bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of an elastic decellularized tendon‐derived scaffold for the vascular tissue engineering application
Authors: Ghazanfari Samaneh , Alberti Kyle A. , Xu Qiaobing , Khademhosseini Ali 
Published: January 2019

AbstractDue to the limited success rate of currently available vascular replacements, tissue engineering has received tremendous attention in recent years. A main challenge in the field of regenerative medicine is creating a mechanically functional tissue with a well‐organized extracellular matrix, particularly of collagen and elastin. In this study, the native collagen scaffold derived from decellularized tendon sections, as a scaffold having the potential to be used for vascular tissue engineering applications, was studied. We showed that the elasticity of the scaffolds was improved when crosslinked with the bovine elastin. The effect of different concentrations of elastin on mechanical properties of the collagen scaffolds was evaluated of which 15% elastin concentration was selected for further analysis based on the results. Addition of 15% elastin to collagen scaffolds significantly decreased Young's modulus and the tensile stress at the maximum load and increased the tensile strain at the maximum load of the constructs as compared to those of the collagen scaffolds or control samples. Moreover, tubular elastin modified collagen scaffolds showed significantly higher burst pressure compared to the control samples. Smooth muscle cells and endothelial cells cultured on the elastin modified collagen scaffolds showed high viability (>80%) after 1, 3, and 7 days. Furthermore, the cells showed a high tendency to align with the collagen fibers within the scaffold and produced their own extracellular matrix over time. In conclusion, the results show that the decellularized tendon sections have a great potential to be used as scaffolds for vascular tissue engineering applications. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 1225–1234, 2019.
Combinatorial effects of inorganic ions on adhesion and proliferation of osteoblast‐like cells
Authors: Obata Akiko , Ogasawara Toru , Kasuga Toshihiro 
Published: January 2019

AbstractCombinatorial effects of three ions, namely silicate (Si), calcium (Ca), and magnesium (Mg) ions, on the adhesion and proliferation of MC3T3‐E1 mouse osteoblast‐like cells were evaluated. The cells were cultured in single‐, dual‐, or triple‐ion‐conditioned culture media with systematically changed ion concentrations. The ranges of Si, Ca, and Mg ion concentrations were set as 10–70, 80–400, and 25–500 ppm, respectively. The numbers of adherent live cells were measured after culturing for 3 h and for 1, 3, and 5 days to examine cell adhesion and proliferation, respectively. Mg ions predominantly enhanced cell adhesion in both the dual‐ion (xSi‐zMg and yCa‐zMg) and triple‐ion (xSi‐yCa‐zMg) systems but had no effect when they acted individually in the single‐ion system. Conversely, Si ions predominantly enhanced cell proliferation in most single‐ and triple‐ion‐conditioned media. Evaluation of the combinatorial effects of the three ions on cell adhesion and proliferation revealed that the dual‐ and triple‐ion‐conditioned media mainly conferred synergistic effects on adhesion but antagonistic effects on proliferation. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 1042–1051, 2019.
Visible‐light‐responsive antibacterial activity of Au‐incorporated TiO2 layers formed on Ti–(0–10)at%Au alloys by air oxidation
Authors: Ueda Takatoshi , Ueda Kyosuke , Ito Koyu , Ogasawara Kouetsu , Kanetaka Hiroyasu , Mokudai Takayuki , Niwano Yoshimi , Narushima Takayuki 
Published: January 2019

AbstractRutile TiO2 layers were formed on substrates of Ti–(0–10)at%Au alloys by a simple process of air oxidation, and their antibacterial activities were evaluated under visible‐light irradiation (λ ≥ 400 nm). Au was introduced into the TiO2 layers on Ti–(1–10)at%Au alloys and existed as both metallic Au nanoparticles and dissolved Au3+ ions. The TiO2 layers that formed on Ti–5at%Au and Ti–10at%Au alloys exhibited visible‐light photocatalytic activity, that is, degradation of stearic acid and antibacterial activity against Escherichia coli. These visible‐light activities were attributed to the surface plasmon resonance of metallic Au nanoparticles and the decrease in bandgap energy caused by dissolved Au3+ ions. The formation of hydroxyl radicals observed under visible‐light irradiation is attributable to antibacterial activity. From a cost perspective, a Ti–5at%Au alloy is more suitable as a substrate for the formation of a TiO2 layer with antibacterial properties than a Ti–10at%Au alloy. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 991–1000, 2019.
Effect of calcium phosphate phases affecting the crosstalk between osteoblasts and osteoclasts in vitro
Authors: Shiwaku Yukari , Tsuchiya Kaori , Xiao Linghao , Suzuki Osamu 
Published: January 2019

AbstractPrevious studies have reported that octacalcium phosphate (OCP) enhances osteoblast differentiation and osteoclast formation during the hydrolysis process to hydroxyapatite (HA). However, the crystal phases that affect the crosstalk between osteoclasts and osteoblasts are unknown, which should determine the bone substitute material's property of OCP. The present study was designed to investigate whether the chemical composition and crystal structure of calcium phosphates affect osteoclast formation and the osteoclast–osteoblast crosstalk. Biodegradable β‐tricalcium phosphate (β‐TCP) was used as the control material. Osteoclasts were cultured on HA/OCP or HA/TCP disks and their cellular responses were assessed. Both OCP and β‐TCP had a similar ability to create multinucleated osteoclasts. However, OCP promoted the expression of complement component 3a (C3a), a positive coupling factor, in osteoclasts, whereas β‐TCP enhanced that of EphrinB2 (EfnB2) and collagen triple helix repeat containing 1 (Cthrc1). During osteoclast culture, phosphate ions were released from the crystals, and OCP‐HA conversion was advanced in HA/OCP mixtures and OCP. X‐ray diffraction analysis revealed no remarkable changes in the crystal structures of HA/TCP mixtures and β‐TCP before and after osteoclast culture. These results indicate that the distinct chemical environment induced by the calcium phosphate phases affects the crosstalk between osteoclasts and osteoblasts. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 1001–1013, 2019.
Cell sheet tissue engineering: Cell sheet preparation, harvesting/manipulation, and transplantation
Authors: Kobayashi Jun , Kikuchi Akihiko , Aoyagi Takao , Okano Teruo 
Published: January 2019

AbstractCell sheet tissue engineering is a concept for creating transplantable two‐dimensional (2D) and three‐dimensional (3D) tissues and organs. This review describes three elements of cell sheet tissue engineering in terms of the chemical and physical effects of material surfaces and the interfacial properties of cell sheets: preparation, harvesting/manipulation and transplantation of cell sheets. An essential technology for the preparation of cell sheets is the use of a temperature‐responsive cell culture surface, where the surface of tissue culture polystyrene (TCPS) dish is modified with thin layer of temperature‐responsive polymer, poly(N‐isopropylacrylamide) (PIPAAm). PIPAAm‐immobilized TCPS allows cultured cells to be harvested as a contiguous cell sheet with extracellular matrices (ECMs) by reducing the temperature, while chemical and physical disruption impair ECMs, cell–cell junction, and membrane proteins. Ligand‐immobilized and porous hydrophilic PIPAAm‐grafted surfaces are able to accelerate cell sheet preparation and harvesting, respectively. In addition, the manipulation of harvested cell sheets with the aid of cell sheet manipulator facilitates the formation of 3D tissues. Cell sheet‐based tissues and their transplantation are in seven clinical settings such as heart, cornea, esophagus, periodontal, middle chamber of ear, knee cartilage, and lung. In order to create thick and large 3D tissues and organs, large production of differentiated parenchymal cells from induced pluripotent stem (iPS) cells and vascularization within 3D tissues are key issues. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 955–967, 2019.
How the Japanese Society for Biomaterials established interdisciplinary studies in biomaterials science
Authors: Suzuki Osamu 
Published: January 2019

AbstractThe Japanese Society for Biomaterials (JSB) was established in December 1978, aiming to develop and improve science and technology regarding materials used in living organisms and their application. Currently, JSB plays important roles as a domestic and international society serving as a center for interdisciplinary studies on biomaterial science and its applied research. Our academic activities are wide‐ranging, from basic science and clinical practice to post‐application medical devices including the following: holding academic lectures, granting academic and other awards, publishing academic journals, developing guidelines for medical devices and bioassays, conducting research associated with clinical trials and studies, and participating in the World Biomaterials Congress and overseas academic meetings on biomaterials. Through such activities, we have actively engaged professionally in diverse discussions and operations. Thanks to your support, JSB recently celebrated its 40th anniversary since establishment. Over the 40‐year history, our predecessors worked hard to establish this interdisciplinary field spanning basic science (engineering, medical, biology, and others) and collaboration with companies. In addition, they contributed to society through the application of biomaterial technology. Their achievements made what we are today. To commemorate this anniversary, this report looks back at their achievements in order to use such information for further academic progress. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 917–929, 2019.
Effects of magnesium coating on bone‐implant interfaces with and without polyether‐ether‐ketone particle interference: A rabbit model based on porous Ti6Al4V implants
Authors: Du Zhe , Yu Xiaoming , Nie Binen , Zhu Zhonglin , Ibrahim Muhammad , Yang Ke , Tan Lili , Wang You 
Published: January 2019

AbstractWe investigated the effects of magnesium (Mg) on osteogenesis and bone resorption at a porous structure interface. A three‐dimensional (3D)‐printed porous Ti6Al4V implant coated with Mg was introduced, and polyether‐ether‐ketone wear particles were added to generate an animal model of implant loosening. We also examined the effects of Mg leach liquor on osteoblast/osteoclast gene expression, alkaline phosphatase activity, collagen secretion, tartrate‐resistant acid phosphatase activity, and bone resorption in vitro. Mg inhibited the early stage of osteoclast differentiation and inhibited bone resorption in vitro and in vivo. However, Mg did not enhance osteogenesis in vitro or in vivo in the porous structures or in peripheral areas around the implants. For implants with porous structures, the Mg coating did not improve the osteogenic ability by itself, but could restrain peri‐implant osteolysis, which may make it favorable for use in patients with osteoporosis. Further studies are needed to examine the precise mechanism of Mg‐induced anti‐osteolysis and the long‐term effects of Mg‐coated implants in humans. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 2388–2396, 2019.
LINC00520 targeting miR‐27b‐3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway
Authors: Tian Xinghan , Ji Yongqiang , Liang Yafeng , Zhang Jing , Guan Lina , Wang Chunting 
Published: January 2019

AbstractBackgroundAcute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy.MethodsBioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real‐time PCR (qRT‐PCR) and western blot. Dual‐luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI.ResultsLINC00520, miR‐27b‐3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR‐27b‐3p or downregulation of OSMR could accelerate the recovery of AKI.ConclusionOverexpression of LINC00520 contributes to the aggravation of AKI by targeting miR‐27b‐3p/
OSMR.
Role of TGF‐β signaling regulatory microRNAs in the pathogenesis of colorectal cancer
Authors: Soleimani Atena , Khazaei Majid , Ferns Gordon A , Ryzhikov Mikhail , Avan Amir , Hassanian Seyed Mahdi 
Published: January 2019

AbstractTransforming growth factor β (TGF‐β) modulates tumor progression by regulating cell proliferation, apoptosis, metastasis, angiogenesis, and drug resistance. Biological and pharmacological agonists/antagonists, the interplay between intracellular signaling pathways, and microRNAs (miRNAs) control the initiation and activation of the TGF‐β signaling pathway. It has been proposed that the expression profiles of tumor suppressor and oncogenic TGF‐β miRNAs may be used for the classification, diagnosis, and prognosis of human malignancies. Deregulated miRNAs and aberrant activation of TGF‐β signaling are frequently found in human colorectal cancers (CRCs), but a little is known about their mechanisms of action in the development and progression of colorectal carcinoma. This review summarizes the current knowledge of the role of TGF‐β signaling regulatory miRNAs in the pathogenesis of CRC for a better understanding and hence better management of this disease.
IGFBP5 suppresses oleate‐induced intramyocellular lipids deposition and enhances insulin signaling
Authors: Xiang Aoqi , Chu Guiyan , Zhu Youbo , Ma Guangjun , Yang Gongshe , Sun Shiduo 
Published: January 2019

AbstractExcess intramyocellular lipids are often accompanied by muscle insulin resistance (IR) and type 2 diabetes. The mechanism of the formation of intramyocellular lipids is unclear yet. In this study, we optimized the cellular model of intramyocellular lipids from differentiated C2C12 cells and identified that the expression of insulin‐like growth factor‐binding protein 5 (IGFBP5) is diminished in this process. Then, we added exogenous recombinant IGFBP5 during myocyte triglyceride (TAG) formation and found decreased lipids accumulation. In addition, IGFBP5 could promote lipolysis when added to the cellular model after the formation of intramyocellular lipids. Moreover, IGFBP5 could enhance myocyte insulin sensitivity by inhibiting the expression of the thioredoxin‐interacting protein (TXNIP) and arrestin domain‐containing 4 (ARRDC4), which are a negative regulator of insulin signaling in both cases. Meanwhile, IGFBP5 also inhibited the expression of glycerol‐3‐phosphate acyltransferase (GPAM) and diglyceride acyltransferase 2 (DGAT2), which were involved in TAG synthesis from a fatty acid. IGFBP5 also reduced TAG storage by promoting lipolysis. Therefore, IGFBP5 may play a role in the excess accumulation of lipid in muscle cells of diabetic patients and serve as a reference for further research and treatment of muscle IR and diabetes.
A 54‐kDa short variant of DHX33 functions in regulating mRNA translation
Authors: Su Dan , Yuan Baolei , Su Chenjing , Zhang Yandong 
Published: January 2019

AbstractDEAH box protein DHX33 has been found to be necessary for cell proliferation and early development of multicellular organisms. It plays diverse roles in regulating gene transcription, ribosome RNA synthesis, and protein translation. Dysregulation of DHX33 has been observed in various human cancers. In this study, we identified a short DHX33 variant in cells. The short DHX33 (hereafter referred to as DHX33‐2) has only 534 amino acids, which completely matches the C‐terminal helicase domain of full‐length DHX33 (DHX33‐1). Different from DHX33‐1, which mainly localizes to the nucleus, DHX33‐2 preferentially localizes to the cytoplasm. Through protein immunoprecipitation and RNA‐ immunoprecipitation analysis, we found that DHX33‐2 interacts with DDX3, eIF3, hnRNPs, poly (A) binding protein, and a subset of mRNAs. Further RNA sequencing analysis showed that DHX33 binds to a subset of mRNAs important in cell proliferation. DHX33‐2 stimulates the translation for specific mRNAs. Our study for the first time demonstrates the function of a short DHX33 variant in protein translation.
Effects of heparin and derivatives on podocytes: An in vitro functional and morphological evaluation
Authors: Delézay Olivier , Hé Zhiguo , Sabido Odile , Hodin Sophie , Bin Valérie , Saleem Moin A. , Mismetti Patrick , Delavenne Xavier 
Published: January 2019

AbstractUnfractionated heparin (UFH) and low molecular heparin derivatives (LMWH) display numerous biological properties in addition to their anticoagulant effects. However, due to the physicochemical heterogeneity of these drugs, a better understanding concerning their effects on human cells is clearly needed. Considering that heparins are mainly excreted by the kidney, we focused our attention on the effect of UFH and LMWH on human podocytes by functional and morphological/phenotypic in vitro analyses. We demonstrated that these products differentially modulate the permeability of podocyte monolayer to albumin. The functional perturbations observed were correlated to significant cellular morphological and cytoskeletal changes, as well as a decrease in the expression of proteins involved in podocyte adherence to the extracellular matrix or intercellular interactions. This point confirms that UFH and the different LMWHs exert specific effects on podocyte permeability and underlines the need of in vitro tests to evaluate new biological nonanticoagulant properties of LMWH.
PGC‐1α/SNAI1 axis regulates tumor growth and metastasis by targeting miR‐128b in gastric cancer
Authors: Wang Ping , Guo Xueyan , Zong Wei , Li Yulong , Liu Guisheng , Lv Yifei , Zhu Yunqing , He Shuixiang 
Published: January 2019

AbstractPeroxisome proliferator‐activated receptor γ coactivator 1α (PGC‐1α) is a transcriptional coactivator that has been characterized as master regulators of mitochondrial biogenesis. It has been reported that aberrant regulation of PGC‐1α is involved in a variety of human cancers. However, whether PGC‐1α is involved in the regulation of tumor growth and metastasis in gastric cancer (GC) remains unknown. In the present study, we found that the expression of PGC‐1α was upregulated in GC tissues and GC cell lines. Inhibition of PGC‐1α inhibited cell viability, migration, and invasion, and promoted cell apoptosis of GC cells. Furthermore, inhibition of PGC‐1α downregulated the SNAI1 expression, whereas upregulated microRNA (miR)‐128b expression. The expression of SNAI1 was upregulated and the expression of miR‐128b was downregulated in GC tissues. We further found that there was a positive correlation between PGC‐1α and SNAI1 expression, and a negative correlation between PGC‐1α and miR‐128b expression or between SNAI1 and miR‐128b expression in GC tissues. Moreover, PGC‐1α inhibition‐induced increased miR‐128b expression, and PGC‐1α overexpression‐induced decreased miR‐128b expression were both markedly suppressed by SNAI1 overexpression. In addition, SNAI1 overexpression or miR‐128b inhibition partly reversed the effects of PGC‐1α inhibition in GC cells. Furthermore, inhibition of PGC‐1α suppressed the tumor growth in a nude mouse model, which may be related with the dysregulation of SNAI1 and miR‐128b. In conclusion, these data indicate that the PGC‐1α/SNAI1/miR‐128b axis plays a vital role in GC via regulating cell viability, migration, invasion, and apoptosis.
PLCε knockdown overcomes drug resistance to androgen receptor antagonist in castration‐resistant prostate cancer by suppressing the wnt3a/β‐catenin pathway
Authors: Li Luo , Du Zhongbo , Gao Yingying , Tang Yu , Fan Yanru , Sun Wei , Li Ting , Liu Nanjing , Yuan Mengjuan , Fan Jiaxin , Niu Lingfang , Yan Jinxiao , Duan Limei , Wu Xiaohou , Luo Chunli 
Published: January 2019

AbstractMost prostate cancers (Pcas) develop into castration‐resistant prostate cancer (CRPC) after receiving androgen deprivation therapy (ADT). The expression levels of PLCε and wnt3a are increased in Pca and regulate androgen receptor (AR) activity. However, the biological function and mechanisms of PLCε and wnt3a in CRPC remain unknown. In this study, we found that the expression levels of PLCε, wnt3a, and AR were significantly increased in CRPC tissues as well as bicalutamide‐resistant‐LNCaP and enzalutamide‐resistant‐LNCaP cells. In addition, PLCε knockdown partly restored the sensitivity of drug‐resistant cells to bicalutamide and enzalutamide by inhibiting the activity of the wnt3a/β‐catenin/AR signaling axis. Interestingly, the resistance of LNCaP cells docetaxel is related to PLCε but not the wnt3a/β‐catenin pathway. We also found that the combination of PLCε knockdown and enzalutamide treatment synergistically suppressed cell proliferation, tumor growth, and bone metastasis using in vitro and in vivo experiments. Our study revealed that PLCε is involved in the progression of drug‐resistance in CRPC and could be a new target for the treatment of CRPC.
The possible structural changes in the adrenal gland cortex after induction of hepatic ischemia–reperfusion injury in male albino rats: Light and electron microscopic study
Authors: El‐Tahawy Nashwa Fathy Gamal , Abozaid Samah Mohammed Mahmoud 
Published: January 2019

AbstractThe adrenal gland is an important endocrine gland in the body that secrets the adrenal hormones. One of the important clinical issues is the hepatic ischemia–reperfusion (IR) injury. Liver IR injury results in many distant organs dysfunctions such as lung, kidney, intestine, pancreas, and myocardium. The aim of the present study was to investigate the possible remote effects of hepatic IR on the structure of the adrenal cortex. Twenty healthy males, Sprague–Dawley albino rats aged 6–8 weeks were randomly divided into two groups (10 rats each): the sham control group (SC‐group) and the ischemia–reperfusion group (IR‐group). Sera were estimated for the following: aspartate transaminase (AST), alanine transaminase (ALT), lactic dehydrogenase (LDH), and corticosterone levels. Also oxidative markers such as malondialdehyde (MDA) and tumor necrosis factor‐α (TNF‐α), and the antioxidative enzyme, catalase were measured. Adrenal glands were processed for light and transmission electron microscopic study. The results showed a significant increase in serum liver enzymes (AST, ALT, and LDH), corticosterone, MDA, and TNF‐α levels and a significant decrease in serum levels of catalase in IR‐group compared with SC‐group. Adrenal cortical tissue of IR‐group showed the loss of normal appearance. Some cells of zona glomerulosa and most of the zona fasciculata cells appeared swollen and degenerated with highly vacuolated cytoplasm. Other cells were shrunken with deeply acidophilic cytoplasm and pyknotic nuclei. Degenerated mitochondria with disrupted cristae, lipid droplets were confluent and dilated smooth endoplasmic reticulum were seen. Few zona reticularis cells had the dark nucleus and cytoplasmic vacuolations. In the different zones, blood capillaries were markedly congested and some inflammatory cells infiltrations were observed. Liver IR affected the structure of the adrenal cortex.