CARDIOVASCULAR PATHOLOGY
·
2017
·
IF 2.359
Lei Zhang,Hailing Cheng,Yuxia Yue,Shuangzhan Li,Daping Zhang,Ruili He
Background Long non-coding RNAs (lncRNAs) have been revealed to participate in the pathological events associated with atherosclerosis . However, the exact role of lncRNA taurine-up-regulated gene 1 (TUG1) and its possible molecular mechanism in atherosclerosis remain unidentified. Methods High-fat diet (HFD)-treated ApoE −/− mice were used as an in vivo model of atherosclerosis. Ox-LDL-induced macrophages and vascular smooth muscle cells (VSMCs) were employed as cell models of atherosclerosis. qRT-PCR was performed to detect the expression of TUG1 and miR-133a. Serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were analyzed by commercially available enzyme kits. Oil red O and hematoxylin and eosin (H&E) staining were conducted to examine atherosclerotic lesion. Luciferase reporter assay combined with RNA immunoprecipitation (RIP) was applied to confirm the interaction between TUG1, miR-133a and FGF1 . Cell proliferation ability was determined by Cell Counting Kit-8 (CCK-8) assay and trypan blue dye exclusion test. Cell apoptosis was evaluated with TUNEL assay. Expression and production of inflammatory cytokines was measured with western blot and ELISA analysis. Results TUG1 expression was up-regulated in HFD-treated ApoE −/− mice, as well as in ox-LDL-induced RAW264.7 and MOVAS cells. TUG1 knockdown inhibited hyperlipidemia , decreased inflammatory response, and attenuated atherosclerotic lesion in HFD-treated ApoE −/− mice. TUG1 could function as a molecular sponge of miR-133a to suppress its expression. TUG1 overexpression accelerated cell growth, improved inflammatory factor expression, and inhibited apoptosis in ox-LDL-stimulated RAW264.7 and MOVAS cells, while this effect was abated after transfection with miR-133 mimic. Moreover, fibroblast growth factor 1 (FGF1) was identified as a direct target of miR-133a. Restored expression of FGF1 overturned the effect of miR-133a on cell proliferation, inflammatory factor secretion and apoptosis in ox-LDL-treated RAW264.7 and MOVAS cells. Finally, TUG1 was revealed to up-regulate FGF1 expression by sponging miR-133a. Conclusion TUG1 knockdown ameliorates atherosclerosis by modulating FGF1 via miR-133a, raising the possibility of targeting TUG1 as an atheroprotective therapeutic strategy.
研究领域:
分子生物学
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心血管疾病
·
遗传学
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产品关联
DOI
PubMed
高影响因子
ACS Applied Polymer Materials
·
2025
·
IF 4.7
Yuwei Gong,Xiaoyan Wang,Fang Ma,Rui Zhang,Meng Zhu,Hui Yang,Ling Qin,Hairong Ma,Jinsong Liu,Hualin Zhang
As temporary skin substitutes, wound dressings should have multiple functions, such as anti-inflammatory, sterilization, and tissue regeneration-promoting effects. In this study, a multilevel construction strategy was used to construct a bilayer tobramycin (TOB)/acid fibroblast growth factor-coloaded composite functional dressing by electrospinning, emulsification cross-linking, and freeze-drying for sustained drug release and wound repair. The dressing simulated the double-layer structure of the skin, with an upper layer composed of a TOB-loaded poly(lactic-co-glycolic acid)/multiwalled carbon nanotube electrospun membrane, which can prevent body fluid loss, resist external bacterial invasion, and act as a protective barrier, and a lower layer composed of an FGF1-loaded calcium alginate microsphere/chitosan composite sponge with hemostatic, moisturizing, cell proliferation- and tissue regeneration-promoting, and wound healing acceleration functions. The morphology, water contact angle, cell proliferation and migration abilities, antibacterial properties, and angiogenic and coagulation effects of the dressing were determined in vitro, and its skin wound repair properties were evaluated in vivo. The upper layer of the dressing was hydrophobic, whereas the lower layer was hydrophilic. Moreover, the dressing significantly promoted L929 cell proliferation and migration; had strong antibacterial effects on Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa; and promoted angiogenesis and the healing of full-thickness skin wounds in Sprague-Dawley (SD) rats, along with possessing good hemostatic properties.
研究领域:
生物医学工程
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药剂学
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材料科学
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组织工程
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微生物学
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产品关联
DOI
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2023
·
IF 8.1
Qingying Liu,Lianghua Xie,Wei Chen
Cell cultured meat is a novel and promising technology, but developing specific culture medium for muscle cells remains one of the main technical obstacles. FGF1 signaling is reported to promote proliferation and maintain proliferative capacity of satellite cells. However, the effect of FGF1 as a supplement to serum-free medium on satellite cells in vitro culture is still unclear. In this study, an efficient method for the production of soluble and biologically active recombinant bovine FGF1 (rbFGF1) protein in Escherichia coli was established. The soluble expression level of TrxA-rbFGF1 fusion protein was 562 mg/L in shake flasks, resulting in 5.5 mg of pure rbFGF1 from 0.1 L of starting culture. In serum-free culture conditions, rbFGF1 effectively promoted the proliferation and regulated the mitochondrial morphology and function of C2C12 myoblasts.rbFGF1 activated extracellular signal-regulated kinases1/2 (ERK1/2) signaling in C2C12 myoblasts, which further stimulated dynamin related protein 1 (DRP1) Ser616 phosphorylation. These findings highlighted the potential application of rbFGF1 in developing effective serum-free medium for cultured meat production.
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 15
Lei Jin,Cao Kun,Chen Huimin,Hou Jinhuan,Li Taiqin,Zhang Ya,Chen Chengxin,Ma Huaxing,Jin Jiliang,Qian Junxue,Li Zhi,Zhang Tian,Zuo Shi,Linghu Kegang,Li Haiyang
Chronic liver fibrosis remains a major healthcare burden with no approved pharmacotherapies currently available that directly target the fibrotic process. Although apoptotic vesicles (apoVs) derived from human umbilical cord mesenchymal stem cells (hUMSCs) hold great therapeutic potential for tissue repair, their mechanisms in alleviating liver fibrosis and their feasibility as siRNA carriers remain unclear. Here, we demonstrate that systemically administered apoVs exhibit robust liver tropism, efficiently delivering miR-6869-5p to both hepatic stellate cells (HSCs) and macrophages. Mechanistically, miR-6869–5p directly targets fibroblast growth factor 1 (FGF1) to suppress the PI3K/AKT/mTOR signaling pathway, thereby inhibiting HSC activation and reducing collagen deposition. Simultaneously, it targets high-mobility group box 1 (HMGB1) to attenuate NF-κB activity and establish an antifibrotic microenvironment through HSC-macrophage crosstalk. In clinical cohorts ( n = 100), serum miR-6869 − 5p levels were inversely correlated with fibrosis indices. Leveraging these unique properties, we engineered apoVs loaded with antifibrotic TANGO1 siRNA (si-apoVs), which blocks collagen secretion; this achieves enhanced antifibrotic efficacy in CCl₄-induced liver fibrosis models while mitigating the pro-inflammatory side effects associated with free siRNA. This study identifies hUMSC-derived apoVs as a liver-targeted, dual-action therapeutic platform, and si-apoVs represent a potent, translation-ready strategy for the treatment of liver fibrosis. Graphical abstract The alternative text for this image may have been generated using AI.
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DOI
PubMed
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
·
2019
·Vol. 193
·期 2
·422-433
·
IF 2.431
Hu Peilin,Du Jie,Zhang Shuai,Wang Ting,Li Jun,Chen Gang,Zhou Guangqian
Osteoarthritis (OA), a common degenerative disease affecting articular cartilage, is caused by multiple factors, and currently, there are few approaches to effectively delay its progression. This study aimed to evaluate whether a strontium compound (in the form of strontium gluconate, Glu-Sr) could reduce OA pathology severity in osteoarthritic rat models by directly targeting chondrocytes, including catabolic/anabolic activities and/or chondrogenic differentiation. Glu-Sr was administered to OA rats by oral gavage beginning during OA induction and continuing for 8 weeks. Glu-Sr treatment was found to significantly reduce cartilage degeneration and delay OA progression. Further examination showed that collagen II, Sox9, and aggrecan (ACAN) genes were up-regulated whereas IL-1β was down-regulated in chondrocytes isolated from Glu-Sr-treated rats. Glu-Sr also antagonized the catabolic effects of IL-1β on chondrocytes. Furthermore, Glu-Sr was shown to promote the chondrogenic differentiation of bone marrow mesenchymal stem cells (BMMSCs), possibly through promoting chondrogenic gene expression, including CTGF and FGF1, as revealed by RNA-sequencing (RNA-seq). These results suggest that systemic administration of Glu-Sr may be useful in prophylactic and therapeutic treatment of chronic cartilage degradation through affecting multiple steps from chondrogenic differentiation of progenitors to matrix formation in mature chondrocytes.
研究领域:
风湿病学
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骨科
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分子生物学
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干细胞研究
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）