scholarly journals Regulation mechanism of biomolecule interaction behaviors on the superlubricity of hydrophilic polymer coatings

Friction ◽  
2020 ◽  
Author(s):  
Caixia Zhang ◽  
Junmin Chen ◽  
Mengmeng Liu ◽  
Yuhong Liu ◽  
Zhifeng Liu ◽  
...  
Keyword(s):  
Surface Characteristics ◽  
Polymer Coatings ◽  
Regulation Mechanism ◽  
Hydrophilic Polymer ◽  
Hydration Properties ◽  
Adsorption Film ◽  
Synergistic Regulation ◽  
Interaction Behaviors ◽  
Phosphate Buffered Saline

AbstractHydrophilic polymer coatings can improve the surface characteristics of artificial implants. However, because they are used in vivo, they inevitably come into contact with biomolecules that affect their interfacial tribological properties. In this paper, the friction behaviors of poly(vinylphosphonic acid) (PVPA)-modified Ti6Al4V and polytetrafluorethylene balls were analyzed using albumin, globulin, aggrecan, and hyaluronic acid as lubricants. The interaction properties and dynamic adsorption characteristics of the biomolecules and PVPA molecules were explored by a quartz crystal microbalance to identify the cause of the friction difference. It was found that protein molecules disturbed the superlubricity of the PVPA-phosphate-buffered saline system because of the formation of a stable adsorption film, which replaced the interfacial characteristics of the PVPA coating. Polysaccharides, with their excellent hydration properties and polymer structure, had an unstable dynamic interaction or zero adsorption with PVPA molecules, and hardly changed the superlubricity of the PVPA and phosphate-buffered-saline system. The influence mechanism of the specific friction of proteins and polysaccharides was analyzed. Interactions were observed among different biomolecules. Polysaccharides can potentially reduce protein adsorption. The result of the synergistic regulation of the friction coefficient for PVPA-modified Ti6Al4V is approximately 0.017. The results of this study will provide a theoretical basis for the use of polymer coatings in vivo.

scholarly journals Aberrantly high activation of a FoxM1–STMN1 axis contributes to progression and tumorigenesis in FoxM1-driven cancers

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Jun Liu ◽  
Jipeng Li ◽  
Ke Wang ◽  
Haiming Liu ◽  
Jianyong Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Poor Prognosis ◽  
Soft Agar ◽  
Transcriptional Level ◽  
Regulation Mechanism ◽  
Strong Positive Correlation ◽  
Cell Viability Assay ◽  
High Level

AbstractFork-head box protein M1 (FoxM1) is a transcriptional factor which plays critical roles in cancer development and progression. However, the general regulatory mechanism of FoxM1 is still limited. STMN1 is a microtubule-binding protein which can inhibit the assembly of microtubule dimer or promote depolymerization of microtubules. It was reported as a major responsive factor of paclitaxel resistance for clinical chemotherapy of tumor patients. But the function of abnormally high level of STMN1 and its regulation mechanism in cancer cells remain unclear. In this study, we used public database and tissue microarrays to analyze the expression pattern of FoxM1 and STMN1 and found a strong positive correlation between FoxM1 and STMN1 in multiple types of cancer. Lentivirus-mediated FoxM1/STMN1-knockdown cell lines were established to study the function of FoxM1/STMN1 by performing cell viability assay, plate clone formation assay, soft agar assay in vitro and xenograft mouse model in vivo. Our results showed that FoxM1 promotes cell proliferation by upregulating STMN1. Further ChIP assay showed that FoxM1 upregulates STMN1 in a transcriptional level. Prognostic analysis showed that a high level of FoxM1 and STMN1 is related to poor prognosis in solid tumors. Moreover, a high co-expression of FoxM1 and STMN1 has a more significant correlation with poor prognosis. Our findings suggest that a general FoxM1-STMN1 axis contributes to cell proliferation and tumorigenesis in hepatocellular carcinoma, gastric cancer and colorectal cancer. The combination of FoxM1 and STMN1 can be a more precise biomarker for prognostic prediction.

scholarly journals In Vivo Expression of Reprogramming Factor OCT4 Ameliorates Myelination Deficits and Induces Striatal Neuroprotection in Huntington’s Disease

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 712
Author(s):  
Ji-Hea Yu ◽  
Bae-Geun Nam ◽  
Min-Gi Kim ◽  
Soonil Pyo ◽  
Jung-Hwa Seo ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cell Fate ◽  
Gabaergic Neurons ◽  
Oligodendrocyte Progenitor Cells ◽  
Adeno Associated Virus ◽  
In Vivo Expression ◽  
Transcription Factor 4 ◽  
Phosphate Buffered Saline

White matter atrophy has been shown to precede the massive loss of striatal GABAergic neurons in Huntington’s disease (HD). This study investigated the effects of in vivo expression of reprogramming factor octamer-binding transcription factor 4 (OCT4) on neural stem cell (NSC) niche activation in the subventricular zone (SVZ) and induction of cell fate specific to the microenvironment of HD. R6/2 mice randomly received adeno-associated virus 9 (AAV9)-OCT4, AAV9-Null, or phosphate-buffered saline into both lateral ventricles at 4 weeks of age. The AAV9-OCT4 group displayed significantly improved behavioral performance compared to the control groups. Following AAV9-OCT4 treatment, the number of newly generated NSCs and oligodendrocyte progenitor cells (OPCs) significantly increased in the SVZ, and the expression of OPC-related genes and glial cell-derived neurotrophic factor (GDNF) significantly increased. Further, amelioration of myelination deficits in the corpus callosum was observed through electron microscopy and magnetic resonance imaging, and striatal DARPP32+ GABAergic neurons significantly increased in the AAV9-OCT4 group. These results suggest that in situ expression of the reprogramming factor OCT4 in the SVZ induces OPC proliferation, thereby attenuating myelination deficits. Particularly, GDNF released by OPCs seems to induce striatal neuroprotection in HD, which explains the behavioral improvement in R6/2 mice overexpressing OCT4.

scholarly journals The Potential of Calcium/Phosphate Containing MAO Implanted in Bone Tissue Regeneration and Biological Characteristics

2021 ◽  
Vol 22 (9) ◽  
pp. 4706
Author(s):  
Shun-Yi Jian ◽  
Salim Levent Aktug ◽  
Hsuan-Ti Huang ◽  
Cheng-Jung Ho ◽  
Sung-Yen Lin ◽  
...  
Keyword(s):  
Corrosion Resistance ◽  
Calcium Phosphate ◽  
Soft Tissues ◽  
Salt Spray ◽  
Surface Characteristics ◽  
Corrosion Current ◽  
Biological Properties ◽  
Bone Tissue Regeneration ◽  
Additional Surgery

Micro arc oxidation (MAO) is a prominent surface treatment to form bioceramic coating layers with beneficial physical, chemical, and biological properties on the metal substrates for biomaterial applications. In this study, MAO treatment has been performed to modify the surface characteristics of AZ31 Mg alloy to enhance the biocompatibility and corrosion resistance for implant applications by using an electrolytic mixture of Ca3(PO4)2 and C10H16N2O8 (EDTA) in the solutions. For this purpose, the calcium phosphate (Ca-P) containing thin film was successfully fabricated on the surface of the implant material. After in-vivo implantation into the rabbit bone for four weeks, the apparent growth of soft tissues and bone healing effects have been documented. The morphology, microstructure, chemical composition, and phase structures of the coating were identified by SEM, XPS, and XRD. The corrosion resistance of the coating was analyzed by polarization and salt spray test. The coatings consist of Ca-P compounds continuously have proliferation activity and show better corrosion resistance and lower roughness in comparison to mere MAO coated AZ31. The corrosion current density decreased to approximately 2.81 × 10−7 A/cm2 and roughness was reduced to 0.622 μm. Thus, based on the results, it was anticipated that the development of degradable materials and implants would be feasible using this method. This study aims to fabricate MAO coatings for orthopedic magnesium implants that can enhance bioactivity, biocompatibility, and prevent additional surgery and implant-related infections to be used in clinical applications.

scholarly journals Titanium oral implants: surface characteristics, interface biology and clinical outcome

2010 ◽  
Vol 7 (suppl_5) ◽  
Author(s):  
Anders Palmquist ◽  
Omar M. Omar ◽  
Marco Esposito ◽  
Jukka Lausmaa ◽  
Peter Thomsen
Keyword(s):  
Surface Properties ◽  
Cellular Response ◽  
Randomized Clinical Trials ◽  
Three Dimensional ◽  
Cell Communication ◽  
Surface Characteristics ◽  
Titanium Implants ◽  
Material Surface ◽  
Oral Implants

Bone-anchored titanium implants have revolutionized oral healthcare. Surface properties of oral titanium implants play decisive roles for molecular interactions, cellular response and bone regeneration. Nevertheless, the role of specific surface properties, such as chemical and phase composition and nanoscale features, for the biological in vivo performance remains to be established. Partly, this is due to limited transfer of state-of-the-art preparation techniques to complex three-dimensional geometries, analytical tools and access to minute, intact interfacial layers. As judged by the available results of a few randomized clinical trials, there is no evidence that any particular type of oral implant has superior long-term success. Important insights into the recruitment of mesenchymal stem cells, cell–cell communication at the interface and high-resolution imaging of the interface between the surface oxide and the biological host are prerequisites for the understanding of the mechanisms of osseointegration. Strategies for development of the next generation of material surface modifications for compromised tissue are likely to include time and functionally programmed properties, pharmacological modulation and incorporation of cellular components.

Enhanced Oral Bioavailability of Curcumin Using a Supersaturatable Self-Microemulsifying System Incorporating a Hydrophilic Polymer; In Vitro and In Vivo Investigations

2017 ◽  
Vol 19 (2) ◽  
pp. 730-740 ◽  
Author(s):  
Patcharawalai Jaisamut ◽  
Kamonthip Wiwattanawongsa ◽  
Potchanapond Graidist ◽  
Yaowaporn Sangsen ◽  
Ruedeekorn Wiwattanapatapee
Keyword(s):  
Oral Bioavailability ◽  
Hydrophilic Polymer

Synergistic regulation mechanism of selectin and integrin on leukocyte adhesion under shear flow

2021 ◽  
pp. 1-32
Author(s):  
Wei Kang ◽  
Long Li ◽  
Jizeng Wang
Keyword(s):  
Shear Flow ◽  
Leukocyte Adhesion ◽  
Hydrodynamic Process ◽  
Regulation Mechanism ◽  
Leukocyte Rolling ◽  
Cooperative Effects ◽  
Inflammatory Site ◽  
Synergistic Regulation ◽  
Effective Phase ◽  
Kinetics Of

Abstract In the process of inflammation, the hydrodynamic process of circulating leukocyte recruitment to the inflammatory site requires the rolling adhesion of leukocytes in blood vessels mediated by selectin and integrin molecules. Although a number of experiments have demonstrated that cooperative effects exist between selectins and integrins in leukocyte rolling adhesion under shear flow, the mechanisms underlying how the mechanics of selectins and integrins synergistically may govern the dynamics of cell rolling is not yet fully resolved. Here we present a mechanical model on selectin- and integrin- jointly mediated rolling adhesion of leukocyte in shear flow, by considering two pairs' binding/unbinding events as Markov processes and describing kinetics of leukocyte by the approach of continuum mechanics. Through examining the dynamics of leukocyte rolling as a function of relative fraction of selectin and integrin pairs, we show that, during recruitment, the elongation of intermittent weak selectin bonds consuming the kinetic energy of rolling leukocyte decelerates the rolling speed and enables the integrin pairs to form strong bonds, therefore achieving the arrestment of leukocyte (firm adhesion). The coexistence of selectins and integrins may also be required for effective phase transition from firm adhesion to rolling adhesion, due to dynamic competition in pairs' formation and elongation. These results are verified by the relevant Monte Carlo simulations and related to reported experimental observations.

scholarly journals Standardizing Patient-Derived Organoid Generation Workflow to Avoid Microbial Contamination From Colorectal Cancer Tissues

2022 ◽  
Vol 11 ◽  
Author(s):  
Mattia Marinucci ◽  
Caner Ercan ◽  
Stephanie Taha-Mehlitz ◽  
Lana Fourie ◽  
Federica Panebianco ◽  
...  
Keyword(s):  
Microbial Contamination ◽  
Living Cells ◽  
Contamination Rate ◽  
Tissue Processing ◽  
Organoid Culture ◽  
Tissue Handling ◽  
Organoid Cultures ◽  
Cancer Tissues ◽  
Phosphate Buffered Saline

The use of patient-derived organoids (PDO) as a valuable alternative to in vivo models significantly increased over the last years in cancer research. The ability of PDOs to genetically resemble tumor heterogeneity makes them a powerful tool for personalized drug screening. Despite the extensive optimization of protocols for the generation of PDOs from colorectal tissue, there is still a lack of standardization of tissue handling prior to processing, leading to microbial contamination of the organoid culture. Here, using a cohort of 16 patients diagnosed with colorectal carcinoma (CRC), we aimed to test the efficacy of phosphate-buffered saline (PBS), penicillin/streptomycin (P/S), and Primocin, alone or in combination, in preventing organoid cultures contamination when used in washing steps prior to tissue processing. Each CRC tissue was divided into 5 tissue pieces, and treated with each different washing solution, or none. After the washing steps, all samples were processed for organoid generation following the same standard protocol. We detected contamination in 62.5% of the non-washed samples, while the use of PBS or P/S-containing PBS reduced the contamination rate to 50% and 25%, respectively. Notably, none of the organoid cultures washed with PBS/Primocin-containing solution were contaminated. Interestingly, addition of P/S to the washing solution reduced the percentage of living cells compared to Primocin. Taken together, our results demonstrate that, prior to tissue processing, adding Primocin to the tissue washing solution is able to eliminate the risk of microbial contamination in PDO cultures, and that the use of P/S negatively impacts organoids growth. We believe that our easy-to-apply protocol might help increase the success rate of organoid generation from CRC patients.

scholarly journals Intravital microscopy confirmed microvascular and ECM preservation in the decellularized rat kidney directly after transplantation

2021 ◽  
Author(s):  
Peter R. Corridon
Keyword(s):  
Jugular Vein ◽  
Rat Kidney ◽  
Multiphoton Microscopy ◽  
Sodium Dodecyl ◽  
Sprague Dawley ◽  
Short Term ◽  
Post Transplantation ◽  
Flow Through ◽  
Phosphate Buffered Saline

AbstractThe aim of the present study was to determine whether decellularized rat kidney microvascular and extracellular matrix (ECM) integrity could be preserved under in vivo conditions directly after transplantation. Whole kidneys were harvested from the Sprague Dawley rat and were decellularized by perfusion with 0.5% sodium dodecyl sulfate (SDS) for 24 hours, followed by phosphate-buffered saline (PBS) for an additional 24 hours. Decellularized kidneys were then transplanted into recipients and vascular high-molecular-weight (150-kDa) FITC dextrans were infused via the jugular vein. Blood was then allowed to flow through the decellularized transplant. Intravital multiphoton microscopy confirmed the suitable confinement of the dextrans within vascular tracks and preservation of the decellularized architecture that was monitored in the shortterm post transplantation.New and NoteworthyThe study confirmed in vivo microvascular and ECM preservation in the short-term post transplantation.

scholarly journals Regulation mechanism of ERM (ezrin/radixin/moesin) protein/plasma membrane association: possible involvement of phosphatidylinositol turnover and Rho-dependent signaling pathway.

1996 ◽  
Vol 135 (1) ◽  
pp. 37-51 ◽  
Author(s):  
M Hirao ◽  
N Sato ◽  
T Kondo ◽  
S Yonemura ◽  
M Monden ◽  
...  
Keyword(s):  
Ionic Strength ◽  
Cytoplasmic Domain ◽  
Insoluble Fraction ◽  
Regulation Mechanism ◽  
Erm Proteins ◽  
Bhk Cells ◽  
High Affinity ◽  
Binding Partners

The ERM proteins, ezrin, radixin, and moesin, are involved in the actin filament/plasma membrane interaction as cross-linkers. CD44 has been identified as one of the major membrane binding partners for ERM proteins. To examine the CD44/ERM protein interaction in vitro, we produced mouse ezrin, radixin, moesin, and the glutathione-S-transferase (GST)/CD44 cytoplasmic domain fusion protein (GST-CD44cyt) by means of recombinant baculovirus infection, and constructed an in vitro assay for the binding between ERM proteins and the cytoplasmic domain of CD44. In this system, ERM proteins bound to GST-CD44cyt with high affinity (Kd of moesin was 9.3 +/- 1.6nM) at a low ionic strength, but with low affinity at a physiological ionic strength. However, in the presence of phosphoinositides (phosphatidylinositol [PI], phosphatidylinositol 4-monophosphate [4-PIP], and phosphatidylinositol 4.5-bisphosphate [4,5-PIP2]), ERM proteins bound with a relatively high affinity to GST-CD44cyt even at a physiological ionic strength: 4,5-PIP2 showed a marked effect (Kd of moesin in the presence of 4,5-PIP2 was 9.3 +/- 4.8 nM). Next, to examine the regulation mechanism of CD44/ERM interaction in vivo, we reexamined the immunoprecipitated CD44/ERM complex from BHK cells and found that it contains Rho-GDP dissociation inhibitor (GDI), a regulator of Rho GTPase. We then evaluated the involvement of Rho in the regulation of the CD44/ERM complex formation. When recombinant ERM proteins were added and incubated with lysates of cultured BHK cells followed by centrifugation, a portion of the recombinant ERM proteins was recovered in the insoluble fraction. This binding was enhanced by GTP gamma S and markedly suppressed by C3 toxin, a specific inhibitor of Rho, indicating that the GTP form of Rho in the lysate is required for this binding. A mAb specific for the cytoplasmic domain of CD44 also markedly suppressed this binding, identifying most of the binding partners for exogenous ERM proteins in the insoluble fraction as CD44. Consistent with this binding analysis, in living BHK cells treated with C3 toxin, most insoluble ERM proteins moved to soluble compartments in the cytoplasm, leaving CD44 free from ERM. These findings indicate that Rho regulates the CD44/ERM complex formation in vivo and that the phosphatidylinositol turnover may be involved in this regulation mechanism.

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