Venular endothelial cells from bovine heart

Schelling, Margaret E.; Meininger, Cynthia J.; Hawker, James; Granger, Harris J.

doi:10.1152/ajpheart.1988.254.6.h1211

Cited by 58 publications

(47 citation statements)

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“…Coronary venular endothelial cells (CVEC) were obtained, as previously described, by a bead-perfusion technique through the coronary sinus (25). Cells were maintained in culture in DME supplemented with 10% bovine calf serum (CS) and antibiotics (100 U/ml penicillin, 100 g/ml streptomycin) on gelatin-coated dishes.…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide synthase lies downstream from vascular endothelial growth factor-induced but not basic fibroblast growth factor-induced angiogenesis.

Ziche

Morbidelli²,

Choudhuri³

et al. 1997

J. Clin. Invest.

859

648

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Section: Methodsmentioning

confidence: 99%

Nitric oxide synthase lies downstream from vascular endothelial growth factor-induced but not basic fibroblast growth factor-induced angiogenesis.

Ziche

Morbidelli²,

Choudhuri³

et al. 1997

J. Clin. Invest.

859

648

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“…Coronary venular endothelial cells (CVECs) were isolated and cultured as described previously (Schelling et al, 1988). Cells between passages 10 and 15 maintaining all of the markers typical of microvascular endothelium were used in the experiments.…”

Section: Methodsmentioning

confidence: 99%

Fibroblast Growth Factor-2 Mediates Angiotensin-Converting Enzyme Inhibitor-Induced Angiogenesis in Coronary Endothelium

Donnini¹,

Solito²,

Giachetti³

et al. 2006

J Pharmacol Exp Ther

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The beneficial effect exerted by angiotensin-converting enzyme inhibitors (ACEI) on vascular endothelium has been attributed to restoration of endothelial cell survival properties and improvement of angiogenesis. Fibroblast growth factor (FGF)-2 is an angiogenic factor for the microvascular endothelium, which tonically promotes endothelial cell growth and survival through an autocrine/ paracrine mechanism. Here, we formulate the hypothesis that FGF-2 might contribute to the prosurvival/proangiogenic effect of ACEI. We investigated zofenoprilat and, in selected experiments, lisinopril, as representatives of ACEI. These compounds induced formation of pseudocapillaries in vessel fragments isolated from porcine coronary and human umbilical arteries by increasing endothelial cell growth up to 5-fold. Angiogenesis was abolished by inhibitors of nitric-oxide synthase (NOS) pathway and by anti-FGF-2 antibodies. Consistently, in cultured coronary endothelial cells (CVECs), ACEI up-regulated endothelial NOS (eNOS) and FGF-2 and induced mitogen-activated protein kinase extracellular signal-regulated kinase 1/2 activation. The overexpression of eNOS/FGF-2 produced, at the functional level, enhanced cell proliferation and migration, the latter effect being dose-dependent and maximal at 0.1 M zofenoprilat. The importance of FGF-2 for the acquisition of the angiogenic phenotype elicited by ACEI was clearly demonstrated by the impairment of endothelial functions following transfection of CVECs with small interference RNA for FGF-2. Moreover, FGF-2 silencing greatly affected the nuclear translocation of the FGF receptor (FGFR)-1, highlighting the autocrine mode of action of FGF-2. At the endothelial membrane level, zofenoprilat appeared to activate the bradykinin B1 receptor, a known stimulant of FGF-2 expression. In conclusion, we show that ACEI exert protective/proangiogenic effects in microvascular coronary endothelial cells by activating the endogenous FGF-2/ FGFR-1 system.

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“…While methods for isolating and cultivating venular EC have been reported (49,59), there is no indication in those studies of the degree of purity, nor is there convincing proof for the venular origin of the resulting cultures, despite the availability of specific markers (19). The same holds for the sole report on the isolation of arteriolar EC (together with cells of venular origin; Ref.…”

Section: Purification Of Constituent Wall Cells Of the Smallest Myocamentioning

confidence: 99%

Wall structures of myocardial precapillary arterioles and postcapillary venules reexamined and reconstructed in vitro for studies on barrier functions

Nees¹,

Juchem²,

Eberhorn³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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The barrier functions of myocardial precapillary arteriolar and postcapillary venular walls (PCA or PCV, respectively) are of considerable scientific and clinical interest (regulation of blood flow and recruitment of immune defense). Using enzyme histochemistry combined with confocal microscopy, we reexamined the cell architecture of human PCA and PVC and reconstructed appropriate in vitro models for studies of their barrier functions. Contrary to current opinion, the PCA endothelial tube is encompassed not by smooth muscle cells but rather by a concentric layer of pericytes cocooned in a thick, microparticlecontaining extracellular matrix (ECM) that contributes substantially to the tightness of the arteriolar wall. This core tube extends upstream into the larger arterioles, there additionally enwrapped by smooth muscle. PCV consist of an inner layer of large, contractile endothelial cells encompassed by a fragile, wide-meshed pericyte network with a weakly developed ECM. Pure pericyte and endothelial cell preparations were isolated from PCA and PCV and grown in sandwich cultures. These in vitro models of the PCA and PCV walls exhibited typical histological and functional features. In both plasma-like (PLM) and serum-containing (SCM) media, the PCA model (including ECM) maintained its low hydraulic conductivity (LP ϭ 3.24 Ϯ 0.52 · 10 Ϫ8 cm·s Ϫ1 · cmH2O Ϫ1 ) and a high selectivity index for transmural passage of albumin (SIAlb ϭ 0.95 Ϯ 0.02). In contrast, LP and SIAlb in the PCV model (almost no ECM) were 2.55 Ϯ 0.32 · 10 Ϫ7 cm·s Ϫ1 · cmH2O Ϫ1 and 0.88 Ϯ 0.03, respectively, in PLM, and 1.39 Ϯ 0.10 · 10 Ϫ6 cm·s Ϫ1 · cmH2O Ϫ1 and 0.49 Ϯ 0.04 in SCM. With the use of these models, systematic, detailed studies on the regulation of microvascular barrier properties now appear to be feasible.

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Venular endothelial cells from bovine heart

Cited by 58 publications

References 0 publications

Nitric oxide synthase lies downstream from vascular endothelial growth factor-induced but not basic fibroblast growth factor-induced angiogenesis.

Nitric oxide synthase lies downstream from vascular endothelial growth factor-induced but not basic fibroblast growth factor-induced angiogenesis.

Fibroblast Growth Factor-2 Mediates Angiotensin-Converting Enzyme Inhibitor-Induced Angiogenesis in Coronary Endothelium

Wall structures of myocardial precapillary arterioles and postcapillary venules reexamined and reconstructed in vitro for studies on barrier functions

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