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1.
Biomed Pharmacother ; 122: 109388, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31919041

RESUMO

Autologous chondrocyte implantation (ACI) is commonly used for the treatment of cartilage defects. Since the cell number for transplantation is limited, the expand culture of chondrocytes in vitro is needed. However, the phenotype of chondrocytes is easy to lose in monolayer cultured in vitro. Traditional growth factors such as transformation growth factor -ß1 (TGF-ß1) have been used for promoting the proliferation and maintained the phenotype of chondrocytes, but the high cost and functional heterogeneity limit their clinical application. It is of significant to develop substitutes that can accelerate proliferation and prevent dedifferentiation of chondrocytes for further study. In our present study, the effect of salidroside on proliferation and phenotype maintenance of chondrocytes and cartilage repair was investigated by performing the cell viability, morphology, glycosaminoglycan (GAG) synthesis, cartilage relative genes expression, macroscopic and histological analyzsis. The TGF-ß/smad3 signal which may involve in the protective effect of salidroside on chondrocytes was also detected by ELISA and qRT-PCR assays. The results indicated that salidroside could promote chondrocytes proliferation and enhance synthesis of cartilage extracellular matrix (ECM). Expression of collagen type I was significantly down-regulated which suggesting that salidroside could prevent chondrocytes from dedifferentiation. The in vivo experiments for cartilage repair also indicated that in the treatment of salidroside, chondrocytes used for ACI significantly accelerated the hyaline cartilage repair. While in the absence of salidroside, the repaired cartilage is mainly the fibrous cartilage. Additional experiments demonstrated that salidroside promotes the proliferation and maintain the phenotype of chondrocytes by activate the TGF-ß/smad3 signal. Salidroside may be a potential agent for ACI to promote the proliferation and maintain the phenotype of chondrocytes expansion in vitro.

2.
Carbohydr Polym ; 231: 115727, 2020 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-31888849

RESUMO

Carbazate groups were grafted on the commercial cellulose membrane (CM) to specifically scavenge the carbonylated proteins for hemodialysis. It confirmed that carbazate groups were successfully covalently attached on the CMs by XPS and EDS, and the modified CMs still saved their original morphology and crystalline structures by SEM and XRD. Furthermore, the modified CMs presented favorable physicochemical stability at wide pH range from 2.5 to 7.4. It was also found that the carbazate modified CMs could selectively remove carbonylated proteins from acrolein treated bovine serum albumin (BSA) or ESRD patient's blood serum in PBS buffer. The modified CMs showed the potential to be utilized as the substitute of dialysis membranes in hemodialysis.

3.
Biomaterials ; 230: 119601, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31711715

RESUMO

Osteoarthritis (OA) is one of the most common musculoskeletal disorders worldwide. Oxidative stress initiated by excessive free radicals such as reactive oxygen species (ROS) is a leading cause of cartilage degradation and OA. However, conventional injection or oral intake of antioxidants usually cannot provide effective treatment due to rapid clearance and degradation or low bioavailability. Here, a new strategy is proposed based on nanofibers made of poly (ε-caprolactone) (PCL) and PCL-grafted lignin (PCL-g-lignin) copolymer. Lignin offers intrinsic antioxidant activity while PCL tailors the mechanical properties. Electrospun PCL-lignin nanofibers show excellent antioxidant activity, low cytotoxicity and excellent anti-inflammatory effects as demonstrated using both H2O2-stimulated human chondrocytes and an OA rabbit model. PCL-lignin nanofibers inhibit ROS generation and activate antioxidant enzymes through autophagic mechanism. Arthroscopic implantation of nanofibrous membrane of PCL-lignin is effective to OA therapy because it is biocompatible, biodegradable and able to provide sustained antioxidant activity.

4.
J Cell Biochem ; 121(3): 2643-2654, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31692043

RESUMO

Immune infiltration is reported to be highly associated with tumor progress. Since butyrophilin subfamily 3 member A2 (BTN3A2) serves as a crucial mediator in immune activation, we aimed to investigate the correlation of BTN3A2 in immune infiltration and tumor prognosis via extensive-cancer analysis. The levels of BTN3A2 expression in extensive cancers were analyzed with Oncomine and TIMER databases. Univariate cox and multivariate cox regression analyses were conducted to assess the associations of BTN3A2 to prognosis of various cancers. The correlations of BTN3A2 with immune infiltration were assessed by TIMER database. It suggested that BTN3A2 was a potential prognosis signature for breast cancer (BRCA) and ovarian cancer (OV). However, immune infiltrations were highly correlated with BTN3A2 in triple-negative breast cancer (TNBC), compared with OV and other subtypes of BRCA. Multivariate cox regression analysis revealed that BTN3A2 was an independently prognostic signature of TNBC, as well as weighted correlation network analysis suggested BTN3A2 was only correlated with TNBC, rather than other subtypes of BRCA. Immune cell subtypes correlation analysis showed that BTN3A2 was highly correlated with general T, CD8+ T, T helper type 1, exhausted T cells, and dendritic cells in TNBC. And the coexpression geneset of BTN3A2 was mainly involved in T-cell receptor interaction and the nuclear factor-κB (NF-κB) signaling pathway. Collectively, BTN3A2 that was positively associated with better prognosis could be served as a special diagnostic and independently prognostic marker for TNBC by regulating the T-cell receptor interaction and NF-κB signaling pathways.

5.
J Cell Physiol ; 235(2): 1746-1758, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31309562

RESUMO

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease, and the pathogenesis of RA is still unknown. Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) are of significance in the pathogenesis of RA. In this study, three microarray profiles (GSE55457, GSE55584, and GSE55235) of human joint FLSs from 33 RA patients and 20 normal controls were extracted from the Gene Expression Omnibus Dataset and analyzed to investigate the underlying pathogenesis of RA. As analyzed by the differently expressed genes, gene ontology, Kyoto Encyclopedia of Genes and Genomes pathway enrichment, and protein-protein interaction network analysis, syndecan-4 (SDC4), a receptor of multiple cytokines and chemokines, which played a key role in the regulation of inflammatory response, was found to be an essential regulator in RA. To further validate these results, the levels of SDC4, reactive oxygen species (ROS), nitric oxide (NO), inflammation, and apoptosis in RA-FLSs were examined. SDC4-silenced RA-FLSs were also used. The results demonstrated that SDC4 and the level of ROS, NO, and inflammation were highly expressed while the apoptosis was decreased in RA-FLSs compared with normal FLSs. SDC4 silencing significantly suppressed the levels of ROS, NO, and inflammation; elevated the expression of nuclear factor erythroid 2-related factor 2; and promoted the apoptosis of RA-FLSs. Collectively, our results demonstrated a new mechanism of SDC4 in initiating the inflammation and inhibiting the apoptosis of RA-FLSs and that a potential target for the diagnosis and treatment of RA in the clinic might be developed.

6.
Mater Sci Eng C Mater Biol Appl ; 104: 109796, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31500029

RESUMO

Nanofibers as niche-biomimetic scaffolds hold promise in guided bone regeneration (GBR). Here we fabricated poly (lactic-co-glycolic acid) (PLGA)/poly(caprolactone) (PCL)-doped octacalcium phosphate (OCP) nanofiber membranes via electrospinning and investigated the osteogenic behavior of marrow mesenchymal stem cells (MSCs) on the membranes. By adjusting different ratio of OCP to PLGA/PCL, three hybrid stents including PLGA/PCL, PLGA/PCL/2 wt%OCP, PLGA/PCL/4wt%OCP were successfully prepared. The PLGA/PCL/OCP membranes showed a decrease in fiber diameter compared with PLGA/PCL, leading to enhanced mechanical strength. In-vitro studies showed that PLGA/PCL/OCP membranes better supported cell adhesion, spreading and proliferation than PLGA/PCL. The incorporation of OCP via electrospinning also endowed the membranes with osteoinductive capacity, as evidenced by activation of ALP activity, increased gene expression of bone specific markers (such as Runx2, ALP, Col 1a1, OPN, OCN, BMP2), and mineral nodules formation compared to PLGA/PCL. Comparatively, PLGA/PCL/4wt%OCP showed better mechanical and biological performance than PLGA/PCL/2 wt%OCP, demonstrating the role of OCP in nanofiber membranes. Thus, the electrospun PLGA/PCL/OCP nanofiber membranes can be potentially developed as a promising hybrid stent for GBR.


Assuntos
Fosfatos de Cálcio/química , Diferenciação Celular , Células-Tronco Mesenquimais/citologia , Nanofibras/química , Osteogênese , Poliésteres/química , Copolímero de Ácido Poliláctico e Ácido Poliglicólico/química , Engenharia Tecidual/métodos , Fosfatase Alcalina/metabolismo , Animais , Apoptose , Biomarcadores/metabolismo , Proliferação de Células , Regulação da Expressão Gênica , Células-Tronco Mesenquimais/metabolismo , Nanofibras/ultraestrutura , Ratos Sprague-Dawley , Espectroscopia de Infravermelho com Transformada de Fourier , Tecidos Suporte/química , Difração de Raios X
7.
Cell Biochem Funct ; 37(5): 359-367, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31066473

RESUMO

This study aimed to investigate the mechanism of nerve growth factor (NGF) from cobra venom and human transforming growth factor-ß1 (TGF-ß1) on the chondrogenic induction of mesenchymal stem cells (MSCs). NGF and TGF-ß1 were used to induce chondrogenesis of MSCs from rabbits for 7 days. Total RNA was extracted for mRNA sequencing. Differentially expressed genes (DEGs), gene ontology (GO), KEGG pathway enrichment, and PPI network analysis were conducted to screen the specific signalling pathways and target genes. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to further confirm the relative target genes. The results showed that NGF could significantly promote the expression of hyaline cartilage specific genes (collagen type II alpha 1 chain, COL2A1) compared with TGF-ß1. PI3K-AKT signalling pathway is commonly involved in the chondrogenesis of MSCs induced by NGF and TGF-ß1. However, the expression levels of the genes in the PI3K-AKT signalling pathway were significantly higher in NGF group than that in the TGF-ß1 group. In the process of chondrogenesis of MSCs induced by NGF and TGF-ß1, integrin (ITGAs) were the targeted hub genes to activate the PI3K-AKT signalling pathway. NGF could activate more proliferation and differentiation genes in the process of chondrogenesis of MSCs than TGF-ß1. TGF-ß1 promoted angiogenesis by targeting the thrombospondin (THBS1) and THBS2 which might contribute to the osteophyte formation. PI3K-AKT was the crucial signalling pathway for chondrogenic differentiation. NGF could activate the PI3K-AKT signalling pathway to a higher level, and NGF had more specificity for promoting expression of specific genes of chondrocyte compared with TGF-ß1. SIGNIFICANCE OF THE STUDY: In our study, we compared two different growth factors in promoting cartilage differentiation of MSCs and found some similarities and differences. We revealed that both NGF and TGF-ß1 could activate the PI3K-AKT signalling pathway (the expression of it in NGF was higher) by targeting the ITGAs in the process of chondrogenesis from MSCs. However, NGF could activate more proliferation and differentiation genes in the process of chondrogenesis of MSCs, whereas TGF-ß1 caused osteophyte formation by activating THBS1 and THBS2. These might be the reason why NGF could promote cartilage differentiation more specifically.


Assuntos
Diferenciação Celular , Condrogênese , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Células-Tronco Mesenquimais/citologia , Células-Tronco Mesenquimais/metabolismo , Animais , Diferenciação Celular/genética , Células Cultivadas , Condrogênese/genética , Fosfatidilinositol 3-Quinases/metabolismo , Coelhos
8.
Cell Biochem Funct ; 37(1): 31-41, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30468518

RESUMO

The purpose of the present study was to investigate the underlying molecular mechanism of osteoarthritis (OA) and rheumatoid arthritis (RA) based on microarray profiles. Three human joint fibroblast-like synoviocytes (FLSs) microarray profiles including 26 OA samples, 33 RA samples, and 20 healthy control (HC) samples were downloaded from the GEO database. Differentially expressed genes (DEGs) between OA and HC (DEGsOA) and RA and HC (DEGsRA) were identified. Co-expressed and specific genes were analysed between DEGsOA and DEGsRA. Gene ontology, KEGG pathway enrichment, PPI network, and GSEA were performed to predict the function of DEGs. Two hundred seventy-six and 410 differential genes in DEGsOA and DEGsRA were observed. One hundred fifty coexpressed genes and 126 OA-specific genes (SELE, SERPINE1, and NFKBIA were the key genes) between DEGsOA and DEGsRA were enriched in the tumour necrosis factor (TNF) signalling pathway. However, 260 RA-specific genes of which the key genes were CCR5, CCR7, CXCR4, CCL5, and CCR4 were enriched in chemokine signalling pathway. Therefore, FLSs might exert an inflammatory effect by regulating TNF signalling pathway, targeting SELE, SERPINE1, and NFKBIA during the process of OA. Although TNF signalling pathway was also involved in the synovitis of RA, chemokine signalling pathway played the key role in RA FLSs mediating cell migration, invasion, and release of chemotaxis. In addition, CCR5, CCR7, CXCR4, CCL5, and CCR4 might be hub genes in RA. The different biomarkers and pathways identified in OA and RA may provide references for further study. SIGNIFICANCE OF THE STUDY: This study revealed the similar and different mechanisms of FLSs and different biomarkers that might with important regulatory effects on RA and OA. In OA, FLSs played an inflammatory role through TNF signalling pathway, targeting SELE, SERPINE1, and NFKBIA. Although TNF signalling pathway was also involved in the synovitis of RA, chemokine signalling pathway was a crucial pathway in mediating FLSs migration, invasion, and release of chemotaxis. CCR5, CCR7, CXCR4, CCL5, and CCR4 might be keys genes in RA. We expect that our results will bring more comprehensively understanding between RA and OA for researchers.


Assuntos
Artrite Reumatoide/genética , Fibroblastos/metabolismo , Fibroblastos/patologia , Análise de Sequência com Séries de Oligonucleotídeos , Osteoartrite/genética , Sinoviócitos/metabolismo , Sinoviócitos/patologia , Artrite Reumatoide/patologia , Biomarcadores/análise , Perfilação da Expressão Gênica , Humanos , Osteoartrite/patologia , Reação em Cadeia da Polimerase em Tempo Real
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