Abstract 17122: Cardioprotection With Proangiogenic Nanomaterials Formulated With CHIR99021 and FGF1

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Chengming Fan ◽  
Yasin Oduk ◽  
Meng Zhao ◽  
Yawen Tang ◽  
Gregory P. Walcott ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Treatment Group ◽  
Cardiac Fibrosis ◽  
Sham Group ◽  
Contractile Function ◽  
Umbilical Vein ◽  
Tunel Staining ◽  
Aurora B ◽  
Lv Remodeling ◽  
Umbilical Vein Endothelial Cells

Introduction: We aimed at to investigate whether activation of both FGF1 and Wnt1 synergistically enhances angiogenesis and render the cardioprotection in hearts with post infarction LV remodeling. Materials and methods: CHIR99021 (a Wnt1 activator) and FGF1 were encapsulated into poly lactic-co-glycolic acid nanoparticles (CHIR99021/FGF1-NPs). Ischemic heart models were generated in C57BL/6 mice or Yorkshire swine by ligation of the left anterior descending coronary. The mice were randomly divided into 6 groups: Myocardial infarction (MI) Only (n=11), MI with nanoparticles (CHIR99021 or/and FGF1 loaded) injection (n=12, each), MI with non-loaded nanoparticles injection (n=11) and Sham group (n=10). The swine were divided into 3 groups: ischemic reperfusion injury (IRI) (n=4), IRI with CHIR99021/FGF-NPs injection (n=4) and Sham group (n=4). Left ventricle function 4 week after surgery were evaluated by Echocardiography. Cell proliferation was assessed via immunostaining in ischemic hearts and in cultivated human umbilical vein endothelial cells (HUVECs) and Human vascular smooth muscle cells (HVSMCs) using the following markers: Ki67, Brdu, PH3, and Aurora B. Apoptosis was determined with TUNEL staining. Cardiac fibrosis was evaluated via Sirius red and Fast green staining (mice) and magnetic resonance imaging (swine). Results: CHIR99021/FGF1-NPs treatment attenuated fibrosis and preserved heart contractile function in mice and swine models of postinfarction LV remodeling. The proportion of cells that expressed cell cycle markers (Ki67; BrdU; Aurora B and PH3) was significantly greater in CHIR99021+FGF1 treatment group than CHIR99021, FGF1 and PBS treatment group. The proportion of apoptotic cells was significantly smaller in CHIR99021+FGF1 treatment group than in groups of control, VEGF, CHIR99021, or FGF1 treatment alone. Conclusions: CHIR99021 and FGF synergistically activate cell cycle and reduce apoptosis, which accompanied by a significant improvement of cardiac function.

Extract of Housefly (Musca domestica) Maggot Anti-Inflammatory Parts could Regulate the Proliferation and Migration of TNF-α- Stimulated Human Umbilical Vein Endothelial Cells

2014 ◽  
Vol 884-885 ◽  
pp. 446-449
Author(s):  
Fu Jiang Chu ◽  
Hong Yan Ma ◽  
Xiao Bao Jin ◽  
Jia Yong Zhu
Keyword(s):  
Endothelial Cells ◽  
Treatment Group ◽  
Umbilical Vein ◽  
House Fly ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells ◽  
Proliferation And Migration

House fly maggot, Musca domestica (Linnaeus) (Diptera: Muscidae) is one of the traditional Chinese medicine (TCM). In our earlier studies, the anti-inflammatory and anti-atherosclerotic functions of the housefly maggot have been found and also the anti-inflammatory effective parts have been acquired. In this study, the effect of housefly maggot anti-inflammatory parts on proliferation and migration of TNF-α-stimulated human umbilical vein endothelial cells (HUVEC) were investigated. And the results showed that the proliferation index and the migration rates of HUVEC which stimulated by TNF-α were decreased significantly in housefly maggot anti-inflammatory parts treatment group. And also the secretion of vascular endothelial growth factor (VEGF) was decreased too compared with only TNF-α treatment group. Based on the above, the housefly maggot anti-inflammatory parts could regulate the endothelial cell dysfunction through decreasing cell proliferation and migration and a reduction in VEGF expression might plays a key role in this process.

scholarly journals Calcitriol Attenuates Doxorubicin-Induced Cardiac Dysfunction and Inhibits Endothelial-to-Mesenchymal Transition in Mice

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 865 ◽  
Author(s):  
Tsai ◽  
Lin ◽  
Hang ◽  
Chen
Keyword(s):  
Myocardial Fibrosis ◽  
Cardiac Fibrosis ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Umbilical Vein ◽  
Active Form ◽  
Mesenchymal Transition ◽  
Endothelial To Mesenchymal Transition ◽  
Umbilical Vein Endothelial Cells

Doxorubicin (Dox) is an effective anti-neoplasm drug, but its cardiac toxicity limits its clinical use. Endothelial-to-mesenchymal transition (EndMT) has been found to be involved in the process of heart failure. It is unclear whether EndMT contributes to Dox-induced cardiomyopathy (DoIC). Calcitriol, an active form Vitamin D3, blocks the growth of cancer cells by inhibiting the Smad pathway. To investigate the effect of calcitriol via inhibiting EndMT in DoIC, C57BL/6 mice and endothelial-specific labeled mice were intraperitoneally administered Dox twice weekly for 4 weeks (32 mg/kg cumulative dose) and were subsequently treated with or without calcitriol for 12 weeks. Echocardiography revealed diastolic dysfunction at 13 weeks following the first Dox treatment, accompanied by increased myocardial fibrosis and up-regulated pro-fibrotic proteins. Calcitriol attenuated Dox-induced myocardial fibrosis, down-regulated pro-fibrotic proteins and improved diastolic function. Endothelial fate tracing revealed that EndMT-derived cells contributed to Dox-induced cardiac fibrosis. In vitro, human umbilical vein endothelial cells and mouse cardiac fibroblasts were treated with Transforming growth factor (TGF)-β with or without calcitriol. Morphological, immunofluorescence staining, and Western blot analyses revealed that TGF-β-induced EndMT and fibroblast-to-myofibroblast transition (FMT) were attenuated by calcitriol by the inhibition of the Smad2 pathway. Collectively, calcitriol attenuated DoIC through the inhibition of the EndMT and FMT processes.

Effects of Bone Powder Extracts with Different Hydroxyapatite Contents on Proliferation, Apoptosis, and Cell Phase of Human Umbilical Vein Endothelial Cells

2021 ◽  
Vol 13 (7) ◽  
pp. 1275-1279
Author(s):  
Yanyi Liu ◽  
Xueyang Zhang ◽  
Yuan Su ◽  
Fei Hu
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cell Morphology ◽  
Umbilical Vein ◽  
Bone Powder ◽  
Group A ◽  
Proliferation Ability ◽  
Umbilical Vein Endothelial Cells ◽  
Experimental Group ◽  
Powder Extract

ABSTRACTBone powder with different contents of hydroxyapatite may have different effects on angiogenesis in bone defect areas. The effects of bone powder with different content of hydroxyapatite on proliferation, apoptosis and cell cycle of vascular endothelial cells (HUVECs) were studied. In the experimental group, HUVECs were cultured in the incubator with different contents of hydroxyapatite bone powder extract. The experimental group was divided into four subgroups: group A had a low hydroxyapatite content of 10–15%; group B had a hydroxyapatite content of 25–30%; group C had a hydroxyapatite content of 80–90%; and group D had a hydroxyapatite content of more than 90%. The control group was treated with the culture of umbilical vein endothelial cells alone. Firstly, we used scanning electron microscope (SEM) to observe the morphology of bone powder with different hydroxyapatite content in normal condition. After that, we carried out a series of experiments to observe the changes of cell morphology, proliferation ability, apoptosis and cell cycle in different culture groups. The results showed that there was no significant difference in cell morphology and proliferation ability among different experimental groups. However, the apoptosis rate in group A was higher than that in group C. The underlying mechanism may be related to G1 arrest and G2 transformation in smaller and higher concentration groups, respectively. We can thus preliminarily conclude that a high concentration of hydroxyapatite in bone powder extract would be most suitable for cell cultures.

scholarly journals Antitumor Potential and Phytochemical Profile of Plants from Sardinia (Italy), a Hotspot for Biodiversity in the Mediterranean Basin

Plants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 26 ◽  
Author(s):  
Concettina Cappadone ◽  
Manuela Mandrone ◽  
Ilaria Chiocchio ◽  
Cinzia Sanna ◽  
Emil Malucelli ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Umbilical Vein ◽  
Sesquiterpene Lactones ◽  
Induce Cell Cycle Arrest ◽  
P53 Expression ◽  
Human Osteosarcoma Cells ◽  
Wide Range ◽  
M Phase ◽  
Centaurea Calcitrapa ◽  
Umbilical Vein Endothelial Cells

Sardinia (Italy), with its wide range of habitats and high degree of endemism, is an important area for plant-based drug discovery studies. In this work, the antitumor activity of 35 samples from Sardinian plants was evaluated on human osteosarcoma cells U2OS. The results showed that five plants were strongly antiproliferative: Arbutus unedo (AuL), Cynara cardunculus (CyaA), Centaurea calcitrapa (CcA), Smilax aspera (SaA), and Tanacetum audibertii (TaA), the latter endemic to Sardinia and Corsica. Thus, their ability to induce cell cycle arrest and apoptosis was tested. All extracts determined cell cycle block in G2/M phase. Nevertheless, the p53 expression levels were increased only by TaA. The effector caspases were activated mainly by CycA, TaA, and CcA, while AuL and SaA did not induce apoptosis. The antiproliferative effects were also tested on human umbilical vein endothelial cells (HUVEC). Except for AuL, all the extracts were able to reduce significantly cell population, suggesting a potential antiangiogenic activity. The phytochemical composition was first explored by 1H NMR profiling, followed by further purifications to confirm the structure of the most abundant metabolites, such as phenolic compounds and sesquiterpene lactones, which might play a role in the measured bioactivity.

Propranolol Suppresses Cobalt Chloride-Induced Hypoxic Proliferation in Human Umbilical Vein Endothelial Cells in vitro

Pharmacology ◽  
2018 ◽  
Vol 103 (1-2) ◽  
pp. 61-67 ◽  
Author(s):  
Li Wei ◽  
Li Li ◽  
Bin Zhang ◽  
Lin Ma
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cyclin D1 ◽  
Cobalt Chloride ◽  
Umbilical Vein ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Background/Aims: To investigate the effect of propranolol on cobalt chloride (CoCl2)-induced hypoxic proliferation in human umbilical vein endothelial cells (HUVECs). Methods: CoCl2 was administrated to HUVECs to mimic hypoxic proliferation in infantile hemangioma. The proliferation of HUVECs was detected by Cell Counting Kit-8. Effects of propranolol on apoptosis and expressions of cell cycle-related genes, CDK4 and cyclin D1, were detected by flow cytometry and RT-PCR respectively. The release of vascular endothelial growth factor (VEGF) and lactate dehydrogenase (LDH) was measured by enzyme-linked immunosorbent assay. Results: Propranolol significantly inhibited the CoCl2-induced hypoxic proliferation of HUVECs in a dose-dependent manner, and also induced apoptosis and suppressed the expression of CDK4 and cyclin D1. Propranolol also decreased the release of VEGF and LDH in the supernatant. Conclusions: Propranolol could inhibit CoCl2-induced hypoxic proliferation of HUVECs through inducing apoptosis and cell cycle arrest.

scholarly journals Platelet Lysate Inhibits NF-κB Activation and Induces Proliferation and an Alert State in Quiescent Human Umbilical Vein Endothelial Cells Retaining Their Differentiation Capability

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 331 ◽  
Author(s):  
Romaldini ◽  
Ulivi ◽  
Nardini ◽  
Mastrogiacomo ◽  
Cancedda ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Endothelial Cells ◽  
Blood Vessel ◽  
Umbilical Vein ◽  
Healing Process ◽  
Primary Cultures ◽  
Platelet Lysate ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

: Injured blood vessel repair and blood circulation re-establishment are crucial events for tissue repair. We investigated in primary cultures of human umbilical vein endothelial cells (HUVEC), the effects of platelet lysate (PL), a cocktail of factors released by activated platelets following blood vessel disruption and involved in the wound-healing process triggering. PL exerted a protective effect on HUVEC in an inflammatory milieu by inhibiting IL-1α-activated NF-κB pathway and by inducing the secretion of PGE2, a pro-resolving molecule in the wound microenvironment. Moreover, PL enhanced HUVEC proliferation, without affecting their capability of forming tube-like structures on matrigel, and activated resting quiescent cells to re-enter cell cycle. In agreement with these findings, proliferation-related pathways Akt and ERK1/2 were activated. The expression of the cell-cycle activator Cyclin D1 was also enhanced, as well as the expression of the High Mobility Group Box-1 (HMGB1), a protein of the alarmin group involved in tissue homeostasis, repair, and remodeling. These in vitro data suggest a possible in vivo contribution of PL to new vessel formation after a wound by activation of cells resident in vessel walls. Our biochemical study provides a rationale for the clinical use of PL in the treatment of wound healing-related pathologies.

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