Growth Factor Expression of Human Arterial Smooth Muscle Cells and Endothelial Cells in a Transfilter Coculture System

Axel, Dorothea I.; Riessen, Reimer; Athanasiadis, Anastasios; Runge, Heike; Köveker, G.; Karsch, Karl R.

doi:10.1006/jmcc.1997.0541

Cited by 35 publications

(23 citation statements)

References 3 publications

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“…2 Active TGF-␤ is produced by ECs in vitro when they are cocultured with pericytes or SMCs. 3 Production of active TGF-␤ has also been found in human arterial SMCs in culture. 4 Active TGF-␤ is detectable in the aortic wall of mice and is decreased in transgenic mice expressing apo(a) as a consequence of apo(a) inhibition of the plasminogen/plasmin system.…”

Section: Tgf-␤mentioning

confidence: 96%

Anti-Inflammatory Mechanisms in the Vascular Wall

Tedgui

Mallat

2001

Circulation Research

378

258

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Abstract-The role of vascular cells during inflammation is critical and is of particular importance in inflammatorydiseases, including atherosclerosis, ischemia/reperfusion, and septic shock. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli. Most of the vascular inflammatory responses are mediated through the IB/nuclear factor-B system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. The anti-inflammatory mechanisms in the vascular wall involve anti-inflammatory external signals and intracellular mediators. The anti-inflammatory external signals include the anti-inflammatory cytokines, transforming growth factor-␤, interleukin-10 and interleukin-1 receptor antagonist, HDL, as well as some angiogenic and growth factors. Physiological laminar shear stress is of particular importance in protecting endothelial cells against inflammatory activation. Its effects are partly mediated through NO production. Finally, endogenous cytoprotective genes or nuclear receptors, such as the peroxisome proliferator-activated receptors, can be expressed by vascular cells in response to proinflammatory stimuli to limit the inflammatory process and the injury. nflammation is a basic pathological mechanism that underlies a variety of diseases. The inflammatory reaction involves the complex interactions between inflammatory cells (neutrophils, lymphocytes, and monocytes/macrophages) and vascular cells (endothelial cells [ECs] and smooth muscle cells [SMCs]). The role of vascular cells during the inflammatory process is critical. Multiple cytokines and growth factors are present at sites of inflammation, and each of these can potentially influence the nature of the inflammatory response. ECs and SMCs must integrate the signals generated by these multiple factors to effectively regulate the immunoinflammatory response through the expression of adhesion molecules, cytokines, chemokines, matrix metalloproteinases, and growth factors. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli and resulting in the identification of major intracellular inflammatory signaling pathways, particularly the IB/nuclear factor-B (NF-B) system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. This might be of particular importance in inflammatory diseases, such as atherosclerosis, septic shock, or ischemia/reperfusion. The purpose of the present review is to describe recent advances in the understanding of the anti-inflammatory mechanisms in vascular cells, focusing on anti-inflammatory external signals and intracellular mediators Original

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Section: Tgf-␤mentioning

confidence: 96%

Anti-Inflammatory Mechanisms in the Vascular Wall

Tedgui

Mallat

2001

Circulation Research

378

258

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“…19,20 SMCs were routinely cultured with a mixture of Weymouth's MB 752/1 and Nutrient Mixture Ham's F-12, supplemented by 10% FCS, 100 U/mL penicillin, and 100 g/mL streptomycin (GIBCO BRL). Vascular SMCs were identified by the characteristic "hill and valley" growth pattern and positive immunocytochemical staining with a monoclonal antibody against smooth muscle ␣-actin (Progen).…”

Section: Cell Culturementioning

confidence: 99%

Cartilage Oligomeric Matrix Protein (Thrombospondin-5) Is Expressed by Human Vascular Smooth Muscle Cells

Riessen

Fenchel

Chen

et al. 2001

ATVB

Self Cite

112

101

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“…To obtain high-titer virus preparations, EC-propagated virus stocks were inoculated with fibroblasts for a single round of infection, harvested at 100% cytopathic effect (CPE), and made cell free by centrifugation. HAEC were isolated from adult human iliac arteries of bypass recipients by mechanically removing the endothelial layer as previously described (1,2) and were cultured in EGM-2 medium (Clonetics, Walkersville, Md.) containing 2% fetal calf serum on culture flasks (Greiner, Frickenhausen, Germany) coated with 2% gelatin.…”

Section: Efficient Lytic Infection Of Haec By Ec-propagated Hcmv Stramentioning

confidence: 99%

Efficient Lytic Infection of Human Arterial Endothelial Cells by Human Cytomegalovirus Strains

Kahl

Siegel-Axel

Stenglein³

et al. 2000

J Virol

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Endothelial cells (EC) are common targets of permissive infection by human cytomegalovirus (HCMV) inEndothelial cells (EC) are major targets of human cytomegalovirus (HCMV) during acute infection of an immunocompromised host (18). In addition to contributing to hematogenous viral dissemination (7,8,13,19,23), infected EC may trigger direct vascular injury if viral induced cytopathogenicity occurs. In support of these in vivo data, susceptibility of cultured human venous EC (HUVEC) to productive lytic HCMV infection has been demonstrated (25). However, studies of interactions of HCMV with human arterial EC (HAEC) have generated conflicting results. Whereas reports about noncytopathic persistence of HCMV in cultured aortic EC (6) raised the possibility of different susceptibilities of EC depending on their vascular origin, Knight et al. (9) have described similar cytopathologies of HCMV in HUVEC, HAEC, and microvascular EC with regard to adhesion molecule induction. The respective usage of fibroblast-propagated and EC-propagated HCMV strains might provide an explanation for the discrepancies. While such interstrain differences in the cytopathic potential of HCMV in HUVEC are well established (11,20,22,24), the lytic potentials of various HCMV strains in HAEC have not yet been determined.In the present investigation we have tested the hypothesis that interstrain differences in viral host cell tropism, rather than properties inherent to EC of different vascular origins, determine the outcome of HCMV infection. To this end we have performed a detailed analysis of viral replication kinetics, long-term evolution of cytopathology, and lytic end points, comparing EC derived from human adult iliac artery, placental microvasculature, and umbilical vein following inoculation with various HCMV strains. Efficient lytic infection of HAEC by EC-propagated HCMV strains.In a first set of experiments, HCMV strains VHL/E (kindly provided by W. J. Waldman) (24) and TB40/E (22) were tested for cytopathic potential in HAEC. Both strains were propagated in HUVEC to preserve the natural endothelial cytopathogenicity of the original isolates. To obtain high-titer virus preparations, EC-propagated virus stocks were inoculated with fibroblasts for a single round of infection, harvested at 100% cytopathic effect (CPE), and made cell free by centrifugation. HAEC were isolated from adult human iliac arteries of bypass recipients by mechanically removing the endothelial layer as previously described (1, 2) and were cultured in EGM-2 medium (Clonetics, Walkersville, Md.) containing 2% fetal calf serum on culture flasks (Greiner, Frickenhausen, Germany) coated with 2% gelatin. For infection, cells were preincubated for 2 h in heparin-free medium, inoculated with cell-free virus at multiplicities of infection (MOI) of 0.1, 1, and 10, and incubated for 90 min before removal of the inoculum. The medium was replaced at 48-h intervals. The kinetics of viral antigen expression in HAEC cultures was analyzed by indirect immunoperoxidase detection of imm...

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Growth Factor Expression of Human Arterial Smooth Muscle Cells and Endothelial Cells in a Transfilter Coculture System

Cited by 35 publications

References 3 publications

Anti-Inflammatory Mechanisms in the Vascular Wall

Anti-Inflammatory Mechanisms in the Vascular Wall

Cartilage Oligomeric Matrix Protein (Thrombospondin-5) Is Expressed by Human Vascular Smooth Muscle Cells

Efficient Lytic Infection of Human Arterial Endothelial Cells by Human Cytomegalovirus Strains

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