• Complex
  • Title
  • Author
  • Keyword
  • Abstract
  • Scholars
Search
High Impact Results & Cited Count Trend for Year Keyword Cloud and Partner Relationship

Query:

学者姓名:夏育民

Refining:

Type

Submit Unfold

Indexed by

Submit Unfold

Language

Submit

Clean All

Export Sort by:
Default
  • Default
  • Title
  • Year
  • WOS Cited Count
  • Impact factor
  • Ascending
  • Descending
< Page ,Total 3 >
TWEAK/Fn14 Interaction Confers Aggressive Properties to Cutaneous Squamous Cell Carcinoma. PubMed SCIE
期刊论文 | 2019 , 139 (4) , 796-806 | The Journal of investigative dermatology
Abstract&Keyword Cite

Abstract :

Recent studies showed that TWEAK/Fn14 signaling participates in the progression of internal malignancies. However, its role in the biological properties of cutaneous squamous cell carcinoma (SCC) remains unclear. This study was designed to explore the effect of TWEAK/Fn14 activation on cutaneous SCC as well as the relevant mechanism. The expression of TWEAK and Fn14 was determined in tissue samples of patients with cutaneous SCC. Human primary keratinocytes and SCC cell lines were cultured in vitro, receiving stimulation of TWEAK. The xenografts of SCC were generated subcutaneously in BALB/c nude mice. The results showed that both TWEAK and Fn14 were highly expressed in human cutaneous SCC. Moreover, TWEAK/Fn14 activation promoted the proliferation, migration, and invasion of cultured SCC cells. Interestingly, TNFR2 was upregulated in cultured SCC cells, and the transfection of TNFR2 small interfering RNA abrogated the effect of TWEAK on these cells. Finally, the favorable effect of TWEAK/Fn14 signals was confirmed in BALB/c nude mice with SCC xenografts. In conclusion, TWEAK/Fn14 signals contribute to the progression of cutaneous SCC, possibly involving the TNF-α-independent TNFR2 signal transduction.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Hu Guanglei , Liang Lili , Liu Yale et al. TWEAK/Fn14 Interaction Confers Aggressive Properties to Cutaneous Squamous Cell Carcinoma. [J]. | The Journal of investigative dermatology , 2019 , 139 (4) : 796-806 .
MLA Hu Guanglei et al. "TWEAK/Fn14 Interaction Confers Aggressive Properties to Cutaneous Squamous Cell Carcinoma." . | The Journal of investigative dermatology 139 . 4 (2019) : 796-806 .
APA Hu Guanglei , Liang Lili , Liu Yale , Liu Jing , Tan Xuanfeng , Xu Meifeng et al. TWEAK/Fn14 Interaction Confers Aggressive Properties to Cutaneous Squamous Cell Carcinoma. . | The Journal of investigative dermatology , 2019 , 139 (4) , 796-806 .
Export to NoteExpress RIS BibTex
Cold atmospheric plasma induces apoptosis of melanoma cells via Sestrin2-mediated nitric oxide synthase signaling. EI PubMed Scopus SCIE
期刊论文 | 2019 , 12 (1) , e201800046 | Journal of biophotonics
WoS CC Cited Count: 3 SCOPUS Cited Count: 2
Abstract&Keyword Cite

Abstract :

Cold atmospheric plasma (CAP) represents a promising therapy for selectively cancer killing. However, the mechanism of CAP-induced cancer cell death remains unclear. Here, we identified the tumor necrosis factor-family members, especially Fas, and overloaded intracellular nitric oxide participated in CAP induced apoptosis in A375 and A875 melanoma cell lines, which was known as extrinsic apoptosis pathway. This progress was mediated by antagonistic protein of reactive oxygen species, Sestrin2. The over expression of Sestrin2 induced by plasma treatment resulted in phosphorylation of p38 mitogen-activated protein kinase (MAPK), followed by increased expression of nitric oxide synthase (iNOS), Fas and Fas ligand. Depletion of Sestrin2 reduced iNOS and Fas expression, which was associated with reduction of plasma-induced apoptosis. In contrast, inhibition of iNOS activity and phosphorylation of p38 did not alter Sestrin2 expression in plasma-treated melanoma cells. Taken together, cold atmospheric plasma increases Sestrin2 expression and further activates downstream iNOS, Fas and p38 MAPK signaling to induce apoptosis of melanoma cell lines. These findings suggest a previously unrecognized mechanism in melanoma cells response to cold atmospheric plasma therapy.

Keyword :

apoptosis Sestrin2 melanoma cold atmospheric plasma iNOS

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Xia Jun , Zeng Weihui , Xia Yumin et al. Cold atmospheric plasma induces apoptosis of melanoma cells via Sestrin2-mediated nitric oxide synthase signaling. [J]. | Journal of biophotonics , 2019 , 12 (1) : e201800046 .
MLA Xia Jun et al. "Cold atmospheric plasma induces apoptosis of melanoma cells via Sestrin2-mediated nitric oxide synthase signaling." . | Journal of biophotonics 12 . 1 (2019) : e201800046 .
APA Xia Jun , Zeng Weihui , Xia Yumin , Wang Bingchuan , Xu Dehui , Liu Dingxin et al. Cold atmospheric plasma induces apoptosis of melanoma cells via Sestrin2-mediated nitric oxide synthase signaling. . | Journal of biophotonics , 2019 , 12 (1) , e201800046 .
Export to NoteExpress RIS BibTex
TWEAK/Fn14 Signals Mediate Burn Wound Repair. PubMed Scopus SCIE
期刊论文 | 2019 , 139 (1) , 224-234 | The Journal of investigative dermatology
WoS CC Cited Count: 1 SCOPUS Cited Count: 1
Abstract&Keyword Cite

Abstract :

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) acts by engaging with fibroblast growth factor-inducible 14 (Fn14) to regulate inflammatory responses, fibrosis, and tissue remodeling, which are central in the repair processes of wounds. This study aims to explore the potential role of the TWEAK/Fn14 pathway in the healing of cutaneous burn wounds. Third-degree burns were introduced in the wild-type and Fn14-deficient BALB/c mice, followed by evaluation of wound areas and histological changes. The downstream cytokines including growth factors were also examined in lesional skin. Moreover, human dermal microvascular endothelial cells (DMECs) and dermal fibroblasts were analyzed in vitro upon TWEAK stimulation. The healing of burn wounds was delayed in Fn14-deficient mice and was accompanied by the suppression of inflammatory responses, growth factor production, and extracellular matrix synthesis. Moreover, TWEAK/Fn14 activation enhanced the migration and cytokine production of both DMECs and dermal fibroblasts. TWEAK also facilitates the expression of α-SMA and palladin in dermal fibroblasts. Furthermore, transfection of Fn14 siRNA abrogated such promotion effect of TWEAK on these cells. In conclusion, TWEAK/Fn14 signals mediate the healing of burn wounds, possibly involving TWEAK regulation of the function of resident cells.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Liu Jing , Liu Yale , Peng Lingling et al. TWEAK/Fn14 Signals Mediate Burn Wound Repair. [J]. | The Journal of investigative dermatology , 2019 , 139 (1) : 224-234 .
MLA Liu Jing et al. "TWEAK/Fn14 Signals Mediate Burn Wound Repair." . | The Journal of investigative dermatology 139 . 1 (2019) : 224-234 .
APA Liu Jing , Liu Yale , Peng Lingling , Li Juxue , Wu Kunyi , Xia Linlin et al. TWEAK/Fn14 Signals Mediate Burn Wound Repair. . | The Journal of investigative dermatology , 2019 , 139 (1) , 224-234 .
Export to NoteExpress RIS BibTex
TWEAK-Fn14轴相关因子在皮肌炎患者中的表达
期刊论文 | 2018 , (3) , 219-222 | 皖南医学院学报
Abstract&Keyword Cite

Abstract :

目的:研究肿瘤坏死因子样弱凋亡诱导因子(TWEAK)与它的受体成纤维细胞生长诱导因子14(Fn14)及其下游的细胞因子单核细胞趋化蛋白(MCP-1)、γ-干扰素诱导蛋白10(IP-10)、调节正常T细胞表达和分泌的活性因子(RANTES)、Ro52在皮肌炎(DM)中的表达.方法:免疫组化检测皮肌炎病人与健康对照组皮肤和肌肉中TWEAK、Fn14、MCP-1、RANTES、IP-10、Ro52的表达水平,并进行半定量分析.结果:免疫组化结果显示,皮肌炎患者皮肤中各蛋白的表达水平高于健康对照组;皮肌炎患者肌肉中各蛋白的表达水平高于健康对照组.结论:TWEAK/Fn14信号轴可能参与皮肌炎的发病机制.

Keyword :

成纤维细胞生长诱导因子14 肿瘤坏死因子样弱凋亡诱导因子 皮肌炎 Ro52 免疫组化

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 童芳 , 夏育民 , 王萍 . TWEAK-Fn14轴相关因子在皮肌炎患者中的表达 [J]. | 皖南医学院学报 , 2018 , (3) : 219-222 .
MLA 童芳 et al. "TWEAK-Fn14轴相关因子在皮肌炎患者中的表达" . | 皖南医学院学报 3 (2018) : 219-222 .
APA 童芳 , 夏育民 , 王萍 . TWEAK-Fn14轴相关因子在皮肌炎患者中的表达 . | 皖南医学院学报 , 2018 , (3) , 219-222 .
Export to NoteExpress RIS BibTex
Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice SCIE PubMed
期刊论文 | 2018 | JOURNAL OF IMMUNOLOGY RESEARCH
Abstract&Keyword Cite

Abstract :

Many studies have demonstrated that anti-dsDNA IgG is closely associated with lupus nephritis. Recently, it was found that activation of the fibroblast growth factor-inducible 14 (Fn14) signaling pathway damages glomerular filtration barrier in MRL/lpr lupus-prone mice. However, MRL/lpr mice have high titers of serum autoantibodies other than anti-dsDNA IgG. The aim of this study was to further explore the effect of Fn14 deficiency on anti-dsDNA IgG-induced glomerular damage in severe combined immunodeficiency (SCID) mice that have no endogenous IgG. Fn14 deficiency was generated in SCID mice. The murine hybridoma cells producing control IgG or anti-dsDNA IgG were intraperitoneally injected into mice. In two weeks, the urine, serum, and kidney tissue samples were harvested from mice at sacrifice. It showed that the injection of anti-dsDNA IgG, but not control IgG hybridoma cells, induced proteinuria and glomerular damage in SCID mice. Between the wild-type (WT) and knockout (KO) mice injected with anti-dsDNA IgG hybridoma cells, the latter showed a decrease in both proteinuria and glomerular IgG deposition. The histopathological changes, inflammatory cell infiltration, and proinflammatory cytokine production were also attenuated in the kidneys of the Fn14-KO mice upon anti-dsDNA IgG injection. Therefore, Fn14 deficiency effectively protects SCID mice from anti-dsDNA IgG-induced glomerular damage.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Wu, Jiawen , Min, Xiaoyun , Wang, Li et al. Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice [J]. | JOURNAL OF IMMUNOLOGY RESEARCH , 2018 .
MLA Wu, Jiawen et al. "Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice" . | JOURNAL OF IMMUNOLOGY RESEARCH (2018) .
APA Wu, Jiawen , Min, Xiaoyun , Wang, Li , Yang, Jie , Wang, Ping , Liu, Xingyin et al. Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice . | JOURNAL OF IMMUNOLOGY RESEARCH , 2018 .
Export to NoteExpress RIS BibTex
Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice SCIE PubMed Scopus
期刊论文 | 2018 , 9 | FRONTIERS IN PHARMACOLOGY | IF: 3.845
WoS CC Cited Count: 3 SCOPUS Cited Count: 3
Abstract&Keyword Cite

Abstract :

The interaction of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor inducible 14 (Fn14) participates in inflammatory responses, fibrosis, and tissue remodeling, which are central in the repair processes of wounds. Fn14 is expressed in main skin cells including dermal fibroblasts. This study was designed to explore the therapeutic effect of TWEAK on experimental burn wounds and the relevant mechanism underlying such function. Third-degree burns were introduced in two BALB/c mouse strains. Recombinant TWEAK was administrated topically, followed by the evaluation of wound areas and histologic changes. Accordingly, the downstream cytokines, inflammatory cell infiltration, and extracellular matrix synthesis were examined in lesional tissue. Moreover, the differentiation markers were analyzed in cultured human dermal fibroblasts upon TWEAK stimulation. The results showed that topical TWEAK accelerated the healing of burn wounds in wild-type mice but not in Fn14-deficient mice. TWEAK strengthened inflammatory cell infiltration, and exaggerated the production of growth factor and extracellular matrix components in wound areas of wild-type mice. Moreover, TWEAK/Fn14 activation elevated the expression of myofibroblastic differentiation markers, including alpha-smooth muscle actin and palladin, in cultured dermal fibroblasts. Therefore, topical TWEAK exhibits therapeutic effect on experimental burn wounds through favoring regional inflammation, cytokine production, and extracellular matrix synthesis. TWEAK/Fn14 activation induces the myofibroblastic differentiation of dermal fibroblasts, partially contributing to the healing of burn wounds.

Keyword :

animal model TWEAK burn wound differentiation dermal fibroblast Fn14

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Liu, Jing , Pang, Lingling , Liu, Yale et al. Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice [J]. | FRONTIERS IN PHARMACOLOGY , 2018 , 9 .
MLA Liu, Jing et al. "Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice" . | FRONTIERS IN PHARMACOLOGY 9 (2018) .
APA Liu, Jing , Pang, Lingling , Liu, Yale , Wu, Kunyi , Wang, Sijia , Wang, Xuening et al. Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice . | FRONTIERS IN PHARMACOLOGY , 2018 , 9 .
Export to NoteExpress RIS BibTex
皮肤性病学双语教学体会
期刊论文 | 2017 , (23) | 现代医药卫生
Abstract&Keyword Cite

Keyword :

皮肤病学 教学模式 教育,医学

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 安金刚 , 夏育民 . 皮肤性病学双语教学体会 [J]. | 现代医药卫生 , 2017 , (23) .
MLA 安金刚 et al. "皮肤性病学双语教学体会" . | 现代医药卫生 23 (2017) .
APA 安金刚 , 夏育民 . 皮肤性病学双语教学体会 . | 现代医药卫生 , 2017 , (23) .
Export to NoteExpress RIS BibTex
皮肤性病学双语教学体会
期刊论文 | 2017 , (23) , 3669-3671 | 现代医药卫生
Abstract&Keyword Cite

Abstract :

为适应医学发展和教学改革的新要求,近年来,该科教研室承担了五年制、七年制和八年制临床专业医学生的双语教学任务.作者总结了双语教学过程中的具体体会,从双语比例分配、教材选择、教学活动的实施等多个方面总结了经验;并且通过与既往文献比较,分析了优缺点,以期进一步改进双语教学的质量.

Keyword :

皮肤病学 教学模式 教育,医学

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 安金刚 , 夏育民 . 皮肤性病学双语教学体会 [J]. | 现代医药卫生 , 2017 , (23) : 3669-3671 .
MLA 安金刚 et al. "皮肤性病学双语教学体会" . | 现代医药卫生 23 (2017) : 3669-3671 .
APA 安金刚 , 夏育民 . 皮肤性病学双语教学体会 . | 现代医药卫生 , 2017 , (23) , 3669-3671 .
Export to NoteExpress RIS BibTex
Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling SCIE Scopus
期刊论文 | 2017 , 43 (2) , 579-588 | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY | IF: 5.5
WoS CC Cited Count: 5 SCOPUS Cited Count: 4
Abstract&Keyword Cite

Abstract :

Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor-inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators. An Fn14-TRAF2-TNFR axis has been suggested in the function of TWEAK/Fn14 signaling, which may serve as a target in the development of novel therapeutic strategies for many diseases that have Fn14-overexpressing cells in affected tissues. The aims of this review are: 1) to present the main results on TWEAK/Fn14 regulation of cell fates, 2) to analyze the mechanism of the Fn14-TRAF2-TNFR axis, and 3) to summarize the potential strategies in the pharmacologic targeting of this axis. (C) 2017 The Author(s) Published by S. Karger AG, Basel

Keyword :

Keratinocyte Proliferation TNFR TWEAK TRAF Apoptosis Fn14

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Wang, Xuening , Xiao, Shengxiang , Xia, Yumin . Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling [J]. | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY , 2017 , 43 (2) : 579-588 .
MLA Wang, Xuening et al. "Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling" . | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY 43 . 2 (2017) : 579-588 .
APA Wang, Xuening , Xiao, Shengxiang , Xia, Yumin . Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling . | CELLULAR PHYSIOLOGY AND BIOCHEMISTRY , 2017 , 43 (2) , 579-588 .
Export to NoteExpress RIS BibTex
TWEAK/Fn14 signaling in tumors SCIE PubMed Scopus
期刊论文 | 2017 , 39 (6) | TUMOR BIOLOGY
WoS CC Cited Count: 10 SCOPUS Cited Count: 10
Abstract&Keyword Cite

Abstract :

TWEAK (tumor necrosis factor-related weak inducer of apoptosis), a member of the tumor necrosis factor superfamily, acts on cells by binding to its only receptor named Fn14 (fibroblast growth factor-inducible 14). Their engagement activates a number of intracellular signal transduction cascades and consequently leads to cell death, proliferation, migration, or survival depending on the cellular contexts. Studies have indicated that the expression of TWEAK and Fn14 is upregulated in many solid tumors compared with healthy tissues. The activation of TWEAK/Fn14 signaling enhances the proliferation, invasion, and migration of tumor cells. Moreover, the angiogenesis, pro-inflammatory cytokine expression, and epithelial-mesenchymal transitions are promoted upon TWEAK/Fn14 activation. Currently, the tumor necrosis factor receptor-associated factor and nuclear factor kappa B signaling pathways are considered two main downstream pathways activated by TWEAK/Fn14 interaction. In view of these facts, some TWEAK- or Fn14-targeting agents are generated to inhibit the progression of tumors and have achieved initial success in clinical and pre-clinical trials. These agents include monoclonal antibodies, fusion proteins, immunotoxins, and nanoparticles. In addition, some relevant signaling pathways are studied to identify new potential therapeutic targets. Overall, these findings suggest that the TWEAK/Fn14 pathway is critical in the development of tumors, and targeting this signaling is a potential therapeutic approach in future tumor therapy.

Keyword :

tumor TWEAK signaling pathway targeted therapy Fn14

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Hu, Guanglei , Zeng, Weihui , Xia, Yumin . TWEAK/Fn14 signaling in tumors [J]. | TUMOR BIOLOGY , 2017 , 39 (6) .
MLA Hu, Guanglei et al. "TWEAK/Fn14 signaling in tumors" . | TUMOR BIOLOGY 39 . 6 (2017) .
APA Hu, Guanglei , Zeng, Weihui , Xia, Yumin . TWEAK/Fn14 signaling in tumors . | TUMOR BIOLOGY , 2017 , 39 (6) .
Export to NoteExpress RIS BibTex
10| 20| 50 per page
< Page ,Total 3 >

Export

Results:

Selected

to

Format:
FAQ| About| Online/Total:3126/70747024
Address:XI'AN JIAOTONG UNIVERSITY LIBRARY(No.28, Xianning West Road, Xi'an, Shaanxi Post Code:710049) Contact Us:029-82667865
Copyright:XI'AN JIAOTONG UNIVERSITY LIBRARY Technical Support:Beijing Aegean Software Co., Ltd.