Vessel graft fabricated by the on-site differentiation of human mesenchymal stem cells towards vascular cells on vascular extracellular matrix scaffold under mechanical stimulation in a rotary bioreactor

Li, Na; Rickel, Alex P.; Sanyour, Hanna J; Hong, Zhongkui

doi:10.1039/c8tb03348j

Cited by 16 publications

(12 citation statements)

References 49 publications

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“…This system is sensitive to ECM stiffness as talin unfolding only occurs on stiff substrates, allowing the recruitment of vinculin and higher force transmission . Ample previous studies have demonstrated the ability of the ECM to alter cell fate and function. − In addition, the transduction of forces to the actin cytoskeleton can induce cytoskeletal remodeling in response to ECM stiffness changes. , …”

Section: Introductionmentioning

confidence: 99%

Extracellular Matrix Proteins and Substrate Stiffness Synergistically Regulate Vascular Smooth Muscle Cell Migration and Cortical Cytoskeleton Organization

Rickel

Sanyour

Leyda

et al. 2020

ACS Appl. Bio Mater.

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Vascular smooth muscle cell (VSMC) migration is a critical step in the progression of cardiovascular disease and aging. Migrating VSMCs encounter a highly heterogeneous environment with the varying extracellular matrix (ECM) composition due to the differential synthesis of collagen and fibronectin (FN) in different regions and greatly changing stiffness, ranging from the soft necrotic core of plaques to hard calcifications within blood vessel walls. In this study, we demonstrate an application of a two-dimensional (2D) model consisting of an elastically tunable polyacrylamide gel of varying stiffness and ECM protein coating to study VSMC migration. This model mimics the in vivo microenvironment that VSMCs experience within a blood vessel wall, which may help identify potential therapeutic targets for the treatment of atherosclerosis. We found that substrate stiffness had differential effects on VSMC migration on type 1 collagen (COL1) and FN-coated substrates. VSMCs on COL1-coated substrates showed significantly diminished migration distance on stiffer substrates, while on FN-coated substrates VSMCs had significantly increased migration distance. In addition, cortical stress fiber orientation increased in VSMCs cultured on more rigid COL1-coated substrates, while decreasing on stiffer FN-coated substrates. On both proteins, a more disorganized cytoskeletal architecture was associated with faster migration. Overall, these results demonstrate that different ECM proteins can cause substrate stiffness to have differential effects on VSMC migration in the progression of cardiovascular diseases and aging.

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Section: Introductionmentioning

confidence: 99%

Extracellular Matrix Proteins and Substrate Stiffness Synergistically Regulate Vascular Smooth Muscle Cell Migration and Cortical Cytoskeleton Organization

Rickel

Sanyour

Leyda

et al. 2020

ACS Appl. Bio Mater.

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“…The proliferation and differentiation of VSMC is a key regulatory process that affects the maturation and development of the vascular system. When vascular intima is damaged, VSMC overproliferation, migration, and synthesis of a large number of cellular matrix can induce cardiovascular diseases such as vascular restenosis, hypertension, and atherosclerosis [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

lncRNA-SNHG14 Promotes Atherosclerosis by Regulating RORα Expression through Sponge miR-19a-3p

Zhu

Liu

Zhao

et al. 2020

Computational and Mathematical Methods in Medicine

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Coronary heart disease (CHD) is the most common cardiovascular disease with high prevalence, disability, and mortality. The balance between proliferation and apoptosis of vascular smooth muscle cells (VSMCs) plays a key role in the initiation of atherosclerosis. In this study, we found a significant decrease in the expression of lncRNA-SNHG14 in atherosclerotic plaque tissues of ApoE-/- mice. Overexpression of lncRNA-SNHG14 can inhibit VSMC proliferation while promoting apoptosis. There is a potential reciprocal regulatory relationship between lncRNASNHG14 and miR-19a-3p, which inhibit each other’s expression in vascular smooth muscle cells. In addition, the luciferase reporter gene analysis results showed that there was a direct interaction between miR-19a-3p and the 3′UTR of RORα. The results of qRT-PCR showed that the level of RORα mRNA was significantly increased in the aortas treated with miR-19a-3p and SNHG14 compared with that treated with miR-19a-3p alone. In conclusion, we demonstrated that lncRNA-SNHG14 regulates the apoptosis/proliferation balance of VSMCs in atherosclerosis.

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“…Another study by Hoerstrup et al developed pulmonary conduits by culturing human umbilical cord cells into a bioabsorbable polymer in a pulse duplicator bioreactor (217). Li et al used a rotary bioreactor to stimulate on-site differentiation of human MSCs to vascular cells on ECM scaffolds and induce the maturation of the vascular scaffold in one system (218). As an example of a vascular disease model, Robert et al developed an atherosclerosis system using primary HUVECs and cord bloodderived myofibroblasts which were cultured on a biodegradable tubular non-woven polyglycolic-acid meshes in a flow bioreactor system (191).…”

Section: Dynamic Culture Conditionsmentioning

confidence: 99%

3D Tissue-Engineered Vascular Drug Screening Platforms: Promise and Considerations

Marei

Samaan

Al-Quradaghi

et al. 2022

Front. Cardiovasc. Med.

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Despite the efforts devoted to drug discovery and development, the number of new drug approvals have been decreasing. Specifically, cardiovascular developments have been showing amongst the lowest levels of approvals. In addition, concerns over the adverse effects of drugs to the cardiovascular system have been increasing and resulting in failure at the preclinical level as well as withdrawal of drugs post-marketing. Besides factors such as the increased cost of clinical trials and increases in the requirements and the complexity of the regulatory processes, there is also a gap between the currently existing pre-clinical screening methods and the clinical studies in humans. This gap is mainly caused by the lack of complexity in the currently used 2D cell culture-based screening systems, which do not accurately reflect human physiological conditions. Cell-based drug screening is widely accepted and extensively used and can provide an initial indication of the drugs' therapeutic efficacy and potential cytotoxicity. However, in vitro cell-based evaluation could in many instances provide contradictory findings to the in vivo testing in animal models and clinical trials. This drawback is related to the failure of these 2D cell culture systems to recapitulate the human physiological microenvironment in which the cells reside. In the body, cells reside within a complex physiological setting, where they interact with and respond to neighboring cells, extracellular matrix, mechanical stress, blood shear stress, and many other factors. These factors in sum affect the cellular response and the specific pathways that regulate variable vital functions such as proliferation, apoptosis, and differentiation. Although pre-clinical in vivo animal models provide this level of complexity, cross species differences can also cause contradictory results from that seen when the drug enters clinical trials. Thus, there is a need to better mimic human physiological conditions in pre-clinical studies to improve the efficiency of drug screening. A novel approach is to develop 3D tissue engineered miniaturized constructs in vitro that are based on human cells. In this review, we discuss the factors that should be considered to produce a successful vascular construct that is derived from human cells and is both reliable and reproducible.

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Vessel graft fabricated by the on-site differentiation of human mesenchymal stem cells towards vascular cells on vascular extracellular matrix scaffold under mechanical stimulation in a rotary bioreactor

Abstract: Stem cell differentiation on a decellularized native blood vessel scaffold under mechanical stimulation for vascular tissue engineering.

Cited by 16 publications

References 49 publications

Extracellular Matrix Proteins and Substrate Stiffness Synergistically Regulate Vascular Smooth Muscle Cell Migration and Cortical Cytoskeleton Organization

Extracellular Matrix Proteins and Substrate Stiffness Synergistically Regulate Vascular Smooth Muscle Cell Migration and Cortical Cytoskeleton Organization

lncRNA-SNHG14 Promotes Atherosclerosis by Regulating RORα Expression through Sponge miR-19a-3p

3D Tissue-Engineered Vascular Drug Screening Platforms: Promise and Considerations

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