issue Editor

Prof. Dr. Tao Wang

E-Mail Website
Guest Editor
School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK
Interests: molecular mechanisms of genetic cardiovascular diseases; iPSC modelling of genetic vascular and neurovascular conditions; neurovascular interactions and vascular dementia; notch signalling in human cardiovascular system; vascular engineering and nano-medicine

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are the leading cause of death globally, imposing a significant health burden. In addition to conventional medication, a considerable proportion of patients require alternative interventions by revascularisation and regeneration approaches, which drives innovations in this field. As a result, many advances have been made towards the application of stem cell biology, tissue engineering, material science, and biofabrications. However, despite effort, challenges remain. Areas including but not limited to the cell type, seeding method, biocompatibility of scaffolds, immune response, fabrication techniques, mechanical strengths, and lifespan of implants are waiting to be significantly further improved. It is still not possible to create a tissue-engineered vascular conduit that fits all patient demands, especially small-diameter vascular grafts used for the coronary bypass operation. In situ vascularisation to repair ischemic tissue damage is also challenging. This Special Issue thus aims to highlight recent developments and advances in the application of engineering and regeneration approaches for the treatment of cardiovascular diseases with a focus on vascular interventions. Additionally, basic studies in understanding the pathophysiological processes of cardiovascular disease at a cellular and molecular level, which have the potential of translation for regeneration or engineering, are areas of interest. Areas in basic stem-cell research related to vascular regeneration are also welcome.

Prof. Dr. Tao Wang
Guest Editor

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Keywords

  • vascular tissue engineering
  • cardiovascular regeneration
  • Induced pluripotent stem cells (iPSCs)
  • mesenchymal stem cells
  • cardiovascular disease
  • microfluidics vascular mimicking

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Published Papers (6 papers)

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Research

26 pages, 3370 KiB  
Article
Patterned Arteriole-Scale Vessels Enhance Engraftment, Perfusion, and Vessel Branching Hierarchy of Engineered Human Myocardium for Heart Regeneration
by Rajeev J. Kant, Kiera D. Dwyer, Jang-Hoon Lee, Collin Polucha, Momoka Kobayashi, Stephen Pyon, Arvin H. Soepriatna, Jonghwan Lee and Kareen L. K. Coulombe
Cells 2023, 12(13), 1698; https://doi.org/10.3390/cells12131698 - 23 Jun 2023
Cited by 2 | Viewed by 2123
Abstract
Heart regeneration after myocardial infarction (MI) using human stem cell-derived cardiomyocytes (CMs) is rapidly accelerating with large animal and human clinical trials. However, vascularization methods to support the engraftment, survival, and development of implanted CMs in the ischemic environment of the infarcted heart [...] Read more.
Heart regeneration after myocardial infarction (MI) using human stem cell-derived cardiomyocytes (CMs) is rapidly accelerating with large animal and human clinical trials. However, vascularization methods to support the engraftment, survival, and development of implanted CMs in the ischemic environment of the infarcted heart remain a key and timely challenge. To this end, we developed a dual remuscularization-revascularization therapy that is evaluated in a rat model of ischemia-reperfusion MI. This study details the differentiation of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for engineering cardiac tissue containing patterned engineered vessels 400 μm in diameter. Vascularized engineered human myocardial tissues (vEHMs) are cultured in static conditions or perfused in vitro prior to implantation and evaluated after two weeks. Immunohistochemical staining indicates improved engraftment of hiPSC-CMs in in vitro-perfused vEHMs with greater expression of SMA+ vessels and evidence of inosculation. Three-dimensional vascular reconstructions reveal less tortuous and larger intra-implant vessels, as well as an improved branching hierarchy in in vitro-perfused vEHMs relative to non-perfused controls. Exploratory RNA sequencing of explanted vEHMs supports the hypothesis that co-revascularization impacts hiPSC-CM development in vivo. Our approach provides a strong foundation to enhance vEHM integration, develop hierarchical vascular perfusion, and maximize hiPSC-CM engraftment for future regenerative therapy. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Vascular Engineering)
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24 pages, 4299 KiB  
Article
Targeted Inhibition of Matrix Metalloproteinase-8 Prevents Aortic Dissection in a Murine Model
by Chengxin Zhang, Kaiyuan Niu, Meixia Ren, Xinmiao Zhou, Zhisheng Yang, Mei Yang, Xinxin Wang, Jun Luo, Yue Shao, Cheng Zhang, Dan Chen, Shan Gao, Shenglin Ge, Qingchen Wu and Qingzhong Xiao
Cells 2022, 11(20), 3218; https://doi.org/10.3390/cells11203218 - 14 Oct 2022
Cited by 5 | Viewed by 2588
Abstract
Aortic dissection (AD) is a lethal aortic pathology without effective medical treatments since the underlying pathological mechanisms responsible for AD remain elusive. Matrix metalloproteinase-8 (MMP8) has been previously identified as a key player in atherosclerosis and arterial remodeling. However, the functional role of [...] Read more.
Aortic dissection (AD) is a lethal aortic pathology without effective medical treatments since the underlying pathological mechanisms responsible for AD remain elusive. Matrix metalloproteinase-8 (MMP8) has been previously identified as a key player in atherosclerosis and arterial remodeling. However, the functional role of MMP8 in AD remains largely unknown. Here, we report that an increased level of MMP8 was observed in 3-aminopropionitrile fumarate (BAPN)-induced murine AD. AD incidence and aortic elastin fragmentation were markedly reduced in MMP8-knockout mice. Importantly, pharmacologic inhibition of MMP8 significantly reduced the AD incidence and aortic elastin fragmentation. We observed less inflammatory cell accumulation, a lower level of aortic inflammation, and decreased smooth muscle cell (SMC) apoptosis in MMP8-knockout mice. In line with our previous observation that MMP8 cleaves Ang I to generate Ang II, BAPN-treated MMP8-knockout mice had increased levels of Ang I, but decreased levels of Ang II and lower blood pressure. Additionally, we observed a decreased expression level of vascular cell adhesion molecule-1 (VCAM1) and a reduced level of reactive oxygen species (ROS) in MMP8-knockout aortas. Mechanistically, our data show that the Ang II/VCAM1 signal axis is responsible for MMP8-mediated inflammatory cell invasion and transendothelial migration, while MMP8-mediated SMC inflammation and apoptosis are attributed to Ang II/ROS signaling. Finally, we observed higher levels of aortic and serum MMP8 in patients with AD. We therefore provide new insights into the molecular mechanisms underlying AD and identify MMP8 as a potential therapeutic target for this life-threatening aortic disease. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Vascular Engineering)
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19 pages, 4540 KiB  
Article
Mitochondrial Membrane Potential Identifies a Subpopulation of Mesenchymal Progenitor Cells to Promote Angiogenesis and Myocardial Repair
by Xiuchun Li, Xiaoliang Wang, Pan He, Edward Bennett, Erin Haggard, Jianjie Ma and Chuanxi Cai
Cells 2022, 11(10), 1713; https://doi.org/10.3390/cells11101713 - 22 May 2022
Cited by 4 | Viewed by 2941
Abstract
Identifying effective donor cells is one of obstacles that limits cell therapy for heart disease. In this study, we sorted a subpopulation of human mesenchymal progenitor cells (hMPCs) from the right atrial appendage using the low mitochondrial membrane potential. Compared to the non-sorted [...] Read more.
Identifying effective donor cells is one of obstacles that limits cell therapy for heart disease. In this study, we sorted a subpopulation of human mesenchymal progenitor cells (hMPCs) from the right atrial appendage using the low mitochondrial membrane potential. Compared to the non-sorted cells, hMPCs hold the capacity for stemness and enrich mesenchymal stem cell markers. The hMPCs display better ability for survival, faster proliferation, less production of reactive oxygen species (ROS), and greater release of cytoprotective cytokines. The hMPCs exhibit decreased expression of senescence genes and increased expression of anti-apoptotic and antioxidant genes. Intramyocardial injection of hMPCs into the infarcted heart resulted in increased left ventricular ejection fraction and reduced cardiac remodeling and infarct size in the group of animals receiving hMPCs. Both in vitro and in vivo studies indicated hMPCs have the potential to differentiate into endothelial cells and smooth muscle cells. Immunohistochemistry staining showed that cell therapy with hMPCs enhances cardiac vascular regeneration and cardiac proliferation, and decreases cardiac cell apoptosis, which is associated with the increased secretion of cytoprotective and pro-angiogenic cytokines. Overall, we discovered a subpopulation of human mesenchymal progenitor cells via their low mitochondrial membrane potential, which might provide an alternative donor cell source for cellular therapy for ischemic heart disease. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Vascular Engineering)
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22 pages, 5559 KiB  
Article
Novel Insights into the Cardioprotective Effects of Calcitriol in Myocardial Infarction
by Simin Yang, Chunmiao Wang, Chengshao Ruan, Meiling Chen, Ran Cao, Liang Sheng, Naiying Chang, Tong Xu, Peiwen Zhao, Xuesheng Liu, Fengqin Zhu, Qingzhong Xiao and Shan Gao
Cells 2022, 11(10), 1676; https://doi.org/10.3390/cells11101676 - 18 May 2022
Cited by 8 | Viewed by 2840
Abstract
Background: Increasing evidence indicates that vitamin D deficiency negatively affects the cardiovascular system. Here we studied the therapeutic effects of calcitriol in myocardial infarction (MI) and investigated its underlying mechanisms. Methods: A MI model of Kun-ming mice induced by left anterior descending coronary [...] Read more.
Background: Increasing evidence indicates that vitamin D deficiency negatively affects the cardiovascular system. Here we studied the therapeutic effects of calcitriol in myocardial infarction (MI) and investigated its underlying mechanisms. Methods: A MI model of Kun-ming mice induced by left anterior descending coronary artery ligation was utilized to study the potential therapeutic effects of calcitriol on MI. AC16 human cardiomyocyte-like cells treated with TNF-α were used for exploring the mechanisms that underlie the cardioprotective effects of calcitriol. Results: We observed that calcitriol reversed adverse cardiovascular function and cardiac remodeling in post-MI mice. Mechanistically, calcitriol suppressed MI-induced cardiac inflammation, ameliorated cardiomyocyte death, and promoted cardiomyocyte proliferation. Specifically, calcitriol exerted these cellular effects by upregulating Vitamin D receptor (VDR). Increased VDR directly interacted with p65 and retained p65 in cytoplasm, thereby dampening NF-κB signaling and suppressing inflammation. Moreover, up-regulated VDR was translocated into nuclei where it directly bound to IL-10 gene promoters to activate IL-10 gene transcription, further inhibiting inflammation. Conclusion: We provide new insights into the cellular and molecular mechanisms underlying the cardioprotective effects of calcitriol, and we present comprehensive evidence to support the preventive and therapeutic effects of calcitriol on MI. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Vascular Engineering)
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17 pages, 10043 KiB  
Article
Novel Blood Vascular Endothelial Subtype-Specific Markers in Human Skin Unearthed by Single-Cell Transcriptomic Profiling
by Yuliang He, Carlotta Tacconi, Lothar C. Dieterich, Jihye Kim, Gaetana Restivo, Epameinondas Gousopoulos, Nicole Lindenblatt, Mitchell P. Levesque, Manfred Claassen and Michael Detmar
Cells 2022, 11(7), 1111; https://doi.org/10.3390/cells11071111 - 25 Mar 2022
Cited by 12 | Viewed by 6041
Abstract
Ample evidence pinpoints the phenotypic diversity of blood vessels (BVs) and site-specific functions of their lining endothelial cells (ECs). We harnessed single-cell RNA sequencing (scRNA-seq) to dissect the molecular heterogeneity of blood vascular endothelial cells (BECs) in healthy adult human skin and identified [...] Read more.
Ample evidence pinpoints the phenotypic diversity of blood vessels (BVs) and site-specific functions of their lining endothelial cells (ECs). We harnessed single-cell RNA sequencing (scRNA-seq) to dissect the molecular heterogeneity of blood vascular endothelial cells (BECs) in healthy adult human skin and identified six different subpopulations, signifying arterioles, post-arterial capillaries, pre-venular capillaries, post-capillary venules, venules and collecting venules. Individual BEC subtypes exhibited distinctive transcriptomic landscapes associated with diverse biological pathways. These functionally distinct dermal BV segments were characterized by their unique compositions of conventional and novel markers (e.g., arteriole marker GJA5; arteriole capillary markers ASS1 and S100A4; pre-venular capillary markers SOX17 and PLAUR; venular markers EGR2 and LRG1), many of which have been implicated in vascular remodeling upon inflammatory responses. Immunofluorescence staining of human skin sections and whole-mount skin blocks confirmed the discrete expression of these markers along the blood vascular tree in situ, further corroborating BEC heterogeneity in human skin. Overall, our study molecularly refines individual BV compartments, whilst the identification of novel subtype-specific signatures provides more insights for future studies dissecting the responses of distinct vessel segments under pathological conditions. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Vascular Engineering)
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15 pages, 3933 KiB  
Article
Fingolimod (FTY720), a Sphinogosine-1-Phosphate Receptor Agonist, Mitigates Choroidal Endothelial Proangiogenic Properties and Choroidal Neovascularization
by Christine M. Sorenson, Mitra Farnoodian, Shoujian Wang, Yong-Seok Song, Soesiawati R. Darjatmoko, Arthur S. Polans and Nader Sheibani
Cells 2022, 11(6), 969; https://doi.org/10.3390/cells11060969 - 11 Mar 2022
Cited by 7 | Viewed by 2843
Abstract
Neovascular or wet age-related macular degeneration (nAMD) causes vision loss due to inflammatory and vascular endothelial growth factor (VEGF)-driven neovascularization processes in the choroid. Due to the excess in VEGF levels associated with nAMD, anti-VEGF therapies are utilized for treatment. Unfortunately, not all [...] Read more.
Neovascular or wet age-related macular degeneration (nAMD) causes vision loss due to inflammatory and vascular endothelial growth factor (VEGF)-driven neovascularization processes in the choroid. Due to the excess in VEGF levels associated with nAMD, anti-VEGF therapies are utilized for treatment. Unfortunately, not all patients have a sufficient response to such therapies, leaving few if any other treatment options for these patients. Sphingosine-1-phosphate (S1P) is a bioactive lipid mediator found in endothelial cells that participates in modulating barrier function, angiogenesis, and inflammation. S1P, through its receptor (S1PR1) in endothelial cells, prevents illegitimate sprouting angiogenesis during vascular development. In the present paper, we show that, in choroidal endothelial cells, S1PR1 is the most abundantly expressed S1P receptor and agonism of S1PR1-prevented choroidal endothelial cell capillary morphogenesis in culture. Given that nAMD pathogenesis draws from enhanced inflammation and angiogenesis as well as a loss of barrier function, we assessed the impact of S1PR agonism on choroidal neovascularization in vivo. Using laser photocoagulation rupture of Bruch’s membrane to induce choroidal neovascularization, we show that S1PR non-selective (FTY720) and S1PR1 selective (CYM5442) agonists significantly inhibit choroidal neovascularization in this model. Thus, utilizing S1PR agonists to temper choroidal neovascularization presents an additional novel use for these agonists presently in clinical use for multiple sclerosis as well as other inflammatory diseases. Full article
(This article belongs to the Special Issue Cardiovascular Disease and Vascular Engineering)
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