scholarly journals Taohong Siwu-Containing Serum Enhances Angiogenesis in Rat Aortic Endothelial Cells by Regulating the VHL/HIF-1α/VEGF Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zhi Tang ◽  
Wangyang Li ◽  
Hongzan Xie ◽  
Shengping Jiang ◽  
Yunqing Pu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Signaling Pathway ◽  
Bone Repair ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Aortic Endothelial Cells ◽  
Vegf Signaling ◽  
Vegf Signaling Pathway ◽  
Aortic Endothelial

Background. The incidence of bone fracture and bone-related diseases is increasing every year. Angiogenesis plays a vital role in fracture healing and bone repair. This study assessed the benefits of Taohong Siwu (TSW) decoction on angiogenesis in isolated rat aortic endothelial cells (RAEC) treated with TSW-containing serum. Methods. The components of TSW decoction were analyzed by liquid chromatography-mass spectrometry (LC-MS). TSW-containing serum was prepared by gavage of TSW decoction to Sprague-Dawley (SD) rats. The effects of TSW-containing serum on the viability, migration, wound healing, and angiogenesis of RAEC were detected by the MTT, transwell, wound healing, and Matrigel lumen formation assays, respectively. In addition, the effects of an HIF-1α inhibitor on TSW-containing serum-induced RAEC were also assessed. The effects of TSW-containing serum on the expression of the HIF-1α signaling pathway were evaluated by qRT-PCR and western blot analysis. Results. LC-MS revealed that TSW decoction primarily contained isomaltulose, choline, D-gluconic acid, L-pipecolic acid, hypotaurine, albiflorin, and tryptophan. TSW-containing serum significantly increased the viability, migration, wound healing, and angiogenesis of RAEC in a dose-dependent manner. Furthermore, our results demonstrated that HIF-1α and VEGF expressions were increased in the cells of TSW-containing serum groups, whereas VHL expression was decreased. The effects of TSW-containing serum were reversed by treatment with an HIF-1α inhibitor. Conclusion. These results suggested that TSW decoction enhanced angiogenesis by regulating the VHL/HIF-1α/VEGF signaling pathway.

scholarly journals Taohong Siwu (TSW) decoction enhances angiogenesis by regulation of VHL/HIF-1α/VEGF pathway

2020 ◽  
Author(s):  
Zhi Tang ◽  
Wangyang Li ◽  
Hongzan Xie ◽  
Shengping Jiang ◽  
Yunqing Pu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Invasion ◽  
Bone Repair ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Vegf Pathway ◽  
Dose Dependent ◽  
Aortic Endothelial

Abstract Background: The incidence of bone fracture and bone-related diseases is increasing year by year. Angiogenesis plays vital role in fracture healing and bone repair. In this study, we assessed the effect of Taohong Siwu (TSW) decoction on angiogenesis by treatment of isolated rat aortic endothelial cell with TSW-containing serum. Method: First, TSW-containing serum was prepared from male Sprague-Dawley by intragastrically administration of TSW decoction. Then, isolated aortic endothelial cells were treated with different dose of TSW-containing serum. The effect of TSW-containing serum on the viability/proliferation of aortic endothelial cells were examined by MTT assay. The effects of TSW-containing serum on endothelial cell invasion, migration/spreading were detected by trans-well assay and scratch/wound-healing assay respectively. In addition, the effect of HIF-1α inhibitor on TSW-induced cell invasion and migration was also assessed. Moreover, the effect of TSW-containing serum on the expression of HIF-1α signaling pathway related protein, including HIF-1α, VHL and VEGF was detected by qRT-PCR and western-blot. Results: Our results showed that TSW decoction significantly increased the endothelial viability, invasion and wound-healing in a dose-dependent manner. Importantly, these enhanced effects induced by TSW were attenuated by HIF-1α inhibitor. Furthermore, our data demonstrated that TSW-containing serum increased the expression of HIF-1α and VEGF in a dose-dependent manner, while decreased the expression of VHL slightly. These effects induced by TSW were reversed by HIF-1α inhibitor. Conclusion: In summary these results for the first time suggested that TSW decoction enhances the angiogenesis by regulating of VHL/HIF-1α/VEGF pathway.

PMA-activated neutrophils decrease ectoenzyme activities in rabbit aortic endothelial cells in culture

1992 ◽  
Vol 263 (6) ◽  
pp. L657-L663
Author(s):  
X. Chen ◽  
M. Tzanela ◽  
M. K. Baumgartner ◽  
J. R. McCormick ◽  
J. D. Catravas
Keyword(s):  
Endothelial Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Endothelial Monolayers ◽  
Activated Neutrophils ◽  
Ace Activity ◽  
Dose Dependent Decrease ◽  
Dose Dependent ◽  
Aortic Endothelial

We have studied the effects of phorbol 12-myristate 13-acetate (PMA)-activated neutrophils [polymorphonuclear leukocytes (PMN)] on endothelial ectoenzyme [angiotensin-converting enzyme (ACE) and 5'-nucleotidase (NCT)] activities in cultured rabbit aortic endothelial cells (EC) with the use of [3H]benzoyl-Phe-Ala-Pro and 14C-labeled AMP as substrates, respectively, under first-order reaction conditions. PMA (1–1,000 ng/ml) or PMN alone had no effect on ACE activity. When PMA was incubated together with PMN (PMN/EC = 1.25:1 or 2.5 x 10(5) neutrophils/ml) for 4 h in Earle's salts, a PMA dose-dependent decrease in ACE activity was observed. Threshold PMA concentration was 2 ng/ml. At 8 ng PMA/ml, ACE activity was totally abolished, without any evidence of cytotoxicity, as inferred from release of 51Cr from prelabeled EC. The decrease in ACE activity was also dependent on PMN concentration and was detectable at PMN/EC values as low as 1.25:10 (0.25 x 10(5) PMN/ml). Inhibition of ACE occurred as early as 1 h after incubation (PMA 10 ng/ml, PMN/EC = 1.25:1). PMA alone caused a small but significant increase in NCT activity, whereas PMA coincubation with PMN produced a significant decrease in NCT activity (20–29%), which was PMA and PMN concentration independent. PMA increased PMN adherence to endothelial monolayers in a concentration-dependent manner. Pretreating PMN with monoclonal antibody 60.3 (raised against the adhesion glycoprotein CD18) or placing a 2-microns filter between PMN and EC, protected the decrease in ACE activity.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Clinopodium tomentosum (Kunth) Govaerts Leaf Extract Influences in vitro Cell Proliferation and Angiogenesis on Primary Cultures of Porcine Aortic Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Irvin Tubon ◽  
Chiara Bernardini ◽  
Fabiana Antognoni ◽  
Roberto Mandrioli ◽  
Giulia Potente ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Primary Cultures ◽  
Ethanolic Extract ◽  
Total Phenolic ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Phenolic Components ◽  
Porcine Aortic Endothelial Cells ◽  
Aortic Endothelial

Clinopodium tomentosum (Kunth) Govaerts is an endemic species in Ecuador, where it is used as an anti-inflammatory plant to treat respiratory and digestive affections. In this work, effects of a Clinopodium tomentosum ethanolic extract (CTEE), prepared from aerial parts of the plant, were investigated on vascular endothelium functions. In particularly, angiogenesis activity was evaluated, using primary cultures of porcine aortic endothelial cells (pAECs). Cells were cultured for 24 h in the presence of CTEE different concentrations (10, 25, 50, and 100 μg/ml); no viability alterations were found in the 10-50 μg/ml range, while a slight, but significant, proliferative effect was observed at the highest dose. In addition, treatment with CTEE was able to rescue LPS-induced injury in terms of cell viability. The CTEE ability to affect angiogenesis was evaluated by scratch test analysis and by an in vitro capillary-like network assay. Treatment with 25-50 μg/ml of extract caused a significant increase in pAEC’s migration and tube formation capabilities compared to untreated cells, as results from the increased master junctions’ number. On the other hand, CTEE at 100 μg/ml did not induce the same effects. Quantitative PCR data demonstrated that FLK-1 mRNA expression significantly increased at a CTEE dose of 25 μg/ml. The CTEE phytochemical composition was assessed through HPLC-DAD; rosmarinic acid among phenolic acids and hesperidin among flavonoids were found as major phenolic components. Total phenolic content and total flavonoid content assays showed that flavonoids are the most abundant class of polyphenols. The CTEE antioxidant activity was also showed by means of the DPPH and ORAC assays. Results indicate that CTEE possesses an angiogenic capacity in a dose-dependent manner; this represents an initial step in elucidating the mechanism of the therapeutic use of the plant.

Stimulation Of Prostacyclin Production In Aortic Endothelial Cells By A Non-Dialysable Serum Factor

1981 ◽  
Author(s):  
E R Hall ◽  
M Rafelson ◽  
K Wu
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Calf Serum ◽  
Dependent Manner ◽  
Freezing And Thawing ◽  
Concentration Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Prostacyclin Production ◽  
Aortic Endothelial

The production of prostacyclin (PGI2) by vascular endothelial cells is thought to be of primary importance in maintaining normal hemostasis. We have investigated the production of prostacyclin in bovine arterial endothelial cells maintained in Dulbecco’s modified Eagle’s medium (DMEM) containing 30% fetal calf serum. Intact, confluent monolayers of endothelial cells (3x106 cells) in passages 2 through 6 were used. The growth medium was removed and the cells were washed in DMEM that did not contain serum. 3 mls of medium alone or containing normal plasma or serum was then added and incubated at 37°C for 15 min. Then, 1 mg of arachidonic acid was added and the cells incubated for an additional hour. The test medium was removed, centrifuged to remove any loose cells and stored at -70°C. To determine the production of PGI2 by the endothelial cells, the medium was assayed for 6-keto-PGF1α, the stable metabolite of PGI2, by radioimmunoassay. The synthesis of prostacyclin by bovine aortic endothelial cells was significantly increased in a concentration dependent manner by both normal platelet poor plasma and normal serum. This increase in prostacyclin production was inhibited by both aspirin and indomethacin, indicating an increase in synthesis rather than the release of PGI2. Furthermore, this increase could be demonstrated in the presence or absence of added arachidonic acid. The active component in plasma and serum was non-dialysable, eliminating the possibility of a small compound such as bradykinin or angiotensin II. This active factor was present after freezing and thawing the plasma and serum and was heat stable (60°C, 5 min). The presence of an endogenous prostacyclin stimulating factor may be significant in the in vivo regulation of prostacyclin production.

scholarly journals Inhibitory effect of serotonin derivatives on high glucose-induced adhesion and migration of monocytes on human aortic endothelial cells

2009 ◽  
Vol 102 (2) ◽  
pp. 264-272 ◽  
Author(s):  
Rosaria Piga ◽  
Yuji Naito ◽  
Satoshi Kokura ◽  
Osamu Handa ◽  
Toshikazu Yoshikawa
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Atherosclerotic Lesion ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Serotonin Derivatives ◽  
And Migration ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Previous reports have shown that safflower-seed extract and its major antioxidant constituents, serotonin hydroxycinnamic amides, attenuated atherosclerotic lesion formation in apoE-deficient mice, as well as inflammation and aortic stiffness in human subjects. In the present report, we examined a still unknown cell-based mechanism of serotonin derivatives against the development of atherosclerosis, focusing our attention on their action against the increase of adhesion molecules and the release of chemotactic factors on human aortic endothelial cells, phenomena that represent the key events in the early stages of atherosclerogenesis. Serotonin derivatives N-(p-coumaroyl)serotonin and N-feruloylserotonin exerted an inhibitory effect on short-term high glucose-induced up-regulation of mRNA and protein of adhesion and migration factors, and the consequent adhesion and migration of monocytes to endothelial cells; they inhibited the activation of transcription factors such as NF-κB, and the overproduction of the mitochondrial superoxide by acting as scavengers of the superoxide radical. In addition, serotonin derivative concentration inside the cells and inside the mitochondria was increased in a time-dependent manner. These results identify a mechanism of action of serotonin derivatives against endothelial damage at a cellular level, and underline their benefits against the disorders and complications related to reactive oxygen species.

Effects of DL-Penicillamine on Cytotoxic Reaction between Baboon Performed Xenoantibodies and Pig Endothelial Cells

1997 ◽  
Vol 20 (7) ◽  
pp. 375-378
Author(s):  
P.A. Kwiatkowski ◽  
J. Puc ◽  
W. Rowinski ◽  
P. Fiedor
Keyword(s):  
Endothelial Cells ◽  
Cytotoxicity Assay ◽  
Dependent Manner ◽  
Elisa Method ◽  
Aortic Endothelial Cells ◽  
Cytotoxic Reaction ◽  
Igg Binding ◽  
Dose Dependent ◽  
Aortic Endothelial

The purpose of this study was to evaluate effects of DL-Penicillamine (DLP), a compound interrupting S-S bonds (IgM pentamers) on binding and cytotoxicity of adult baboon performed xenoantibodies to pig endothelial cells. Pooled baboon serum was treated with different concentrations of DLP during various periods of time. Complement-mediated cytotoxicity assay was used to determine the reactivity of baboon xenoantibodies to pig aortic endothelial cells (PAEC). To assess IgM and IgG binding to PAEC, ELISA method was applied. Serum treated with DLP revealed significant reduction of cytotoxicity in a dose dependent manner. Cytotoxicity was also reduced during time prolongation of DLP exposure to PAEC. Results indicate that baboon performed IgM and IgG xenoantibodies bind to pig endothelial cells, but only IgM is able to cause degradation of the complement. DLP significantly reduces cytotoxicity and eliminates binding of IgMs to PAEC in spite of continued binding of IgG xenoantibodies to the surface of endothelium.

O185 miR-199b induces iPS cell differentiation into endothelial cells by targeting JAG1 and VEGF signaling pathway

Global Heart ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e52-e53
Author(s):  
li zhang ◽  
Ting Chen ◽  
zhoubin li ◽  
yutao wu ◽  
hui yan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Differentiation ◽  
Signaling Pathway ◽  
Ips Cell ◽  
Vegf Signaling ◽  
Vegf Signaling Pathway

scholarly journals Shear-induced tyrosine phosphorylation in endothelial cells requires Rac1-dependent production of ROS

1999 ◽  
Vol 276 (4) ◽  
pp. C838-C847 ◽  
Author(s):  
Li-Hong Yeh ◽  
Young J. Park ◽  
Riple J. Hansalia ◽  
Imraan S. Ahmed ◽  
Shailesh S. Deshpande ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Map Kinase ◽  
Tyrosine Phosphorylation ◽  
Protein Detection ◽  
Pyrrolidine Dithiocarbamate ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

The shear-induced intracellular signal transduction pathway in vascular endothelial cells involves tyrosine phosphorylation and activation of mitogen-activated protein (MAP) kinase, which may be responsible for the sustained release of nitric oxide. MAP kinase is known to be activated by reactive oxygen species (ROS), such as H2O2, in several cell types. ROS production in ligand-stimulated nonphagocytic cells appears to require the participation of a Ras-related small GTP-binding protein, Rac1. We hypothesized that Rac1 might serve as a mediator for the effect of shear stress on MAP kinase activation. Exposure of bovine aortic endothelial cells to laminar shear stress of 20 dyn/cm2for 5–30 min stimulated total cellular and cytosolic tyrosine phosphorylation as well as tyrosine phosphorylation of MAP kinase. Treating endothelial cells with the antioxidants N-acetylcysteine and pyrrolidine dithiocarbamate inhibited in a dose-dependent manner the shear-stimulated increase in total cytosolic and, specifically, MAP kinase tyrosine phosphorylation. Hence, the onset of shear stress caused an enhanced generation of intracellular ROS, as evidenced by an oxidized protein detection kit, which were required for the shear-induced total cellular and MAP kinase tyrosine phosphorylation. Total cellular and MAP kinase tyrosine phosphorylation was completely blocked in sheared bovine aortic endothelial cells expressing a dominant negative Rac1 gene product (N17rac1). We concluded that the GTPase Rac1 mediates the shear-induced tyrosine phosphorylation of MAP kinase via regulation of the flow-dependent redox changes in endothelial cells in physiological and pathological circumstances.

scholarly journals Sulfation of 25-hydroxycholesterol by SULT2B1b decreases cellular lipids via the LXR/SREBP-1c signaling pathway in human aortic endothelial cells

2011 ◽  
Vol 214 (2) ◽  
pp. 350-356 ◽  
Author(s):  
Qianming Bai ◽  
Leyuan Xu ◽  
Genta Kakiyama ◽  
Melissa Ann Runge-Morris ◽  
Phillip B. Hylemon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Aortic Endothelial Cells ◽  
Cellular Lipids ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Volatile Anesthetics Affect Calcium Mobilization in Bovine Endothelial Cells

1996 ◽  
Vol 85 (5) ◽  
pp. 1147-1156 ◽  
Author(s):  
Thomas N. Pajewski ◽  
Ning Miao ◽  
Carl III Lynch ◽  
Roger A. Johns
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Adenosine Triphosphate ◽  
Volatile Anesthetic ◽  
Volatile Anesthetics ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Inhalational Anesthetics ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

Background The site where volatile anesthetics inhibit endothelium-dependent, nitric oxide-mediated vasodilation is unclear. To determine whether anesthetics could limit endothelium-dependent nitric oxide production by inhibiting receptor-mediated increases in cytosolic Ca2+, experiments were performed to see if the inhalational anesthetics halothane, isoflurane, and enflurane affect intracellular Ca2+ ([Ca2+]i) transients induced by the agonists bradykinin and adenosine triphosphate in cultured bovine aortic endothelial cells. Methods Bovine aortic endothelial cells, which had been loaded with the fluorescent Ca2+ indicator Fura-2, were added to medium preequilibrated with volatile anesthetic (1.25% and 2.5% for isoflurane, 1.755 and 3.5% for enflurane, and 0.75% and 1.5% for halothane). In Ca(2+)-containing medium, intracellular Ca2+ transients were elicited in response to bradykinin (10 nM and 1 microM) or adenosine triphosphate (1 microM and 100 microM). Results Both bradykinin and adenosine triphosphate triggered a rapid rise to peak [Ca2+]i followed by a gradual decline to a plateau above the resting level. Although basal [Ca2+]i was unaltered by the anesthetics, both halothane and enflurane, in a dose-dependent manner, depressed the peak and plateau of the [Ca2+]i transient elicited by 10 nM bradykinin, whereas isoflurane had no effect. When [Ca2+]i transients were elicited by 1 microM bradykinin, halothane (1% and 5%) did not alter peak and plateau levels. Halothane and enflurane also decreased [Ca2+]i transients evoked by 1 microM and 100 microM adenosine triphosphate, whereas isoflurane also had no effect in this setting. Conclusions Halothane and enflurane, but not isoflurane, inhibit bradykinin- and adenosine triphosphate-stimulated Ca2+ transients in endothelial cells. Limitations of Ca2+ availability to activate constitutive endothelial nitric oxide synthase could allow for part, but not all, of the inhibition of endothelium-dependent nitric oxide-mediated vasodilation by inhalational anesthetics.

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