scholarly journals Tuning of Titanium Microfiber Scaffold with UV-Photofunctionalization for Enhanced Osteoblast Affinity and Function

2020 ◽  
Vol 21 (3) ◽  
pp. 738 ◽  
Author(s):  
Chika Iwasaki ◽  
Makoto Hirota ◽  
Miyuki Tanaka ◽  
Hiroaki Kitajima ◽  
Masako Tabuchi ◽  
...  

Titanium (Ti) is an osteoconductive material that is routinely used as a bulk implant to fix and restore bones and teeth. This study explored the effective use of Ti as a bone engineering scaffold. Challenges to overcome were: (1) difficult liquid/cell infiltration into Ti microfiber scaffolds due to the hydrophobic nature of Ti; and (2) difficult cell attachment on thin and curved Ti microfibers. A recent discovery of UV-photofunctionalization of Ti prompted us to examine its effect on Ti microfiber scaffolds. Scaffolds in disk form were made by weaving grade 4 pure Ti microfibers (125 µm diameter) and half of them were acid-etched to roughen the surface. Some of the scaffolds with original or acid-etched surfaces were further treated by UV light before cell culture. Ti microfiber scaffolds, regardless of the surface type, were hydrophobic and did not allow glycerol/water liquid to infiltrate, whereas, after UV treatment, the scaffolds became hydrophilic and immediately absorbed the liquid. Osteogenic cells from two different origins, derived from the femoral and mandibular bone marrow of rats, were cultured on the scaffolds. The number of cells attached to scaffolds during the early stage of culture within 24 h was 3–10 times greater when the scaffolds were treated with UV. The development of cytoplasmic projections and cytoskeletal, as well as the expression of focal adhesion protein, were exclusively observed on UV-treated scaffolds. Osteoblastic functional phenotypes, such as alkaline phosphatase activity and calcium mineralization, were 2–15 times greater on UV-treated scaffolds, with more pronounced enhancement on acid-etched scaffolds compared to that on the original scaffolds. These effects of UV treatment were associated with a significant reduction in atomic carbon on the Ti microfiber surfaces. In conclusion, UV treatment of Ti microfiber scaffolds tunes their physicochemical properties and effectively enhances the attachment and function of osteoblasts, proposing a new strategy for bone engineering.

Materials ◽  
2020 ◽  
Vol 14 (1) ◽  
pp. 151
Author(s):  
Kourosh Nakhaei ◽  
Manabu Ishijima ◽  
Takayuki Ikeda ◽  
Amirreza Ghassemi ◽  
Juri Saruta ◽  
...  

Early establishment of soft-tissue adhesion and seal at the transmucosal and transcutaneous surface of implants is crucial to prevent infection and ensure the long-term stability and function of implants. Herein, we tested the hypothesis that treatment of titanium with ultraviolet (UV) light would enhance its interaction with epithelial cells. X-ray spectroscopy showed that UV treatment significantly reduced the atomic percentage of surface carbon on titanium from 46.1% to 28.6%. Peak fitting analysis revealed that, among the known adventitious carbon contaminants, C–C and C=O groups were significantly reduced after UV treatment, while other groups were increased or unchanged in percentage. UV-treated titanium attracted higher numbers of human epithelial cells than untreated titanium and allowed more rapid cell spread. Hemi-desmosome-related molecules, integrin β4 and laminin-5, were upregulated at the gene and protein levels in the cells on UV-treated surfaces. The result of the detachment test revealed twice as many cells remaining adherent on UV-treated than untreated titanium. The enhanced cellular affinity of UV-treated titanium was equivalent to laminin-5 coating of titanium. These data indicated that UV treatment of titanium enhanced the attachment, adhesion, and retention of human epithelial cells associated with disproportional removal of adventitious carbon contamination, providing a new strategy to improve soft-tissue integration with implant devices.


2013 ◽  
Vol 305 (2) ◽  
pp. C215-C227 ◽  
Author(s):  
Ransom H. Poythress ◽  
Cynthia Gallant ◽  
Susanne Vetterkind ◽  
Kathleen G. Morgan

Turnover of focal adhesions (FAs) is known to be critical for cell migration and adhesion of proliferative vascular smooth muscle (VSM) cells. However, it is often assumed that FAs in nonmigratory, differentiated VSM (dVSM) cells embedded in the wall of healthy blood vessels are stable structures. Recent work has demonstrated agonist-induced actin polymerization and Src-dependent FA phosphorylation in dVSM cells, suggesting that agonist-induced FA remodeling occurs. However, the mechanisms and extent of FA remodeling are largely unknown in dVSM. Here we show, for the first time, that a distinct subpopulation of dVSM FA proteins, but not the entire FA, remodels in response to the α-agonist phenylephrine. Vasodilator-stimulated phosphoprotein and zyxin displayed the largest redistributions, while β-integrin and FA kinase showed undetectable redistribution. Vinculin, metavinculin, Src, Crk-associated substrate, and paxillin displayed intermediate degrees of redistribution. Redistributions into membrane fractions were especially prominent, suggesting endosomal mechanisms. Deconvolution microscopy, quantitative colocalization analysis, and Duolink proximity ligation assays revealed that phenylephrine increases the association of FA proteins with early endosomal markers Rab5 and early endosomal antigen 1. Endosomal disruption with the small-molecule inhibitor primaquine inhibits agonist-induced redistribution of FA proteins, confirming endosomal recycling. FA recycling was also inhibited by cytochalasin D, latrunculin B, and colchicine, indicating that the redistribution is actin- and microtubule-dependent. Furthermore, inhibition of endosomal recycling causes a significant inhibition of the rate of development of agonist-induced dVSM contractions. Thus these studies are consistent with the concept that FAs in dVSM cells, embedded in the wall of the aorta, remodel during the action of a vasoconstrictor.


1997 ◽  
Vol 60 (6) ◽  
pp. 639-643 ◽  
Author(s):  
FUENG-LIN KUO ◽  
JOHN B. CAREY ◽  
STEVEN C. RICKE

The effects were investigated of 254-nm UV radiation on populations of Salmonella typhimurium, aerobes, and molds on the shells of eggs. In the first experiment, the CFU of attached S. typhimurium cells on unwashed clean shell eggs were determined after 0, 1, 3, 5, and 7 min of UV treatment (620 μW/cm2) on both ends of the egg. All UV treatments significantly reduced S. typhimurium CFU (P < .01). UVtreatment (620 μW/cm2) in 1-min alternating light and dark cycles for 5 min (three light and two dark) was compared to 0, 3, and 5 min of UV treatment. No significant differences in microbial populations were observed among light and dark cycles and the other UV treatments. In a subsequent experiment, the same UV treatments were utilized to evaluate photoreactivation. After UV exposure, eggs were exposed to 1 h of fluorescent light or I h of darkness or cultured immediately. S. typhimurium CFU were significantly (P < .01) reduced by the UV treatments. However, no significant differences between microbial populations exposed to UV treatment and UV radiation plus photoreactivation were detected. For studies of aerobic bacteria and molds, different UV treatment times (0, 15, and 30 min) at the intensity of 620 μW/cm2 and different intensities (620, 1350, and 1720 μW/cm2) for 15 min were evaluated. Mold CFU per egg were either 0 or 1 for all UV treatments and a 99% reduction of CFU of aerobic bacteria per egg were observed for all UV treatments. It appears from these studies that UV light can significantly reduce populations of S. typhimurium, aerobes, and molds on shell eggs.


Channels ◽  
2021 ◽  
Vol 15 (1) ◽  
pp. 229-238
Author(s):  
Maria Papanikolaou ◽  
Shawn M. Crump ◽  
Geoffrey W. Abbott

Oncogene ◽  
2021 ◽  
Author(s):  
Qiuping Xu ◽  
Jingwei Zhang ◽  
Brian A. Telfer ◽  
Hao Zhang ◽  
Nisha Ali ◽  
...  

AbstractThere is overwhelming clinical evidence that the extracellular-regulated protein kinase 5 (ERK5) is significantly dysregulated in human breast cancer. However, there is no definite understanding of the requirement of ERK5 in tumor growth and metastasis due to very limited characterization of the pathway in disease models. In this study, we report that a high level of ERK5 is a predictive marker of metastatic breast cancer. Mechanistically, our in vitro data revealed that ERK5 was critical for maintaining the invasive capability of triple-negative breast cancer (TNBC) cells through focal adhesion protein kinase (FAK) activation. Specifically, we found that phosphorylation of FAK at Tyr397 was controlled by a kinase-independent function of ERK5. Accordingly, silencing ERK5 in mammary tumor grafts impaired FAK phosphorylation at Tyr397 and suppressed TNBC cell metastasis to the lung without preventing tumor growth. Collectively, these results establish a functional relationship between ERK5 and FAK signaling in promoting malignancy. Thus, targeting the oncogenic ERK5-FAK axis represents a promising therapeutic strategy for breast cancer exhibiting aggressive clinical behavior.


Author(s):  
Siamack Sabrkhany ◽  
Marijke J. E. Kuijpers ◽  
Mirjam G. A. oude Egbrink ◽  
Arjan W. Griffioen

AbstractPlatelets have an important role in tumor angiogenesis, growth, and metastasis. The reciprocal interaction between cancer and platelets results in changes of several platelet characteristics. It is becoming clear that analysis of these platelet features could offer a new strategy in the search for biomarkers of cancer. Here, we review the human studies in which platelet characteristics (e.g., count, volume, protein, and mRNA content) are investigated in early-stage cancer. The main focus of this paper is to evaluate which platelet features are suitable for the development of a blood test that could detect cancer in its early stages.


Behaviour ◽  
1991 ◽  
Vol 119 (1-2) ◽  
pp. 1-29 ◽  
Author(s):  
Kyra Garnetzke-Stollmann ◽  
Dierk Franck

AbstractSpectacled parrotlets live in a complex system of individual relationships throughout their lives. The adults form exclusive pair bonds, addressing all friendly and sexual behaviour patterns to each other. Pair mates cooperate in agonistic situations. As long as they stay close together they hold the same rank-order position. In mate-choice experiments females (not males) significantly preferred a mate which formerly held a high social position. There are also non-exclusive pair bonds, which are far less stable than exclusive ones. Only exclusive pairs have a good chance to occupy a breeding cavity. All group members are synchronized in many of their activities, such as foraging, preening or resting. They are keenly interested in unusual activities of other group members. Social learning, including copying sexual techniques, seems to be essential. After fledging the parents keep their offspring at a distance from a very early stage. Instead of a close parent-offspring relationship the fledglings form sibling groups with their nest mates. Over a period of months siblings remain the main interaction partners for all friendly and playful activities. They also support one another in agonistic situations. In the first months of life even courtship feeding and sexual behaviour are addressed predominantly to siblings. Thus a pair-like relationship is established between siblings, anticipating the permanent pair bond of adults. Single fledglings, deprived of the experience of a sibling group, remained poorly integrated into the group. They developed alternative socialisation tactics, namely (1) joining a host group of unrelated siblings, (2) renewing a friendly partnership with the parents, (3) helping to protect and feed younger siblings or even unrelated fledglings and (4) seeking early partnership with unrelated group members. Out of 10 single fledglings only the one that was accepted by a host sibling group immediately after fledging became well integrated into the whole group and reproduced well. It is argued that sibling groups offer good opportunities for learning partnership and function as a safe basis for exploring the social environment. It is tentatively proposed that single fledglings have a decreased probability of reproductive success.


2017 ◽  
Vol 474 (3) ◽  
pp. 333-355 ◽  
Author(s):  
Chris Ugbode ◽  
Yuhan Hu ◽  
Benjamin Whalley ◽  
Chris Peers ◽  
Marcus Rattray ◽  
...  

Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer's disease (AD). These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease-modifying therapies for AD, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic support, neurotransmission and synaptic architecture. Therefore, specific targeting of individual transporter families has the potential to suppress neurodegeneration, a characteristic hallmark of AD. A small number of the 400 transporter superfamilies are expressed in astrocytes, with evidence highlighting a fraction of these are implicated in AD. Here, we review the current evidence for six astrocytic transporter subfamilies involved in AD, as reported in both animal and human studies. This review confirms that astrocytes are indeed a viable target, highlights the complexities of studying astrocytes and provides future directives to exploit the potential of astrocytes in tackling AD.


2003 ◽  
Vol 358 (1433) ◽  
pp. 869-873 ◽  
Author(s):  
Gerrit van Meer ◽  
Jasja Wolthoorn ◽  
Sophie Degroote

In higher eukaryotes, glucosylceramide is the simplest member and precursor of a fascinating class of membrane lipids, the glycosphingolipids. These lipids display an astounding variation in their carbohydrate head groups, suggesting that glycosphingolipids serve specialized functions in recognition processes. It is now realized that they are organized in signalling domains on the cell surface. They are of vital importance as, in their absence, embryonal development is inhibited at an early stage. Remarkably, individual cells can live without glycolipids, perhaps because their survival does not depend on glycosphingolipid–mediated signalling mechanisms. Still, these cells suffer from defects in intracellular membrane transport. Various membrane proteins do not reach their intracellular destination, and, indeed, some intracellular organelles do not properly differentiate to their mature stage. The fact that glycosphingolipids are required for cellular differentiation suggests that there are human diseases resulting from defects in glycosphingolipid synthesis. In addition, the same cellular differentiation processes may be affected by defects in the degradation of glycosphingolipids. At the cellular level, the pathology of glycosphingolipid storage diseases is not completely understood. Cell biological studies on the intracellular fate and function of glycosphingolipids may open new ways to understand and defeat not only lipid storage diseases, but perhaps other diseases that have not been connected to glycosphingolipids so far.


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