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While many endothelial cell lines exist, few are of human origin with characteristics close to the parent endothelial cell. We derived a subline (HUVEC-CS) of immortalized human umbilical vein endothelial cells (HUVEC-C) that proliferate in standard growth media and exhibit positive acetylated low-density lipoprotein (AcLDL) uptake, express eNOS, CD31 and ve-cadherin, and spontaneously form capillary-like structures when grown on Matrigel. HUVEC-CS also maintain endothelial cell characteristics at the level of mitogenesis, kinase activation and vasodilator production. Like primary HUVEC cells, HUVEC-CS express many of the key proteins necessary for vasodilator production, including epithelial nitric oxide synthase (eNOS), HSP 90, cav-1 and -2, cPLA2, and COX-1 and -2. Prostaglandin I synthase (PGIS) was not detectable by Western blot analysis, consistent with primary HUVEC in which PGI2 production is minimal. Receptors were detected for angiotensin II (AII), bradykinin, ATP and growth factors. ATP induced a dose- and time-dependent rise in the intracellular free Ca2+ concentration ([Ca2+]i). Initially, ATP stimulates P2Y receptors rather than P2X receptors, as demonstrated by the inability of ATP to initiate a Ca2+ response subsequent to emptying of the internal Ca2+ stores by thapsigargin. AII, bradykinin, epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) also caused a rise in [Ca2+]i in a subset of the cells. ATP, basic fibroblastic growth factor (bFGF), EGF and VEGF induced mitogenesis and caused a rise in ERK 2 activation within 10 min. L-Arginine to L-citrulline conversion assays showed that ATP, EGF and VEGF induced a significant rise in eNOS activity, and this correlates with an ability to induce Ca2+ mobilization and ERK 2 activation. In conclusion, HUVEC-CS are indeed endothelial cells and appear to be functionally very similar to primary HUVEC. These cells will prove a valuable tool for future studies in both basic and therapeutic sciences.
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The newly formed corpus luteum (CL) rapidly develops after ovulation and has the features of active vascularisation and mitosis of steroidogenic cells. These stage-specific mechanisms also may contribute to gain the function of prostaglandin F2 alpha (PGF2 alpha)-resistant CL at this stage. Recent studies suggest that the vasoactive peptide angiotensin II (Ang II) regulates luteal function. Thus, this study aimed to investigate (i) the expression of angiotensin-converting enzyme (ACE) mRNA by RT-PCR and the ACE protein expression by immunohistochemistry, (ii) the effects of angiogenic growth factors, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), on the secretion of Ang II, PGF2 alpha, progesterone and oxytocin (OT), and (iii) the effects of luteal vasoactive peptides (Ang II and endothelin-1 (ET-1)) or OT on the secretion of PGF2 alpha, progesterone and OT from bovine early CL (days 3--4 of the oestrous cycle), and evaluate a possible interaction of these substances with PGF2 alpha. The expression of mRNA for ACE was found in theca interna of mature follicle, early CL and endothelial cells from developing CL as well as pituitary and kidney, but granulosa cells of mature follicle were negative. The immunohistochemical analysis revealed that blood capillaries (endothelial cells) were stained for ACE, but luteal cells were negative in early CL. To examine the effects of substances on the secretory function of the CL, an in vitro microdialysis system was used as a model. The infusion of bFGF and VEGF stimulated Ang II and PGF2 alpha secretion as well as progesterone, but not OT secretion in early CL. The infusion of Ang II after PGF2 alpha infusion continued the stimulatory effect on progesterone and OT release within early CL until 3 h thereafter. However, the infusion of ET-1 alone had no effect on progesterone or OT release. The infusion of luteal peptides such as Ang II and OT stimulated PGF2 alpha secretion, whereas the infusion of ET-1 did not. In conclusion, the overall results of this study indicate that a functional angiotensin system exists on the endothelial cells of early CL, and that angiogenic factors bFGF and VEGF upregulate luteal Ang II and PGF2 alpha secretion, which fundamentally supports the mechanism of progesterone secretion in bovine early CL. This idea supports the concept that the local regulatory mechanism involved in active angiogenesis ensures the progesterone secretion in the developing CL in vivo.
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Ocular diseases such as proliferative diabetic retinopathy are the major cause of blindness in industrialized countries. The main pathologic features of these diseases are hypoxia and overproduction of growth factors resulting in pathologic proliferation of endothelial cells and new vessel formation. Particularly, hypoxia and growth factors, such as VEGF, IGF-1, bFGF and TGF beta(2), show a complex interaction in the onset and progression of the diseases. Therefore, to date, most therapeutic strategies for proliferative retinopathies have targeted proliferation of endothelial cells evoked by growth factors. Recently, a synthetic analog of somatostatin, octreotide, has been shown to inhibit the proliferation of various cells in vitro, including endothelial cells. In this study, we have investigated the proliferative response of bovine retinal endothelial cells (BREC) to growth factors under hypoxic conditions and the modulation by octreotide. We found a dose-dependent increase of cell proliferation with VEGF, IGF-1 and bFGF, and inhibition of hypoxia-induced cell proliferation with TGF beta(2). Moreover, growth factor-induced, but not hypoxia-induced, cell proliferation was attenuated in the presence of octreotide. In contrast, TGF beta(2) abolished hypoxia-induced BREC proliferation. Similar to octreotide BIM23027, a somatastatin receptor subtype 2 (SSTR2) receptor agonist was able to attenuate the growth factor-induced proliferation of BREC expressing mRNA and protein for SSTR2. Therefore, we postulate that octreotide exerts its effects mainly through binding to the SSTR2. Taken together, our findings point to octreotide as a promising candidate for the treatment of eye disorders involving growth factor-dependent proliferation of endothelial cells.
Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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Albany Medical College,
Stratton VA Medical Center, 106 New Scotland Ave, Albany, New York 12208, USA
Taichung Poah-Ai Hospital, Taipei, Taiwan
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hypertrophy. In addition, we investigated the expression of two highly potent angiogenic markers, vascular endothelial growth factor (VEGF) and hypoxia inducible factor (HIF-1α) in the hypertrophied bladder. Materials and Methods
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seminiferous cord formation? What composes the VEGFA ligand receptor family and how does VEGFA signal through its receptors and co-receptors? The VEGF family was a logical growth factor family to evaluate its involvement in endothelial cell migration within the
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angiogenesis of the pituitary tumors ( Elias & Weiner 1987 ). It has been shown previously that estrogen exposure can increase the levels of angiogenic factors, like basic fibroblast growth factor and vascular endothelial growth factor (VEGF; Banerjee et al
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(VEGF) production by endothelial cells and so support vascular remodeling indirectly ( Kazi & Koos 2007 ). Beyond ERA and ERB, others have sought to implicate the G-protein-coupled estrogen receptor, GPR30 in maternal regulation of blood flow, but
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vascular endothelial growth factor (VEGF) 164 , VEGF 188 , basic fibroblast growth factor (bFGF or FGF2), angiopoietin-1 and Tie-2 ( Wang et al . 2003 ) and bFGF in neovascularisation around infarction areas ( Zheng et al . 2004 ). More recently, T 4
St Mary’s Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK
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specifically, renal dysfunction. These placental factors include excess release of soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble Endoglin (sENG) which sequester circulating vascular endothelial growth factor (VEGF) and placental growth factor (PIGF
Stark Diabetes Center, Division of Endocrinology, University of Texas Medical Branch, Galvestone, Texas, USA
Renal Unit, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium
Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
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Stark Diabetes Center, Division of Endocrinology, University of Texas Medical Branch, Galvestone, Texas, USA
Renal Unit, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium
Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
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Stark Diabetes Center, Division of Endocrinology, University of Texas Medical Branch, Galvestone, Texas, USA
Renal Unit, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium
Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
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Stark Diabetes Center, Division of Endocrinology, University of Texas Medical Branch, Galvestone, Texas, USA
Renal Unit, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium
Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
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Stark Diabetes Center, Division of Endocrinology, University of Texas Medical Branch, Galvestone, Texas, USA
Renal Unit, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium
Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
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Stark Diabetes Center, Division of Endocrinology, University of Texas Medical Branch, Galvestone, Texas, USA
Renal Unit, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium
Department of Cell Biology, Institute of Anatomy, Aarhus University, Aarhus, Denmark
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accumulation, while mRNAs for vascular endothelial growth factor A (VEGF-A), VEGF receptor 2 (VEGFR-2) and nephrin were used as markers for renal permeability. Materials and Methods Animals Adult female NMRI mice
