scholarly journals Amphiphilic Carboxymethyl Dextran Nanomicelles for Antibacterial Coating on Titanium

2021 ◽  
Author(s):  
Hongbo Wei ◽  
Minghao Zhou ◽  
Weiliang Ye ◽  
Luxuan Zhang ◽  
Jingwei Yu
Keyword(s):  
Drug Release ◽  
Umbilical Vein ◽  
Drug Carriers ◽  
Bacterial Invasion ◽  
Cross Linking ◽  
Antibacterial Coating ◽  
Live Bacteria ◽  
The Stability ◽  
Umbilical Vein Endothelial Cells ◽  
Carboxymethyl Dextran

Peri-implantitis occurs at a significant rate, which is the leading cause of implant failure. The main reason for this unwanted complication is bacterial invasion and biofilm formation. To reduce the incidence of peri-implantitis, we constructed a carboxymethyl dextran (CMD) based nanomicelles antibacterial coating on microarc-oxidized titanium (MAO-Ti) surface. After cross-linking, the drug-loaded nanomicelles were spherical with a particle size of 130nm and uniformly dispersed. Zeta potential was negative, and the absolute value was greater than 10 mV, effectively avoiding micelles aggregation. It was observed by dynamic light scattering (DLS) that the stability of nanomicelles was significantly improved after cross-linking. The hemolysis rate of micelles was less than 5%, and the overall survival rate of human umbilical vein endothelial cells was more than 90%. After being coated on MAO-Ti surface, the cumulative drug release rate of drug-loaded nanomicelles reached 86.6% after 360 hours. Fluorescence staining of immobilized bacteria showed more dead bacteria on the coating surface, and the number of live bacteria was significantly reduced. It was concluded that dextran-based nanomicelles, which showed long-term drug release properties and excellent biocompatibility, are potential drug carriers for fabricating antibacterial coating on titanium surfaces.

scholarly journals Circ_CLASP2 Regulates High Glucose-Induced Dysfunction of Human Endothelial Cells Through Targeting miR-140-5p/FBXW7 Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Qin Zhang ◽  
Jing Long ◽  
Nannan Li ◽  
Xuelian Ma ◽  
Lisheng Zheng
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Colony Formation ◽  
Umbilical Vein ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Proliferation And Apoptosis ◽  
The Stability ◽  
Umbilical Vein Endothelial Cells ◽  
Related Proteins

Hyperglycemia exposure results in the dysfunction of endothelial cells (ECs) and the development of diabetic complications. Circular RNAs (circRNAs) have been demonstrated to play critical roles in EC dysfunction. The current study aimed to explore the role and mechanism of circRNA CLIP–associating protein 2 (circ_CLASP2, hsa_circ_0064772) on HG-induced dysfunction in human umbilical vein endothelial cells (HUVECs). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the levels of circ_CLASP2, miR-140-5p and F-box, and WD repeat domain-containing 7 (FBXW7). The stability of circ_CLASP2 was identified by the actinomycin D and ribonuclease (RNase) R assays. Cell colony formation, proliferation, and apoptosis were measured by a standard colony formation assay, colorimetric 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) assay, and flow cytometry, respectively. Western blot analysis was performed to determine the expression of related proteins. Targeted correlations among circ_CLASP2, miR-140-5p, and FBXW7 were confirmed by dual-luciferase reporter assay. High glucose (HG) exposure downregulated the expression of circ_CLASP2 in HUVECs. Circ_CLASP2 overexpression or miR-140-5p knockdown promoted proliferation and inhibited apoptosis of HUVECs under HG conditions. Circ_CLASP2 directly interacted with miR-140-5p via pairing to miR-140-5p. The regulation of circ_CLASP2 overexpression on HG-induced HUVEC dysfunction was mediated by miR-140-5p. Moreover, FBXW7 was a direct target of miR-140-5p, and miR-140-5p regulated HG-induced HUVEC dysfunction via FBXW7. Furthermore, circ_CLASP2 mediated FBXW7 expression through sponging miR-140-5p. Our current study suggested that the overexpression of circ_CLASP2 protected HUVEC from HG-induced dysfunction at least partly through the regulation of the miR-140-5p/FBXW7 axis, highlighting a novel therapeutic approach for the treatment of diabetic-associated vascular injury.

scholarly journals Design of silk–vaterite microsphere systems as drug carriers with pH-responsive release behavior

2015 ◽  
Vol 3 (42) ◽  
pp. 8314-8320 ◽  
Author(s):  
S. S. Liu ◽  
L. J. Liu ◽  
L. Y. Xiao ◽  
Q. Lu ◽  
H. S. Zhu ◽  
...  
Keyword(s):  
Thermal Treatment ◽  
Drug Release ◽  
Drug Carriers ◽  
Treatment Method ◽  
Release Behavior ◽  
Ph Responsive ◽  
The Stability

A simple thermal treatment method was developed to control the stability of silk–vaterite microspheres and achieve tunable drug release behaviors.

Osteoblastic alkaline phosphatase mRNA is stabilized by binding to vimentin intermediary filaments

2015 ◽  
Vol 396 (3) ◽  
pp. 253-260 ◽  
Author(s):  
Yvonne Schmidt ◽  
Martin Biniossek ◽  
G. Björn Stark ◽  
Günter Finkenzeller ◽  
Filip Simunovic
Keyword(s):  
Tissue Engineering ◽  
Alkaline Phosphatase ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Sirna Transfection ◽  
The Stability ◽  
Umbilical Vein Endothelial Cells ◽  
Mrna Binding

Abstract Vascularization is essential in bone tissue engineering and recent research has focused on interactions between osteoblasts (hOBs) and endothelial cells (ECs). It was shown that cocultivation increases the stability of osteoblastic alkaline phosphatase (ALP) mRNA. We investigated the mechanisms behind this observation, focusing on mRNA binding proteins. Using a luciferase reporter assay, we found that the 3′-untranslated region (UTR) of ALP mRNA is necessary for human umbilical vein endothelial cells (HUVEC)-mediated stabilization of osteoblastic ALP mRNA. Using pulldown experiments and nanoflow-HPLC mass spectrometry, vimentin was identified to bind to the 3′-UTR of ALP mRNA. Validation was performed by Western blotting. Functional experiments inhibiting intermediate filaments with iminodipropionitrile and specific inhibition of vimentin by siRNA transfection showed reduced levels of ALP mRNA and protein. Therefore, ALP mRNA binds to and is stabilized by vimentin. This data add to the understanding of intracellular trafficking of ALP mRNA, its function, and have possible implications in tissue engineering applications.

scholarly journals Klotho Contributes to Pravastatin Effect on Suppressing IL-6 Production in Endothelial Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Weiwei Xia ◽  
Aihua Zhang ◽  
Zhanjun Jia ◽  
Jun Gu ◽  
Hongbing Chen
Keyword(s):  
Endothelial Cells ◽  
Mononuclear Cells ◽  
Umbilical Vein ◽  
Vascular Diseases ◽  
Peripheral Blood Mononuclear ◽  
Inflammatory Stimuli ◽  
The Stability ◽  
Umbilical Vein Endothelial Cells

Both statins and klotho have been shown to be beneficial in vascular diseases. Interleukin- (IL-) 6 is evidenced as an indicator reflecting the stability of atherosclerotic plaque and involved in the pathogenesis of artery atherosclerosis. However, the relationship between statin, klotho, and IL-6 under an inflammatory environment is unknown. Using primary human umbilical vein endothelial cells (HUVECs), pravastatin dose-dependently induced klotho expression in contrast to remarkable suppression to IL-6 expressions determined by qRT-PCR. Moreover, TNF-α-induced IL-6 was partly but significantly blunted by pravastatin detected by ELISA. To further study the role of klotho in modulating IL-6 expression, endothelial cells with klotho overexpression were treated with TNF-α. Importantly, TNF-α-induced IL-6 production was markedly attenuated in klotho-overexpressed cells. In agreement with in vitro data, a marked reduction of klotho mRNA expression was found in isolated peripheral blood mononuclear cells (PBMCs) from patients with atherosclerosis. Together, these data suggested that pravastatin could suppress IL-6 production via promoting klotho expression in endothelial cells under inflammatory stimuli.

Ultrastructural observations on the in vitro cytoadherence of Plasmodium falciparum infected red blood cells

1990 ◽  
Vol 48 (3) ◽  
pp. 914-915
Author(s):  
D.J.P. Ferguson ◽  
A.R. Berendt ◽  
J. Tansey ◽  
K. Marsh ◽  
C.I. Newbold
Keyword(s):  
Plasmodium Falciparum ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Umbilical Vein ◽  
Cell Types ◽  
Amelanotic Melanoma ◽  
Cytoplasmic Process ◽  
Umbilical Vein Endothelial Cells

In human malaria, the most serious clinical manifestation is cerebral malaria (CM) due to infection with Plasmodium falciparum. The pathology of CM is thought to relate to the fact that red blood cells containing mature forms of the parasite (PRBC) cytoadhere or sequester to post capillary venules of various tissues including the brain. This in vivo phenomenon has been studied in vitro by examining the cytoadherence of PRBCs to various cell types and purified proteins. To date, three Ijiost receptor molecules have been identified; CD36, ICAM-1 and thrombospondin. The specific changes in the PRBC membrane which mediate cytoadherence are less well understood, but they include the sub-membranous deposition of electron-dense material resulting in surface deformations called knobs. Knobs were thought to be essential for cytoadherence, lput recent work has shown that certain knob-negative (K-) lines can cytoadhere. In the present study, we have used electron microscopy to re-examine the interactions between K+ PRBCs and both C32 amelanotic melanoma cells and human umbilical vein endothelial cells (HUVEC).We confirm previous data demonstrating that C32 cells possess numerous microvilli which adhere to the PRBC, mainly via the knobs (Fig. 1). In contrast, the HUVEC were relatively smooth and the PRBCs appeared partially flattened onto the cell surface (Fig. 2). Furthermore, many of the PRBCs exhibited an invagination of the limiting membrane in the attachment zone, often containing a cytoplasmic process from the endothelial cell (Fig. 2).

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