scholarly journals Human epicardium-derived cells fuse with high efficiency with skeletal myotubes and differentiate toward the skeletal muscle phenotype: a comparison study with stromal and endothelial cells

2011 ◽  
Vol 22 (5) ◽  
pp. 581-592 ◽  
Author(s):  
Antonietta Gentile ◽  
Gabriele Toietta ◽  
Vincenzo Pazzano ◽  
Vasileios D. Tsiopoulos ◽  
Ada Francesca Giglio ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Efficiency ◽  
Low Frequency ◽  
Mdx Mice ◽  
Skeletal Myoblasts ◽  
Primary Myoblasts ◽  
Multipotent Cells ◽  
Nonmuscle Cells ◽  
Cell Adhesion Molecule 1

Recent studies have underscored a role for the epicardium as a source of multipotent cells. Here, we investigate the myogenic potential of adult human epicardium-derived cells (EPDCs) and analyze their ability to undergo skeletal myogenesis when cultured with differentiating primary myoblasts. Results are compared to those obtained with mesenchymal stromal cells (MSCs) and with endothelial cells, another mesodermal derivative. We demonstrate that EPDCs spontaneously fuse with pre-existing myotubes with an efficiency that is significantly higher than that of other cells. Although at a low frequency, endothelial cells may also contribute to myotube formation. In all cases analyzed, after entering the myotube, nonmuscle nuclei are reprogrammed to express muscle-specific genes. The fusion competence of nonmyogenic cells in vitro parallels their ability to reconstitute dystrophin expression in mdx mice. We additionally show that vascular cell adhesion molecule 1 (VCAM1) expression levels of nonmuscle cells are modulated by soluble factors secreted by skeletal myoblasts and that VCAM1 function is required for fusion to occur. Finally, treatment with interleukin (IL)-4 or IL-13, two cytokines released by differentiating myotubes, increases VCAM1 expression and enhances the rate of fusion of EPDCs and MSCs, but not that of endothelial cells.

scholarly journals High efficiency transduction of human VEGF165 into human skeletal myoblasts: in vitro studies

2003 ◽  
Vol 35 (5) ◽  
pp. 412-420 ◽  
Author(s):  
Lei Ye ◽  
Husnain Kh Haider ◽  
Shujia Jiang ◽  
Ruowen Ge ◽  
Peter K Law ◽  
...  
Keyword(s):  
High Efficiency ◽  
In Vitro Studies ◽  
Skeletal Myoblasts

Inhibition of proinflammatory genes in anti-GBM glomerulonephritis by targeted dexamethasone-loaded AbEsel liposomes

2008 ◽  
Vol 294 (3) ◽  
pp. F554-F561 ◽  
Author(s):  
Sigrídur A. Ásgeirsdóttir ◽  
Peter J. Zwiers ◽  
Henriëtte W. Morselt ◽  
Hendrik E. Moorlag ◽  
Hester I. Bakker ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Endothelial Cells ◽  
Targeted Delivery ◽  
Therapeutic Strategy ◽  
Disease Onset ◽  
Endothelial Activation ◽  
Pcr Analysis ◽  
Endothelial Cell Marker ◽  
Cell Adhesion Molecule 1

E-selectin-directed targeted drug delivery was analyzed in anti-glomerular basement membrane glomerulonephritis. Liposomes conjugated with anti-E-selectin antibodies (AbEsel liposomes) were internalized by activated endothelial cells in vitro through E-selectin-mediated endocytosis. At the onset of glomerulonephritis in mice, E-selectin was expressed on glomerular endothelial cells, which resulted in homing of AbEsel liposomes to glomeruli after intravenous administration. Accumulation of AbEsel liposomes in the kidney was 3.6 times higher than nontargeted IgG liposomes, whereas the accumulation of both liposomes in the clearance organs liver and spleen and in heart and lungs was comparable. In glomeruli, the AbEsel liposomes colocalized with the endothelial cell marker CD31. Quantitative RT-PCR analysis of laser-microdissected arterioles, glomeruli, and postcapillary venules demonstrated that targeted delivery of dexamethasone by AbEsel liposomes reduced glomerular endothelial expression of P-selectin, E-selectin, and vascular cell adhesion molecule-1 by 60–70%. The expression of these genes was not modulated in endothelial cells in nontargeted renal microvasculatures. Decrease of glomerular endothelial activation at disease onset was followed by reduced albuminuria at day 7. This study demonstrates the potential of vascular bed-specific drug delivery aimed at disease-induced epitopes on the microvascular endothelial cells as a therapeutic strategy for glomerulonephritis.

α-Lipoic acid reduces expression of vascular cell adhesion molecule-1 and endothelial adhesion of human monocytes after stimulation with advanced glycation end products

1999 ◽  
Vol 96 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Thomas KUNT ◽  
Thomas FORST ◽  
Axel WILHELM ◽  
Hans TRITSCHLER ◽  
Andreas PFUETZNER ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lipoic Acid ◽  
Cell Adhesion Molecule ◽  
Vascular Cell Adhesion ◽  
Advanced Glycation ◽  
Vascular Cell ◽  
Glycation End Products ◽  
End Products ◽  
Cell Adhesion Molecule 1

Advanced glycation end products (AGEs) have been identified as relevant mediators of late diabetic complications such as atherosclerotic disease. The endothelial migration of monocytes is one of the first steps in atherogenesis and monocyte–endothelial interaction itself is linked to the expression of adhesion molecules like vascular cell adhesion molecule-1 (VCAM-1). Recently, stimulation of VCAM-1 by AGEs has been demonstrated. Since endothelial stimulation by AGEs is followed by generation of oxygen free radicals with subsequent activation of nuclear transcription factor κB, we investigated the influence of α-lipoic acid on the expression of VCAM-1 and monocyte adherence to endothelial cells in vitro by means of cell-associated chemiluminescence assays and quantitative reverse transcriptase polymerase chain reaction using a constructed recombinant RNA standard. We found that α-lipoic acid was able to decrease the number of VCAM-1 transcripts from 41.0±11.2 to 9.5±4.7 RNA copies per cell in AGE-stimulated cell cultures. Furthermore, expression of VCAM-1 was suppressed in a time- and dose-dependent manner by α-lipoic acid as shown by chemiluminescence endothelial cell assay. Pretreatment of endothelial cells with 0.5 ;mM or 5 ;mM α-lipoic acid reduced AGE-induced endothelial binding of monocytes from 22.5±2.9% to 18.3±1.9% and 13.8±1.8% respectively. Thus, we suggest that extracellularly administered α-lipoic acid reduces AGE-albumin-induced endothelial expression of VCAM-1 and monocyte binding to endothelium in vitro. These in vitro results may contribute to the understanding of a potential antioxidative treatment of atherosclerosis.

Extremely low frequency electromagnetic fields (ELF-EMFs) induce in vitro angiogenesis process in human endothelial cells

2008 ◽  
Vol 29 (8) ◽  
pp. 640-648 ◽  
Author(s):  
Simona Delle Monache ◽  
Riccardo Alessandro ◽  
Roberto Iorio ◽  
Giancaterino Gualtieri ◽  
Rosella Colonna
Keyword(s):  
Endothelial Cells ◽  
Electromagnetic Fields ◽  
Low Frequency ◽  
Human Endothelial Cells ◽  
Extremely Low Frequency ◽  
Angiogenesis Process ◽  
In Vitro Angiogenesis

scholarly journals A transmigratory cup in leukocyte diapedesis both through individual vascular endothelial cells and between them

2004 ◽  
Vol 167 (2) ◽  
pp. 377-388 ◽  
Author(s):  
Christopher V. Carman ◽  
Timothy A. Springer
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Vascular Endothelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Definitive Evidence ◽  
Highly Correlated ◽  
Oriented Parallel ◽  
Cell Adhesion Molecule 1

The basic route and mechanisms for leukocyte migration across the endothelium remain poorly defined. We provide definitive evidence for transcellular (i.e., through individual endothelial cells) diapedesis in vitro and demonstrate that virtually all, both para- and transcellular, diapedesis occurs in the context of a novel “cuplike” transmigratory structure. This endothelial structure was comprised of highly intercellular adhesion molecule-1– and vascular cell adhesion molecule-1–enriched vertical microvilli-like projections that surrounded transmigrating leukocytes and drove redistribution of their integrins into linear tracks oriented parallel to the direction of diapedesis. Disruption of projections was highly correlated with inhibition of transmigration. These findings suggest a novel mechanism, the “transmigratory cup”, by which the endothelium provides directional guidance to leukocytes for extravasation.

scholarly journals Cytokine-Mediated Activation of Cultured CNS Microvessels: A System for Examining Antigenic Modulation of CNS Endothelial Cells, and Evidence for Long-Term Expression of the Adhesion Protein E-Selectin

1994 ◽  
Vol 14 (5) ◽  
pp. 837-844 ◽  
Author(s):  
Paula Dore-Duffy ◽  
Ruth A. Washington ◽  
Roumen Balabanov
Keyword(s):  
Endothelial Cells ◽  
Cultured Cells ◽  
Umbilical Vein ◽  
Necrosis Factor Alpha ◽  
Antigenic Modulation ◽  
Adhesion Protein ◽  
Activation Antigens ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

Much of what is known of endothelial responses to cytokines has been derived from in vitro studies using cultured human umbilical vein endothelial cells (EC). Less is known of CNS EC responses and whether intact endothelium responds similarly to cultured cells. We have used techniques by which rat CNS microvessels can be isolated, then cultured in vitro, to study the response of intact endothelium to activation with cytokines. These microvessels are composed of viable EC and perivascular cells, predominantly pericytes. Expression of EC activation antigens in multicellular systems such as cultured microvessels can be assessed quantitatively using immunofluorescence laser cytometry. Interferon gamma increased immunologically reactive major histocompatibility complex class II antigens (<300 to 2,398 ± 225 average fluorescence intensity), while tumor necrosis factor alpha induced an increase in vascular cell adhesion molecule-1 (2,167 ± 171) and E-selectin (1,628 ± 315). CNS EC appeared to respond similarly to cultured EC with the exception that E-selectin expression was not transiently expressed but was maintained by microvessel EC for 24 and 48 h. Cultured CNS microvessels provide a good system for studying EC activation.

Regulation and distribution of MAdCAM-1 in endothelial cells in vitro

2001 ◽  
Vol 281 (4) ◽  
pp. C1096-C1105 ◽  
Author(s):  
Tadayuki Oshima ◽  
Kevin P. Pavlick ◽  
F. Stephen Laroux ◽  
S. Kris Verma ◽  
Paul Jordan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Extracellular Signal ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Cell Adhesion Molecule 1

Mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is a 60-kDa endothelial cell adhesion glycoprotein that regulates lymphocyte trafficking to Peyer's patches and lymph nodes. Although it is widely agreed that MAdCAM-1 induction is involved in chronic gut inflammation, few studies have investigated regulation of MAdCAM-1 expression. We used two endothelial lines [bEND.3 (brain) and SVEC (high endothelium)] to study the signal paths that regulate MAdCAM-1 expression in response to tumor necrosis factor (TNF)-α using RT-PCR, blotting, adhesion, and immunofluorescence. TNF-α induced both MAdCAM-1 mRNA and protein in a dose- and time-dependent manner. This induction was tyrosine kinase (TK), p42/44, p38 mitogen-activated protein kinase (MAPK), and nuclear factor (NF)-κB/poly-ADP ribose polymerase (PARP) dependent. Because MAdCAM-1 is regulated via MAPKs, we examined mitogen/extracellular signal-regulated kinase (MEK)-1/2 activation in SVEC. We found that MEK-1/2 is activated by TNF-α within minutes and is dependent on TK and p42/44 MAPKs. Similarly, TNF-α activated NF-κB through TK, p42/44, p38 MAPKs, and PARP pathways in SVEC cells. MAdCAM-1 was also shown to be frequently distributed to endothelial junctions both in vitro and in vivo. Cytokines like TNF-α stimulate MAdCAM-1 in high endothelium via TK, p38, p42/22 MAPKs, and NF-κB/PARP. MAdCAM-1 expression requires NF-κB translocation through both direct p42/44 and indirect p38 MAPK pathways in high endothelial cells.

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