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  • SAGE Publications  (14)
  • 1
    Online Resource
    Online Resource
    Mechanism of Mir-218-5P in Autophagy, Apoptosis and Oxidative Stress in Rheumatoid Arthritis Synovial Fibroblasts is Mediated by Klf9 and Jak/Stat3 Pathways
    SAGE Publications ; 2021
    In:  Journal of Investigative Medicine Vol. 69, No. 4 ( 2021-04), p. 824-832
    Details
    In: Journal of Investigative Medicine, SAGE Publications, Vol. 69, No. 4 ( 2021-04), p. 824-832
    Abstract: This study was aimed to investigate the effects of miR-218-5p on the proliferation, apoptosis, autophagy, and oxidative stress of rheumatoid arthritis synovial fibroblasts (RASFs), and the related mechanisms. Quantitative reverse transcription-PCR showed that the expression of miR-218-5p in rheumatoid arthritis synovial tissue was significantly higher than that in healthy synovial tissue. Compared with healthy synovial fibroblasts, miR-218-5p expression was obviously upregulated in RASFs, while KLF9 protein expression was markedly downregulated. Mechanistically, miR-218-5p could directly bind to the 3′ untranslated region of KLF9 to inhibit the expression of KLF9. Additionally, transfection of miR-218-5p small interfering RNA (siRNA) inhibited the proliferation but promoted apoptosis and autophagy of RASFs. Simultaneously, miR-218-5p silencing reduced reactive oxygen species and malondialdehyde levels and increased superoxide dismutase and glutathione peroxidase activity to improve oxidative stress in RASFs. More importantly, the introduction of KLF9 siRNA reversed the effects of miR-218-5p siRNA transfection on RASF proliferation, apoptosis, autophagy, and oxidative stress. What is more, silencing miR-218-5p inhibited the activation of JAK2/STAT3 signaling pathway by targeting KLF9. Collectively, knockdown of miR-218-5p could regulate the proliferation, apoptosis, autophagy and oxidative stress of RASFs by increasing the expression of KLF9 and inhibiting the activation of the JAK2/STAT3 signaling pathway, which may provide a potential target for the mechanism research of RA.
    Type of Medium: Online Resource
    ISSN: 1081-5589 , 1708-8267
    URL: Article
    DOI: 10.1136/jim-2020-001437
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2021
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  • 2
    Online Resource
    Online Resource
    Reversibly Immortalized Mouse Articular Chondrocytes Acquire Long-Term Proliferative Capability While Retaining Chondrogenic Phenotype
    SAGE Publications ; 2015
    In:  Cell Transplantation Vol. 24, No. 6 ( 2015-06), p. 1053-1066
    Details
    In: Cell Transplantation, SAGE Publications, Vol. 24, No. 6 ( 2015-06), p. 1053-1066
    Abstract: Cartilage tissue engineering holds great promise for treating cartilaginous pathologies including degenerative disorders and traumatic injuries. Effective cartilage regeneration requires an optimal combination of biomaterial scaffolds, chondrogenic seed cells, and biofactors. Obtaining sufficient chondrocytes remains a major challenge due to the limited proliferative capability of primary chondrocytes. Here we investigate if reversibly immortalized mouse articular chondrocytes (iMACs) acquire long-term proliferative capability while retaining the chondrogenic phenotype. Primary mouse articular chondrocytes (MACs) can be efficiently immortalized with a retroviral vector-expressing SV40 large T antigen flanked with Cre/loxP sites. iMACs exhibit long-term proliferation in culture, although the immortalization phenotype can be reversed by Cre recombinase. iMACs express the chondrocyte markers Col2a1 and aggrecan and produce chondroid matrix in micromass culture. iMACs form subcutaneous cartilaginous masses in athymic mice. Histologic analysis and chondroid matrix staining demonstrate that iMACs can survive, proliferate, and produce chondroid matrix. The chondrogenic growth factor BMP2 promotes iMACs to produce more mature chondroid matrix resembling mature articular cartilage. Taken together, our results demonstrate that iMACs acquire long-term proliferative capability without losing the intrinsic chondrogenic features of MACs. Thus, iMACs provide a valuable cellular platform to optimize biomaterial scaffolds for cartilage regeneration, to identify biofactors that promote the proliferation and differentiation of chondrogenic progenitors, and to elucidate the molecular mechanisms underlying chondrogenesis.
    Type of Medium: Online Resource
    ISSN: 0963-6897 , 1555-3892
    URL: Article
    DOI: 10.3727/096368914X681054
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2015
    detail.hit.zdb_id: 2020466-8
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  • 3
    Online Resource
    Online Resource
    Overexpression of Smac/DIABLO in Hep-2 Cell Line: Possible Role in Potentiating the Sensitivity of Chemotherapeutic Drugs
    SAGE Publications ; 2010
    In:  Tumori Journal Vol. 96, No. 2 ( 2010-03), p. 310-315
    Details
    In: Tumori Journal, SAGE Publications, Vol. 96, No. 2 ( 2010-03), p. 310-315
    Abstract: The major obstacles for tumor chemotherapy are drug resistance and/or adverse effects on the host. In the present study we investigated the role of the second mitochondria-derived activator of caspase (Smac/DIABLO) in the action of cisplatin (DDP), 5-fluorouracil (5-FU), and the combination of both in Hep-2 cells. Methods and study design Hep-2 laryngeal carcinoma cells exposed to DDP, 5-FU and the combination of both were investigated. Cell viability was determined by MTT assay. Apoptosis was measured by Ho.33342 and PI double staining and flow cytometry. The expression of Smac/DIABLO at the mRNA and protein level was assayed by RT-PCR and Western blotting. Results DDP, 5-FU and the combination of both drugs reduced the cell survival rates in a concentration- and time-dependent manner. The drug combination not only exerted a stronger inhibitory effect, but also at a lower concentration compared with the single drugs. Apoptosis was concomitant in a caspase-dependent manner. The expression of Smac/DIABLO increased significantly at both mRNA and protein levels after cell exposure to the combination compared with single drugs. Conclusions Smac/DIABLO plays a pivotal role in attaining a synergistic effect in Hep-2 cells in response to this combined strategy.
    Type of Medium: Online Resource
    ISSN: 0300-8916 , 2038-2529
    URL: Article
    DOI: 10.1177/030089161009600220
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
    detail.hit.zdb_id: 280962-X
    detail.hit.zdb_id: 2267832-3
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  • 4
    Online Resource
    Online Resource
    Dehydrocorydaline attenuates bone cancer pain by shifting microglial M1/M2 polarization toward the M2 phenotype
    SAGE Publications ; 2018
    In:  Molecular Pain Vol. 14 ( 2018-01), p. 174480691878173-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 14 ( 2018-01), p. 174480691878173-
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1177/1744806918781733
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2018
    detail.hit.zdb_id: 2174252-2
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  • 5
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    Online Resource
    SOX11: friend or foe in tumor prevention and carcinogenesis?
    SAGE Publications ; 2019
    In:  Therapeutic Advances in Medical Oncology Vol. 11 ( 2019-01), p. 175883591985344-
    Details
    In: Therapeutic Advances in Medical Oncology, SAGE Publications, Vol. 11 ( 2019-01), p. 175883591985344-
    Abstract: Sex-determining region Y-related high-mobility-group box transcription factor 11 (SOX11) is an essential member of the SOX transcription factors and has been highlighted as an important regulator in embryogenesis. SOX11 studies have only recently shifted focus from its role in embryogenesis and development to its function in disease. In particular, the role of SOX11 in carcinogenesis has become of major interest in the field. SOX11 expression is elevated in a wide variety of tumors. In many cancers, dysfunctional expression of SOX11 has been correlated with increased cancer cell survival, inhibited cell differentiation, and tumor progression through the induction of metastasis and angiogenesis. Nevertheless, in a limited number of malignancies, SOX11 has also been identified to function as a tumor suppressor. Herein, we review the correlation between the expression of SOX11 and tumor behaviors. We also summarize the mechanisms underlying the regulation of SOX11 expression and activity in pathological conditions. In particular, we focus on the pathological processes of cancer targeted by SOX11 and discuss whether SOX11 is protective or detrimental during tumor progression. Moreover, SOX11 is highlighted as a clinical biomarker for the diagnosis and prognosis of various human cancer. The information reviewed here should assist in future experimental designs and emphasize the potential of SOX11 as a therapeutic target for cancer.
    Type of Medium: Online Resource
    ISSN: 1758-8359 , 1758-8359
    URL: Article
    DOI: 10.1177/1758835919853449
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2019
    detail.hit.zdb_id: 2503443-1
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  • 6
    Online Resource
    Online Resource
    The external jugular vein is a feasible and safe alternative access for retrieval of inferior vena cava filter
    SAGE Publications ; 2022
    In:  The Journal of Vascular Access
    Details
    In: The Journal of Vascular Access, SAGE Publications
    Abstract: The purpose is to analyze whether the external jugular vein (EJV) is a feasible and safe alternative access for the retrieval IVCFs designed for the jugular approach. Methods: This study was designed as a nonrandomized, controlled study. The patients were divided into two groups: the IJV or EJV access groups. All operations were performed by the vascular surgery team. The main outcome was the technical success rate. The secondary outcomes included (1) the IVCF retrieval rate; (2) the time required to puncture the access vein (min); (3) the number of punctures required for access, and other aspects. Results: A total of 119 patients were recruited for IVCF retrieval. Seventeen patients refused to join this trial, leaving 58 patients in the IJV group and 44 patients in the EJV group. In the IJV group, technical success was not achieved in one patient who started in the EJV group and was transferred to the IJV group. There was no significant difference in age, comorbidities, or technical success rate between the two groups. Significant differences were observed in puncture time (min), number of punctures, and inadvertent puncture of the carotid artery. All of the patients were discharged 1 or 2 days after the operation. Conclusion: EJV is safe and feasible alternative access for the retrieval of IVCFs that are designed for jugular approaches.
    Type of Medium: Online Resource
    ISSN: 1129-7298 , 1724-6032
    URL: Article
    DOI: 10.1177/11297298211064467
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2022
    detail.hit.zdb_id: 2079292-X
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  • 7
    Online Resource
    Online Resource
    Meta-analysis reveals significant association between FOXP3 polymorphisms and susceptibility to Graves’ disease
    SAGE Publications ; 2021
    In:  Journal of International Medical Research Vol. 49, No. 4 ( 2021-04), p. 030006052110041-
    Details
    In: Journal of International Medical Research, SAGE Publications, Vol. 49, No. 4 ( 2021-04), p. 030006052110041-
    Abstract: This meta-analysis aimed to determine the associations between the rs3761547, rs3761548, and rs3761549 single-nucleotide polymorphisms (SNPs) of the forkhead box P3 ( FOXP3) gene and susceptibility to Graves’ disease (GD). Methods Case–control studies with information on the associations between the rs3761547, rs3761548, and rs3761549 FOXP3 SNPs and GD published before 01 May 2020 were identified in the PubMed, Embase, Web of Science, and China National Knowledge Infrastructure databases. Data from the studies were analyzed using RevMan version 5.3. Results Seven independent case–control studies including 4051 GD patients and 4569 controls were included in the meta-analysis. The overall pooled analysis indicated that FOXP3/rs3761548 and FOXP3/rs3761549 polymorphisms were significantly associated with GD susceptibility (rs3761548: A vs. C, odds ratio [OR] = 1.32, 95% confidence interval [CI] 1.05–1.67; rs3761549: TT vs. CC, OR = 1.98, 95%CI 1.49–2.65; (TT + TC) vs. CC, OR = 1.44, 95%CI 1.11–1.88). In contrast, the FOXP3/rs3761547 polymorphism was not associated with GD susceptibility. Subgroup analysis according to ethnicity showed that rs3761548 was associated with GD in Asians but not in Caucasians, whereas rs3761549 was associated in both Asians and Caucasians. Conclusion This meta-analysis demonstrated that FOXP3/rs3761548 and FOXP3/rs3761549 SNPs were significantly associated with susceptibility to GD, at least in Asian populations.
    Type of Medium: Online Resource
    ISSN: 0300-0605 , 1473-2300
    URL: Article
    DOI: 10.1177/03000605211004199
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2021
    detail.hit.zdb_id: 2082422-1
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  • 8
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    Online Resource
    Wnt signaling in bone formation and its therapeutic potential for bone diseases
    SAGE Publications ; 2013
    In:  Therapeutic Advances in Musculoskeletal Disease Vol. 5, No. 1 ( 2013-02), p. 13-31
    Details
    In: Therapeutic Advances in Musculoskeletal Disease, SAGE Publications, Vol. 5, No. 1 ( 2013-02), p. 13-31
    Abstract: The Wnt signaling pathway plays an important role not only in embryonic development but also in the maintenance and differentiation of the stem cells in adulthood. In particular, Wnt signaling has been shown as an important regulatory pathway in the osteogenic differentiation of mesenchymal stem cells. Induction of the Wnt signaling pathway promotes bone formation while inactivation of the pathway leads to osteopenic states. Our current understanding of Wnt signaling in osteogenesis elucidates the molecular mechanisms of classic osteogenic pathologies. Activating and inactivating aberrations of the canonical Wnt signaling pathway in osteogenesis results in sclerosteosis and osteoporosis respectively. Recent studies have sought to target the Wnt signaling pathway to treat osteogenic disorders. Potential therapeutic approaches attempt to stimulate the Wnt signaling pathway by upregulating the intracellular mediators of the Wnt signaling cascade and inhibiting the endogenous antagonists of the pathway. Antibodies against endogenous antagonists, such as sclerostin and dickkopf-1, have demonstrated promising results in promoting bone formation and fracture healing. Lithium, an inhibitor of glycogen synthase kinase 3β, has also been reported to stimulate osteogenesis by stabilizing β catenin. Although manipulating the Wnt signaling pathway has abundant therapeutic potential, it requires cautious approach due to risks of tumorigenesis. The present review discusses the role of the Wnt signaling pathway in osteogenesis and examines its targeted therapeutic potential.
    Type of Medium: Online Resource
    ISSN: 1759-720X , 1759-7218
    URL: Article
    DOI: 10.1177/1759720X12466608
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2013
    detail.hit.zdb_id: 2516075-8
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  • 9
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    The surface characterization of microporous titanium carbide coating on titanium alloys
    SAGE Publications ; 2014
    In:  Proceedings of the Institution of Mechanical Engineers, Part J: Journal of Engineering Tribology Vol. 228, No. 5 ( 2014-05), p. 521-528
    Details
    In: Proceedings of the Institution of Mechanical Engineers, Part J: Journal of Engineering Tribology, SAGE Publications, Vol. 228, No. 5 ( 2014-05), p. 521-528
    Abstract: Surface composition, the pore size and pore distribution of microporous titanium carbide were investigated to understand the potential use of titanium alloys in the field of artificial joints. The tribological behaviours of the ultra-high-molecular-weight polyethylene (UHMWPE) were investigated to evaluate the potential value of microporous titanium carbide coating on titanium alloys. The result showed that the uniform microporous titanium carbide coating was formed on the substrate of titanium alloys with a porosity of 24.4% after sequential carburization. It was found that the nanohardness values of the bottom and the edges of the pore were significantly increased and kept approximately the same value. Finally, the results also revealed that microporous titanium carbide could not only decrease the friction coefficient, but also decrease the wear rate of UHMWPE.
    Type of Medium: Online Resource
    ISSN: 1350-6501 , 2041-305X
    URL: Article
    DOI: 10.1177/1350650113517375
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2014
    detail.hit.zdb_id: 2032767-5
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  • 10
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    XRCC2 Arg188His polymorphism and colorectal cancer risk: a meta-analysis
    SAGE Publications ; 2021
    In:  Journal of International Medical Research Vol. 49, No. 10 ( 2021-10), p. 030006052110394-
    Details
    In: Journal of International Medical Research, SAGE Publications, Vol. 49, No. 10 ( 2021-10), p. 030006052110394-
    Abstract: To investigate the potential correlation between the Arg188His (rs3218536) polymorphism of X-ray repair cross-complementing 2 ( XRCC2) and colorectal cancer (CRC) risk, as the association remains unclear. Methods The CNKI, PubMed, EMBASE and Cochrane library databases were systematically searched for relevant studies published up to July 2021. Data were extracted from included studies, and analysed for pooled or subgroup odds ratios (ORs) with 95% confidence intervals (CIs) using STATA 12.0 software. Results Seven published studies were included. Pooled analysis revealed that the XRCC2 Arg188His polymorphism was associated with increased CRC risk (His versus Arg: OR 1.14, 95% CI 1.01, 1.29). Trial Sequential Analysis to test the power of the results showed that they were unreliable and the meta-analysis required additional studies. Conclusion The current meta-analysis suggests that the XRCC2 Arg188His polymorphism may be a risk factor for CRC.
    Type of Medium: Online Resource
    ISSN: 0300-0605 , 1473-2300
    URL: Article
    DOI: 10.1177/03000605211039473
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2021
    detail.hit.zdb_id: 2082422-1
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