Differential analyses of angiogenesis and expression of growth factors in micro- and macrovascular endothelial cells of type 2 diabetic rats

Wang, X.H.; Chen, SF; Jin, Hongyue; Hu, RM

doi:10.1016/j.lfs.2008.12.010

Cited by 43 publications

(30 citation statements)

References 45 publications

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“…MAECs were isolated and cultured as described previously with minor modifications (27). Described briefly, 8-12-week-old C57BL/6, CAV1 2/2 , and TLR4…”

Section: Animalsmentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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High mobility group box 1 (HMGB1) plays an important role in the pathologic processes of endothelial permeability under oxidative stress. Trophoblast oxidative stress has been implicated in the pathophysiology of preeclampsia (PE). HMGB1 serum levels are increased in PE. However, the potential roles of HMGB1 in endothelial permeability in PE remain unclear. We assessed the effects of the hypoxic trophoblast on the permeability of the endothelial monolayer. Our results showed that the hypoxic trophoblast displayed higher HMGB1 mRNA, intracellular HMGB1 protein, and HMGB1 in conditioned medium than those of the normoxic trophoblast did. The hypoxic trophoblast conditioned medium increased the endothelial monolayer permeability and increased TLR 4 and caveolin-1 (CAV-1) protein expression in endothelial cells, which was inhibited by glycyrrhizic acid and HMGB1 small interfering RNA transfection to trophoblasts before hypoxia. The increased endothelial permeability induced by hypoxic trophoblast conditioned medium could be inhibited with TLR4 or CAV-1 gene silencing in endothelial cells. Immunoprecipitation showed that CAV-1 and TLR4 are colocalized in HUVECs and C57BL/6 mouse kidney. TLR4 small interfering RNA suppressed CAV-1 protein expression in endothelial cells upon stimulation of hypoxic trophoblast conditioned medium or HMGB1. We conclude that hypoxic trophoblasts play an important role in the mechanism of general edema (including protein urine) in PE via increasing endothelial monolayer permeability through the HMGB1/TLR4/CAV-1 pathway.

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“…MAECs were isolated and cultured as described previously with minor modifications (27). Described briefly, 8-12-week-old C57BL/6, CAV1 2/2 , and TLR4…”

Section: Animalsmentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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“…Micro-and macrovascular ECs not only respond differently to positive/negative modulators of angiogenesis but also express unlike amounts of growth factors, enzymes and receptors. Interestingly, it seems that microvasculature is in general more reactive compared with endothelium from the macrovasculature (Murthi et al, 2007;Sobrevia et al, 2011;Wang et al, 2009) (see also Scheme 1). Therefore, the characteristics of ECs of different origins may determine the angiogenesis behavior/impairments of micro-and macrovasculature.…”

Section: Resultsmentioning

confidence: 99%

“…To measure the rate of healing, the area between the wound edges is measured and compared relative to the area of the original wound at t ¼ 0. As indicated by Figure 3 and contrary to HUVECs, rat mesenteric endothelial cells showed remarkable migration ability measured by the cell scratch wound healing assay (Brouillet et al, 2010;Wang et al, 2009) and repopulated the wound, completely, after 24 h.…”

Section: Evaluation Of Endothelial Cell Proliferation and Migrationmentioning

confidence: 87%

Anin vitromodel for spontaneous angiogenesis using rat mesenteric endothelial cells: Possible therapeutic perspective for obesity and related disorders

Mansouri

Khodarahmi

Ghadami

2013

Pharmaceutical Biology

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Context: Abnormal obesity and the related diseases, such as diabetes and cardiovascular disease, are the main causes of mortality, around the world. A key feature of the adipogenesis and obesity is angiogenesis-dependent tissue growth accompanied with extracellular remodeling. In this way, suppression of angiogenesis may be a key point for preventing the adipogenesis. Objective: In the present study, to provide a deeper insight to understand obesity and screening for more effective therapeutics, we have developed a three-dimensional in vitro model of microvessel formation under collagen matrix culture using endothelial cells, extracted from a suitable tissue. Materials and methods: In a successful approach for developing an angiogenesis model, the rat mesenteric microvascular endothelial cells (RMMECs) were isolated, coated on dextran beads and then suspended in collagen gel. Additionally, the proliferation as well as migration of endothelial cells were analyzed and compared with human umbilical vein endothelial cells (HUVECs). Results: RMMECs showed remarkable migration ability and had higher growth during the logarithmic growth phase, when compared with HUVECs. Also, no significance differences in morphogenesis were observed between HUVECs and RMMECs. Discussion and conclusion: The model may be useful in providing insights to develop potential intervention strategies in vivo against obesity-related disorders. Targeting endothelial cells is an interesting and exciting possibility that may be raised in further investigations.

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“…MMVECs (1×10 5 cells/well) and MCs (1×10 5 cells/well) were co-cultured in DMEM as described previously in the presence or absence of compound 48/80 (5 µg/mL) for 8 h (18). MMVECs were further incubated with MCGs for 8 h at 37°C in humidified 95% air-5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

Wang

Zhu

Jiang

et al. 2013

Braz J Med Biol Res

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Angiopoietin (Ang)-1 and Ang-2 interact in angiogenesis to activate the Tie-2 receptor, which may be involved in new vessel maturation and regression. Mast cells (MCs) are also involved in formation of new blood vessels and angiogenesis. The present study was designed to test whether MCs can mediate angiogenesis in myocardial microvascular endothelial cells (MMVECs). Using a rat MMVEC and MC co-culture system, we observed that Ang-1 protein levels were very low even though its mRNA levels were increased by MCs. Interestingly, MCs were able to enhance migration, proliferation, and capillary-like tube formation, which were associated with suppressed Ang-2 protein expression, but not Tie-2 expression levels. These MCs induced effects that could be reversed by either tryptase inhibitor [N-tosyl-L-lysine chloromethyl ketone (TLCK)] or chymase inhibitor (N-tosyl-L-phenylalanyl chloromethyl ketone), with TLCK showing greater effects. In conclusion, our data indicated that MCs can interrupt neovessel maturation via suppression of the Ang-2/Tie-2 signaling pathway.

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Differential analyses of angiogenesis and expression of growth factors in micro- and macrovascular endothelial cells of type 2 diabetic rats

Cited by 43 publications

References 45 publications

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Anin vitromodel for spontaneous angiogenesis using rat mesenteric endothelial cells: Possible therapeutic perspective for obesity and related disorders

Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

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