Anti-inflammatory effects of the immobilization of SEMA4D on titanium surfaces in an endothelial cell/macrophage indirect coculture model

Abstract In this study, we established a procedure to prepare a SEMA4D-immobilized titanium surface and explored its effects on macrophage behaviors in an endothelial cell/macrophage indirect coculture model. The SEMA4D-BSA complex was immobilized onto a preprocessed poly L-lysine (PLL) titanium surface through NaOH hydrothermal treatment and self-assembly technology. All titanium specimens were examined for surface microstructure, surface element composition, and surface wettability by field emission scanning electron microscopy (FE-SEM), X-ray photoelectron spectroscopy (XPS), and water contact angle (WCA) measurement, respectively. Subsequently, we constructed an endothelial cell/macrophage indirect coculture model and evaluated the activation of NF-κB signaling pathway and the expression of proinflammatory cytokines (TNFα, IL-6, and IL-1β) in macrophages. In XPS analysis, the SEMA4D-immobilized titanium surface appeared as a loose porous structure covered with uniform film, which exhibited better hydrophilicity than the control smooth titanium surface. In the indirect coculture model, SEMA4D attenuated the activation of NF-κB signaling pathway of LPS-stimulated THP-1 macrophages, thereby downregulating the expression of proinflammatory cytokines in macrophages. In conclusion, SEMA4D could be immobilized on titanium surfaces through NaOH hydrothermal treatment and self-assembly technology. Meanwhile, SEMA4D immobilization altered the characteristics of the titanium surfaces, which negatively regulated macrophage behaviors in the endothelial cell/macrophage indirect coculture model.

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Surface Modification of Titanium with Hydrothermal Treatment

Materials Science Forum ◽

10.4028/www.scientific.net/msf.561-565.1521 ◽

2007 ◽

Vol 561-565 ◽

pp. 1521-1524

Author(s):

Akiko Obata ◽

Toshihiro Kasuga

Keyword(s):

Surface Modification ◽

Hydrothermal Treatment ◽

Titanium Surface ◽

Deionized Water ◽

Laser Raman Spectroscopy ◽

Titanium Plate ◽

Laser Raman ◽

Naoh Solution ◽

Titanium Surfaces ◽

Modification Of Titanium

Hydrothermal treatment was performed on a titanium plate for its surface modification to enhance its bioactivity. The titanium plate was autoclaved in deionized water (DW) or 0.05 mol/l NaOH solution at 120, 200 and 240 °C for 24 hr. The titanium surfaces autoclaved in DW were homogeneously coated with nano-sized particles and polygonal deposits with the sizes of several hundreds nanometers. The deposits were regarded as anatase according to the results of laser Raman spectroscopy (LRS). In the case of autoclaving in 0.05 mol/l NaOH solution, leaf-like, needle-like and pyramid deposits were observed on titanium surfaces and regarded to consist of anatase or brookite by LRS analysis. The formation of the deposits significantly depended on the autoclaving temperature. The deposits adhered on the titanium surface though a tape-test; the adhesion of the particle was found to be excellent.

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Apatite-forming ability on titanium surface modified by hydrothermal treatment and ultraviolet irradiation

Journal of Materials Research ◽

10.1557/jmr.2008.0385 ◽

2008 ◽

Vol 23 (12) ◽

pp. 3169-3175 ◽

Cited By ~ 6

Author(s):

Akiko Obata ◽

Tianshu Zhai ◽

Toshihiro Kasuga

Keyword(s):

Hydrothermal Treatment ◽

Uv Irradiation ◽

Calcium Ions ◽

Titanium Surface ◽

Oh Groups ◽

Titanium Surfaces ◽

Surface Modified ◽

Titania Coatings ◽

Phosphate Groups ◽

Titania Coating

Titania coatings with various morphologies were formed on titanium surfaces by hydrothermal treatment using a dilute alkaline solution and evaluated in their hydroxyapatite (HA)-forming abilities in simulated body fluid (1.5SBF) under ultraviolet (UV) irradiation. The HA formation on the titania coating in 1.5SBF was enhanced by UV irradiation. The amount of phosphate groups adsorbed on the titania, after soaking in 1.5SBF for 24 h under UV irradiation, was estimated to be larger than that of calcium ions, whereas that of calcium ions on the titania, after soaking without UV irradiation, was larger than that of phosphate groups. It was suggested that the titania generated much basic Ti–OH groups at its surface by UV irradiation and subsequently adsorbed phosphate groups, such as H2PO4−, resulting in the formation of a new surface rich in the amount of the groups, which eventually enhanced the HA formation in 1.5SBF.

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Construction of Chitosan/Alginate Nano-Drug Delivery System for Improving Dextran Sodium Sulfate-Induced Colitis in Mice

Nanomaterials ◽

10.3390/nano11081884 ◽

2021 ◽

Vol 11 (8) ◽

pp. 1884

Author(s):

Mengfei Jin ◽

Shangyong Li ◽

Yanhong Wu ◽

Dandan Li ◽

Yantao Han

Keyword(s):

Self Assembly ◽

Average Diameter ◽

Mucosal Healing ◽

Plga Nanoparticles ◽

Narrow Particle Size Distribution ◽

Layer By Layer ◽

Systemic Side Effects ◽

Assembly Technology ◽

The Fourier Transform ◽

Polyelectrolyte Film

(1) Background: In the treatment of ulcerative colitis (UC), accurate delivery and release of anti-inflammatory drugs to the site of inflammation can reduce systemic side effects. (2) Methods: We took advantage of this goal to prepare resveratrol-loaded PLGA nanoparticles (RES-PCAC-NPs) by emulsification solvent volatilization. After layer-by-layer self-assembly technology, we deposited chitosan and alginate to form a three-layer polyelectrolyte film. (3) Results: It can transport nanoparticles through the gastric environment to target inflammation sites and slowly release drugs at a specific pH. The resulting RES-PCAC-NPs have an ideal average diameter (~255 nm), a narrow particle size distribution and a positively charged surface charge (~13.5 mV). The Fourier transform infrared spectroscopy showed that resveratrol was successfully encapsulated into PCAC nanoparticles, and the encapsulation efficiency reached 87.26%. In addition, fluorescence imaging showed that RES-PCAC-NPs with positive charges on the surface can effectively target and accumulate in the inflammation site while continuing to penetrate downward to promote mucosal healing. Importantly, oral RES-PCAC-NPs treatment in DSS-induced mice was superior to other results in significantly improved inflammatory markers of UC. (4) Conclusions: Our results strongly prove that RES-PCAC-NPs can target the inflamed colon for maximum efficacy, and this oral pharmaceutical formulation can represent a promising formulation in the treatment of UC.

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Microcystin-leucine arginine blocks vasculogenesis and angiogenesis through impairing cytoskeleton and impeding endothelial cell migration by downregulating integrin-mediated Rho/ROCK signaling pathway

Environmental Science and Pollution Research ◽

10.1007/s11356-021-15337-9 ◽

2021 ◽

Author(s):

Qilong Wang ◽

Guoliang Chen ◽

Qian Zhang ◽

Mingxing Wang ◽

Guixue Wang ◽

...

Keyword(s):

Cell Migration ◽

Endothelial Cell ◽

Signaling Pathway ◽

Endothelial Cell Migration ◽

Vasculogenesis And Angiogenesis

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Ambient Particulate Matter Induces Vascular Smooth Muscle Cell Phenotypic Changes via NOX1/ROS/NF-κB Dependent and Independent Pathways: Protective Effects of Polyphenols

Antioxidants ◽

10.3390/antiox10050782 ◽

2021 ◽

Vol 10 (5) ◽

pp. 782

Author(s):

Chia-Chi Ho ◽

Yu-Cheng Chen ◽

Ming-Hsien Tsai ◽

Hui-Ti Tsai ◽

Chen-Yi Weng ◽

...

Keyword(s):

Smooth Muscle ◽

Particulate Matter ◽

Vascular Smooth Muscle ◽

Signaling Pathway ◽

Proinflammatory Cytokines ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Cytokine Secretion ◽

Ambient Particulate Matter ◽

Migration Ability ◽

Cytokines Secretion

Epidemiological studies have demonstrated an association between ambient particulate matter (PM) exposure and vascular diseases. Here, we observed that treatment with ambient PM increased cell migration ability in vascular smooth muscle cells (VSMCs) and pulmonary arterial SMCs (PASMCs). These results suggest that VSMCs and PASMCs transitioned from a differentiated to a synthetic phenotype after PM exposure. Furthermore, treatment with PM increased intracellular reactive oxygen species (ROS), activated the NF-κB signaling pathway, and increased the expression of proinflammatory cytokines in VSMCs. Using specific inhibitors, we demonstrated that PM increased the migration ability of VSMCs via the nicotinamide–adenine dinucleotide phosphate (NADPH) oxidase 1 (NOX1)/ROS-dependent NF-κB signaling pathway, which also partially involved in the induction of proinflammatory cytokines. Finally, we investigated whether nature polyphenolic compounds prevent PM-induced migration and proinflammatory cytokines secretion in VSMCs. Curcumin, resveratrol, and gallic acid prevented PM2.5-induced migration via the ROS-dependent NF-κB signaling pathway. However, honokiol did not prevent PM2.5-induced migration or activation of the ROS-dependent NF-κB signaling pathway. On the other hand, all polyphenols prevented PM2.5-induced cytokines secretion. These data indicated that polyphenols prevented PM-induced migration and cytokine secretion via blocking the ROS-dependent NF-κB signaling pathway in VSMCs. However, other mechanisms may also contribute to PM-induced cytokine secretion.

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Long-lasting renewable antibacterial porous polymeric coatings enable titanium biomaterials to prevent and treat peri-implant infection

Nature Communications ◽

10.1038/s41467-021-23069-0 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Shuyi Wu ◽

Jianmeng Xu ◽

Leiyan Zou ◽

Shulu Luo ◽

Run Yao ◽

...

Keyword(s):

Dental Implant ◽

Pathogenic Bacteria ◽

Titanium Surface ◽

Polymeric Coating ◽

Antibacterial Efficacy ◽

Polymeric Coatings ◽

Implant Infection ◽

Titanium Surfaces

AbstractPeri-implant infection is one of the biggest threats to the success of dental implant. Existing coatings on titanium surfaces exhibit rapid decrease in antibacterial efficacy, which is difficult to promisingly prevent peri-implant infection. Herein, we report an N-halamine polymeric coating on titanium surface that simultaneously has long-lasting renewable antibacterial efficacy with good stability and biocompatibility. Our coating is powerfully biocidal against both main pathogenic bacteria of peri-implant infection and complex bacteria from peri-implantitis patients. More importantly, its antibacterial efficacy can persist for a long term (e.g., 12~16 weeks) in vitro, in animal model, and even in human oral cavity, which generally covers the whole formation process of osseointegrated interface. Furthermore, after consumption, it can regain its antibacterial ability by facile rechlorination, highlighting a valuable concept of renewable antibacterial coating in dental implant. These findings indicate an appealing application prospect for prevention and treatment of peri-implant infection.

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Intracisternal administration of transforming growth factor-β evokes fever through the induction of cyclooxygenase-2 in brain endothelial cells

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00181.2007 ◽

2008 ◽

Vol 294 (1) ◽

pp. R266-R275 ◽

Cited By ~ 3

Author(s):

Shigenobu Matsumura ◽

Tetsuro Shibakusa ◽

Teppei Fujikawa ◽

Hiroyuki Yamada ◽

Kiyoshi Matsumura ◽

...

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Growth Factor ◽

Proinflammatory Cytokines ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Cyclooxygenase 2 ◽

Dependent Manner ◽

Cox 2 ◽

Β Receptor

Transforming growth factor-β (TGF-β), a pleiotropic cytokine, regulates cell proliferation, differentiation, and apoptosis, and plays a key role in development and tissue homeostasis. TGF-β functions as an anti-inflammatory cytokine because it suppresses microglia and B-lymphocyte functions, as well as the production of proinflammatory cytokines. However, we previously demonstrated that the intracisternal administration of TGF-β induces fever like that produced by proinflammatory cytokines. In this study, we investigated the mechanism of TGF-β-induced fever. The intracisternal administration of TGF-β increased body temperature in a dose-dependent manner. Pretreatment with cyclooxygenase-2 (COX-2)-selective inhibitor significantly suppressed TGF-β-induced fever. COX-2 is known as one of the rate-limiting enzymes of the PGE2 synthesis pathway, suggesting that fever induced by TGF-β is COX-2 and PGE2 dependent. TGF-β increased PGE2 levels in cerebrospinal fluid and increased the expression of COX-2 in the brain. Double immunostaining of COX-2 and von Willebrand factor (vWF, an endothelial cell marker) revealed that COX-2-expressing cells were mainly endothelial cells. Although not all COX-2-immunoreactive cells express TGF-β receptor, some COX-2-immunoreactive cells express activin receptor-like kinase-1 (ALK-1, an endothelial cell-specific TGF-β receptor), suggesting that TGF-β directly or indirectly acts on endothelial cells to induce COX-2 expression. These findings suggest a novel function of TGF-β as a proinflammatory cytokine in the central nervous system.

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