scholarly journals Nanofiber Electrospinning Combined with Rotary Bioprinting for Fabricating Small-Diameter Vessels with Endothelium and Smooth Muscle

2021 ◽  
Author(s):  
Qianheng Jin ◽  
Yi Fu ◽  
Guangliang Zhang ◽  
Lei Xu ◽  
Guangzhe Jin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Tissue ◽  
Umbilical Vein ◽  
Three Dimensional ◽  
Small Diameter ◽  
Muscle Cells ◽  
Research Area ◽  
Speed Increase

Abstract Background: Cardiovascular disease is responsible for a large number of deaths each year. Autologous vascular transplantation is still the best surgical intervention option, but the success rate is affected by many factors. Tissue engineering is a growing research area of great interest because it can produce bionic grafts to replace autologous tissue. Although many molding strategies have been tried, precellularization of small-diameter vascular grafts remains a research challenge. Here, a novel approach for fabricating bionic small-diameter vascular vessels with endothelial and smooth muscle cells is developed through combining nanofiber electrospinning and a specially-designed rotary bioprinter.Results: Combining and utilizing the advantages of nanofiber electrospinning and rotary printing, a tissue-engineered vascular tissue more suitable for biological transplantation is fabricated. Electrospun poly(ε-caprolactone) (PCL) provides good elasticity, and the electrospinning modification is beneficial for adhesion and functionalization of endothelial cells. A flat monolayer on the surface of PCL is formed after 7 days cultivation. Modification of the traditional three-dimensional (3D) bioprinter to increase rotation of the central axis used dual motors rotating clockwise and anticlockwise at the same speed increase stability during the printing process. This allowed a uniform dense methacrylated gelatin (GelMA) structure containing smooth muscle cells to be bioprinted with the cells are arranged linearly along the horizontal axis of rotation. Perfused with umbilical vein endothelial cells, a monolayer endothelial structure is formed. The two type cells maintain viability and proliferation in the structure during the process of cultivation. In addition, the bionic structureis superior to the natural blood vessel in anti-burst pressure and suture retention strength.Conclusion: By combining nanofiber electrospinning and modified rotary bioprinter, we successfully formed a small-diameter bionic vascular vessel with smooth muscle cells and endothelial cells. This method takes advantages of two advanced technologies and provides a new strategy for the development of bionic blood vascular tissue.

Ascorbate and glutathione homeostasis in vascular smooth muscle cells: cooperation with endothelial cells

1998 ◽  
Vol 275 (4) ◽  
pp. C1031-C1039 ◽  
Author(s):  
Ilia Voskoboinik ◽  
Karin Söderholm ◽  
Ian A. Cotgreave
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Steady State ◽  
Smooth Muscle Cells ◽  
Umbilical Vein ◽  
State Level ◽  
Muscle Cells ◽  
Free Access ◽  
Steady State Level ◽  
Human Umbilical Vein

Human umbilical vein smooth muscle cells (HUVSMCs) utilize extracellular cystine, glutathione (GSH), and N-acetylcysteine (NAC) to synthesize cellular GSH. Extracellular cystine was effective from 5 μM, whereas GSH and NAC were required at 100 μM for comparable effects. The efficacy of extracellular GSH was dependent on de novo GSH synthesis, indicating a dependence on cellular γ-glutamyltransferase (glutamyl transpeptidase). Coculture of syngenetic HUVSMCs and corresponding human umbilical vein endothelial cells (HUVECs) on porous supports restricted cystine- or GSH-stimulated synthesis of HUVSMC GSH when supplied on the “luminal” endothelial side. Thus HUVSMC GSH rapidly attained a steady-state level below that achieved in the absence of interposed HUVECs. HUVSMCs also readily utilize both reduced ascorbate (AA) and oxidized dehydroascorbate (DHAA) over the range 50–500 μM. Phloretin effectively blocked both AA- and DHAA-stimulated assimilation of intracellular AA, indicating a role for a glucose transporter in their transport. Uptake of extracellular AA was also sensitive to extracellular, but not intracellular, thiol depletion. When AA was applied to the endothelial side of the coculture model, assimilation of intracellular AA in HUVSMCs was restricted to a steady-state level below that achieved by free access.

scholarly journals IL-8 reduces VCAM-1 secretion of smooth muscle cells by increasing p-ERK expression when 3-D co-cultured with vascular endothelial cells

2011 ◽  
Vol 34 (3) ◽  
pp. 138 ◽  
Author(s):  
Zhi Zhang ◽  
Guang Chu ◽  
Hong-Xian Wu ◽  
Ni Zou ◽  
Bao-Gui Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Type I Collagen ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Muscle Cells ◽  
Type I ◽  
Vascular Endothelial ◽  
Culture Model

Objective: The goal of this study was to investigate the crosstalk between vascular endothelial cells (ECs) and smooth muscle cells (SMCs) using a three-dimensional (3-D) co-culture model. In addition, the role of IL-8 in this crosstalk was investigated. Methods: A 3-D co-culture model was constructed using a Transwell chamber system and type I collagen gel. Human umbilical artery smooth muscle cells (HUASMCs) were suspended in the gel and added to the upper compartment of the Transwell. Human umbilical vein endothelial cells (HUVECs) were then grown on the surface of the gel. The growth of HUASMCs was tested with a CFDA SE cell proliferation kit. IL-8 and other bioactive substances were investigated by ELISA and real-time PCR. The alteration of p-ERK expression related to the change in IL-8 levels was also examined by Western blot analysis. Results: The proliferation rate of HUASMCs in the 3-D co-culture model was 0.679 ± 0.057. Secretion and transcription of VEGF, t-PA, NO and VCAM-1 in the 3-D co-culture model were different than in single (2-D) culture. When 3-D co-cultured, IL-8 released by HUVECs was significantly increased (2.35 ± 0.16 fold) (P﹤0.05) and the expression of VCAM-1 from HUASMCs was reduced accordingly (0.55±0.09 fold). In addition, increasing or decreasing the level of IL-8 changed the level of p-ERK and VCAM-1 expression. The reduction of VCAM-1, resulting from increased IL-8, could be blocked by the MEK inhibitor, PD98059. Conclusion: Crosstalk between HUVECs and HUASMCs occurred and was probably mediated by IL-8 in this 3-D co-culture model.

scholarly journals Fibrinogen induces adhesion, spreading, and microfilament organization of human endothelial cells in vitro.

1987 ◽  
Vol 104 (5) ◽  
pp. 1403-1411 ◽  
Author(s):  
E Dejana ◽  
S Colella ◽  
L R Languino ◽  
G Balconi ◽  
G C Corbascio ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Fiber Type ◽  
Umbilical Vein ◽  
Deae Cellulose ◽  
Muscle Cells ◽  
Binding Activity ◽  
Sequence Of Events

Human umbilical vein endothelial cells (ECs) have been shown to attach to a substratum of fibrinogen (fg). Later, ECs undergo spreading, organization of thick microfilament bundles of the stress fiber type, and formation of focal contacts (adhesion plaques) that correspond to accumulation of vinculin at the cytoplasmic aspect of the ventral membrane. The rate of attachment to fg and the type of spreading is virtually identical to that obtained on substrata coated with fibronectin (FN). Antibodies to fg, but not to FN, prevent EC adhesion to fg; conversely, antibodies to FN, but not to fg, prevent adhesion of ECs to a FN-coated substratum. The removal of residual FN contamination from fg preparations by means of DEAE-cellulose chromatography does not result in any difference in EC adhesion on fg. Moreover, pretreatment of cells with inhibitors of synthesis and release of proteins does not impair their adhesion capacity on an fg-coated substratum. In contrast, human arterial smooth muscle cells do not adhere and spread on fg substrata but do so on FN. The synthetic peptides (Gly-Arg-Gly-Asp[GRGD] and Gly-Arg-Gly-Asp-Ser-Pro[GRGDSP]) containing the tripeptide Arg-Gly-Asp (RGD), originally found to be responsible for the cell binding activity of FN, have been found to inhibit EC spreading and the redistribution of their cytoskeleton, including the formation of stress fibers and the localization of vinculin either on fg or on FN. Conversely, the synthetic peptide Arg-Gly-Gly (RGG) was completely uneffective in inhibiting the adhesion and the sequence of events leading to spreading and cytoskeletal organization. These results indicate that ECs, but not smooth muscle cells, specifically adhere and spread on an fg substratum and this occurs by recognition mechanisms similar to those reported for FN.

scholarly journals Chlamydia pneumoniae Infection of Human Endothelial Cells Induces Proliferation of Smooth Muscle Cells via an Endothelial Cell-Derived Soluble Factor(s)

1999 ◽  
Vol 67 (6) ◽  
pp. 2909-2915 ◽  
Author(s):  
Brian K. Coombes ◽  
James B. Mahony
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cells ◽  
Chlamydia Pneumoniae ◽  
Umbilical Vein ◽  
Muscle Cells ◽  
Cell Counting ◽  
Soluble Factor ◽  
Dose Dependent

ABSTRACT An association of Chlamydia pneumoniae with atherosclerosis and coronary heart disease has been determined epidemiologically and by the detection of C. pneumoniaeorganisms in atherosclerotic lesions in both humans and animal models of atherosclerosis. Previously, it has been shown that C. pneumoniae is capable of replicating in cell types found within atheromatous lesions, viz., endothelial cells, smooth muscle cells (SMC), and macrophages, yet the role of C. pneumoniae in the pathogenesis of atherosclerosis has not been determined. Since intimal thickening is a hallmark of atherosclerosis, we investigated whether C. pneumoniae infection of human umbilical vein endothelial cells (HUVEC) could induce the expression of a soluble factor(s) with mitogenic potential for SMC by using [3H]thymidine incorporation and direct cell counting. Conditioned medium harvested from HUVEC infected with C. pneumoniae stimulated SMC replication in a time- and dose-dependent fashion. Infection studies using various multiplicities of infection (MOIs) ranging from 0.001 to 1 demonstrated a dose-dependent production of the soluble factor(s). At an MOI of 1, SMC stimulation indices were 8.4 (P < 0.01) and 12.2 (P < 0.01) for conditioned media harvested at 24 and 48 h, respectively. To determine whether viable C. pneumoniae was required for production of the soluble factor(s), HUVEC were infected with heat-inactivated C. pneumoniae or with viable organisms in the presence of chloramphenicol. Both treatments produced stimulation indices similar to those for liveC. pneumoniae in the absence of chloramphenicol (P > 0.05), indicating that the factor(s) was produced by HUVEC and not by C. pneumoniae and that signal transduction events following chlamydia endocytosis may be important in the production of a soluble factor(s). The ability of C. pneumoniae to elicit an endothelial cell-derived soluble factor(s) that stimulates SMC proliferation may be important in the pathogenesis of atherosclerosis.

scholarly journals Exosomal MFGE8 from high glucose induced endothelial cells is involved in calcification/senescence of vascular smooth muscle cells

2021 ◽  
Author(s):  
Yu-Qing Ni ◽  
Shuang Li ◽  
Xiao Lin ◽  
Yan-Jiao Wang ◽  
Jie-Yu He ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Milk Fat ◽  
Umbilical Vein ◽  
Muscle Cells

AbstractVascular calcification/aging is a crucial feature of diabetic macro vasculopathy, resulting in serious cardiovascular diseases. The calcification/senescence of vascular smooth muscle cells (VSMCs) induced by hyperglycemia can cause diabetic vascular calcification/aging. However, the mechanism of VSMCs calcification/senescence involved in diabetic vascular calcification/aging remains unknown. The purpose of this study was to determine how the high glucose (HG) information in circulating blood is transmitted from vascular endothelial cells (ECs) to VSMCs, which are not contacted with blood directly. Exosomes have attracted much attention for their vital roles in regulating cell-to-cell communication. In this study, we found that milk fat globule epidermal growth factor 8 (MFGE8) was enriched in high glucose induced human umbilical vein endothelial cell exosomes (HG-HUVEC-Exo) and regulate VSMCs calcification/senescence, characterized by up-regulated expressions of alkaline phosphatase (ALP) and Runt-related transcription factor 2 (Runx2), as well as the increased mineralized nodules and senescence-associated β-galactosidase (SA-β-gal) positive cells. Upstream mechanism studies showed that sirtuin1 (SIRT1) was involved in VSMCs calcification/senescence by affecting the expression of MFGE8. We also found that inflammatory response mediated by IL-1β, IL-6, and IL-8 was closely associated with MFGE8 and played a key role in regulating HG-HUVEC-Exo-induced VSMCs calcification/senescence. These findings provide a new insight into the mechanism of exosomal MFGE8 as a potential preventive and therapeutic target for the intervention of diabetic vascular calcification/aging.

scholarly journals TAGLN, a canonical marker of smooth muscle cells, is present in endothelial cells and involved in angiogenesis

2021 ◽  
Author(s):  
Kiyomi Tsuji-Tamura ◽  
Saori Morino-Koga ◽  
Shingo Suzuki ◽  
Minetaro Ogawa
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Embryonic Stem ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Promoter Activation

Elongation of vascular endothelial cells (ECs) is an important process of angiogenesis. However, the molecular mechanisms remain unknown. An actin cross-linking protein TAGLN (Transgelin, SM22 or SM22alpha) is abundantly expressed in smooth muscle cells (SMCs) and widely used as its canonical marker. In the course of studies using embryonic stem cells (ESCs) carrying an Tagln promoter-driven fluorescence marker, we noticed the activation of Tagln promoter in EC elongation. Tagln promoter activation co-occurred with EC elongation by vascular endothelial growth factor (VEGF). Inhibition of PI3K-Akt and mTORC1 also induced EC elongation and Tagln promoter activation. Human umbilical vein endothelial cells (HUVECs) elongated, activated TAGLN promoter and increased TAGLN transcripts in angiogenesis model. Genetic disruption of TAGLN augmented angiogenic behaviors of HUVECs, as did the disruption of TAGLN2 and TAGLN3 genes. Tagln expression was found in ECs in mouse embryos. Our results identify TAGLN as a novel putative regulator of angiogenesis whose expression is activated in elongating ECs. This finding provides insight into the cytoskeletal regulation of EC elongation and an improved understanding of the molecular mechanisms underlying the regulation of angiogenesis.

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