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学者姓名:刘健康

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< Page ,Total 17 >
Transmembrane protein 215 promotes angiogenesis by maintaining endothelial cell survival. PubMed Scopus SCIE
期刊论文 | 2019 , 234 (6) , 9525-9534 | Journal of cellular physiology
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Abstract :

Sprouting angiogenesis is a major form of neovascularization of tissues suffering from hypoxia and other related stress. Endothelial cells (ECs) undergo proliferation, differentiation, programmed death, and migration during angiogenic sprouting, but the underlying molecular mechanisms regulating ECs in angiogenesis have been incompletely elucidated. Here we report that the transmembrane protein 215 (TMEM215) is involved in angiogenesis by regulating EC survival. The murine TMEM215 gene, which possesses two transcriptional starting sites as determined by 5'-rapid amplification of complementary DNA (cDNA) ends (RACE), encodes a two-pass TMEM. The TMEM215 transcripts were detected in ECs in addition to other tissues by quantitative reverse transcription-polymerase chain reaction. Immunofluorescence showed that TMEM215 was expressed in the vasculature in retina, liver, and tumor, and colocalized with EC markers. We show that knockdown of TMEM215 in ECs induced strong cell death of ECs in vitro without affecting cell proliferation and migration, suggesting that TMEM215 was required for EC survival. Downregulation of TMEM215 expression compromised lumen formation and sprouting capacities of ECs in vitro. Moreover, intravitreous injection of TMEM215 small interfering RNA resulted in delayed and abnormal development of retinal vasculature with poor perfusion. These results identified TMEM215 as a novel molecule involved in angiogenesis by regulating the survival of ECs.

Keyword :

apoptosis angiogenesis retina ECs TMEM215

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GB/T 7714 Liu Yuan , Zheng Qijun , He Guangbin et al. Transmembrane protein 215 promotes angiogenesis by maintaining endothelial cell survival. [J]. | Journal of cellular physiology , 2019 , 234 (6) : 9525-9534 .
MLA Liu Yuan et al. "Transmembrane protein 215 promotes angiogenesis by maintaining endothelial cell survival." . | Journal of cellular physiology 234 . 6 (2019) : 9525-9534 .
APA Liu Yuan , Zheng Qijun , He Guangbin , Zhang Mei , Yan Xianchun , Yang Ziyan et al. Transmembrane protein 215 promotes angiogenesis by maintaining endothelial cell survival. . | Journal of cellular physiology , 2019 , 234 (6) , 9525-9534 .
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Cornulin Is Induced in Psoriasis Lesions and Promotes Keratinocyte Proliferation via Phosphoinositide 3-Kinase/Akt Pathways. PubMed Scopus SCIE
期刊论文 | 2019 , 139 (1) , 71-80 | The Journal of investigative dermatology
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Psoriasis is a chronic inflammatory skin disease characterized by abnormal proliferation of epidermal keratinocytes and infiltration of inflammatory cells. CRNN is a major component of the cornified cell envelope and implicated in several epithelial malignancies. Here, we show that CRNN expression was increased in the lesioned epidermis from the patients with psoriasis vulgaris and skin lesions from the imiquimod (IMQ)-treated mice. Expression of CRNN in cultured keratinocytes (HEKa and HaCaT) was also induced by M5, a mixture of five pro-inflammatory cytokines (i.e., IL-17A, IL-22, IL-1α, oncostatin M, and TNF-α). Lentiviral expression of CRNN increased cell proliferation by inducing cyclin D1. Conversely, knockdown of CRNN by small interfering RNA suppressed G1/S transition and attenuated the M5-induced proliferation. In addition, CRNN overexpression increased the phosphorylation and activation of phosphoinositide 3-kinase and Akt. Inactivation of the phosphoinositide 3-kinase and Akt pathways using small interfering RNA or selective inhibitors (LY294002 and MK2206) reduced the proliferative effects of CRNN. Furthermore, topical use of anti-psoriatic calcipotriol effectively decreased expression of CRNN, inhibited the Akt activation and improved the IMQ-stimulated psoriasis-like pathologies. Taken together, these results suggest that induced expression of CRNN may contribute to the pathogenesis of psoriasis.

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GB/T 7714 Li Changji , Xiao Lei , Jia Jinjing et al. Cornulin Is Induced in Psoriasis Lesions and Promotes Keratinocyte Proliferation via Phosphoinositide 3-Kinase/Akt Pathways. [J]. | The Journal of investigative dermatology , 2019 , 139 (1) : 71-80 .
MLA Li Changji et al. "Cornulin Is Induced in Psoriasis Lesions and Promotes Keratinocyte Proliferation via Phosphoinositide 3-Kinase/Akt Pathways." . | The Journal of investigative dermatology 139 . 1 (2019) : 71-80 .
APA Li Changji , Xiao Lei , Jia Jinjing , Li Fan , Wang Xin , Duan Qiqi et al. Cornulin Is Induced in Psoriasis Lesions and Promotes Keratinocyte Proliferation via Phosphoinositide 3-Kinase/Akt Pathways. . | The Journal of investigative dermatology , 2019 , 139 (1) , 71-80 .
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Proinflammatory macrophages impair skeletal muscle differentiation in obesity through secretion of tumor necrosis factor-α via sustained activation of p38 mitogen-activated protein kinase. PubMed Scopus SCIE
期刊论文 | 2019 , 234 (3) , 2566-2580 | Journal of cellular physiology
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Obesity is associated with skeletal muscle loss and impaired myogenesis. Increased infiltration of proinflammatory macrophages in skeletal muscle is noted in obesity and is associated with muscle insulin resistance. However, whether the infiltrated macrophages can contribute to obesity-induced muscle loss is unclear. In this study, we investigate macrophage and muscle differentiation markers in the quadriceps (QC), gastrocnemius, tibia anterior, and soleus muscles from obese mice that were fed a high-fat diet for 16 weeks. Then, we examined the effect and mediator of macrophage-secreted factors on myoblast differentiation in vitro. We found markedly increased levels of proinflammatory macrophage markers (F4/80 and CD11c) in the QC muscle compared with the other three muscle groups. Consistent with the increased levels of proinflammatory macrophage infiltration, the QC muscle also showed a significant reduction in the expression of muscle differentiation makers MYOD1 and myosin heavy chain. In in vitro studies, treatment of C2C12 myoblasts with Raw 264.7 macrophage-conditioned medium (CM) significantly promoted cell proliferation and inhibited myoblast differentiation. Neutralization of tumor necrosis factor α (TNF-α) in Raw 264.7 macrophage CM reversed the reduction of myoblast differentiation. Finally, we found that both macrophage CM and TNF-α induced sustained activation of p38 mitogen-activated protein kinase (MAPK) in C2C12 myoblasts. Together, our findings suggest that the increased infiltration of proinflammatory macrophages could contribute toward obesity-induced muscle loss by secreting inflammatory cytokine TNF-α via the p38 MAPK signaling pathway.

Keyword :

skeletal muscle obesity TNF-α C2C12 differentiation macrophage

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GB/T 7714 Wang Xueqiang , Zhao Daina , Cui Yajuan et al. Proinflammatory macrophages impair skeletal muscle differentiation in obesity through secretion of tumor necrosis factor-α via sustained activation of p38 mitogen-activated protein kinase. [J]. | Journal of cellular physiology , 2019 , 234 (3) : 2566-2580 .
MLA Wang Xueqiang et al. "Proinflammatory macrophages impair skeletal muscle differentiation in obesity through secretion of tumor necrosis factor-α via sustained activation of p38 mitogen-activated protein kinase." . | Journal of cellular physiology 234 . 3 (2019) : 2566-2580 .
APA Wang Xueqiang , Zhao Daina , Cui Yajuan , Lu Shemin , Gao Dan , Liu Jiankang . Proinflammatory macrophages impair skeletal muscle differentiation in obesity through secretion of tumor necrosis factor-α via sustained activation of p38 mitogen-activated protein kinase. . | Journal of cellular physiology , 2019 , 234 (3) , 2566-2580 .
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Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. PubMed
期刊论文 | 2019 , 128 , 26-37 | Journal of molecular and cellular cardiology
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DNA methylation is a well-defined epigenetic modification that regulates gene transcription. However, the role of DNA methylation in the cardiac hypertrophy seen in hypertension is unclear. This study was performed to investigate genome-wide DNA methylation profiles in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKY), and the cardioprotective effect of choline. Eight-week-old male SHRs received intraperitoneal injections of choline (8 mg/kg/day) for 8 weeks. SHRs showed aberrant methylation distribution on chromosomes and genome regions, with decreased methylation levels at CHG and CHH sites. A total of 91,559 differentially methylated regions (DMRs) were detected between SHRs and WKY rats, of which 28,197 were demethylated and 63,362 were methylated. Choline treatment partly restored the DMRs in SHRs, which were related to 131 genes. Gene ontology analysis and Kyoto Encyclopedia of Genes and Genomes analysis of DMRs suggested that choline partly reversed the dysfunctions of biological processes, cellular components and molecular functions in SHRs. Moreover, the inhibition of 2-oxoglutarate accumulation by choline, thereby inhibiting excessive activation of ten-eleven translocation methylcytosine dioxygenase enzymes, may correlate with the beneficial effects of choline on methylation levels, cardiac hypertrophy and cardiac function of SHRs, as indicated by decreased heart rate and blood pressure, and increased ejection fraction and fractional shortening. This study provides the first genome-wide DNA methylation profile of the hypertrophic myocardium of SHRs and suggests a novel role for this epigenetic modification in hypertension. Choline treatment may represent a promising approach for modification of DNA methylation and optimization of the epigenetic profile for antihypertensive therapy.

Keyword :

DNA methylation Cardiac hypertrophy 2-oxoglutarate Hypertension Choline Spontaneously hypertensive rat

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GB/T 7714 Liu Longzhu , He Xi , Zhao Ming et al. Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. [J]. | Journal of molecular and cellular cardiology , 2019 , 128 : 26-37 .
MLA Liu Longzhu et al. "Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats." . | Journal of molecular and cellular cardiology 128 (2019) : 26-37 .
APA Liu Longzhu , He Xi , Zhao Ming , Yang Si , Wang Shengpeng , Yu Xiaojiang et al. Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. . | Journal of molecular and cellular cardiology , 2019 , 128 , 26-37 .
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Mitochondrial metabolic remodeling involved in the progression of Alzheimer's disease CPCI-S SCIE
会议论文 | 2018 , 120 , S147-S147 | 19th Biennial Meeting of the Society-for-Free-Radical-Research-International (SFRRI)
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GB/T 7714 Long, Jiangang , Liu, Jiankang . Mitochondrial metabolic remodeling involved in the progression of Alzheimer's disease [C] . 2018 : S147-S147 .
MLA Long, Jiangang et al. "Mitochondrial metabolic remodeling involved in the progression of Alzheimer's disease" . (2018) : S147-S147 .
APA Long, Jiangang , Liu, Jiankang . Mitochondrial metabolic remodeling involved in the progression of Alzheimer's disease . (2018) : S147-S147 .
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ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma SCIE PubMed Scopus
期刊论文 | 2018 , 9 | NATURE COMMUNICATIONS
WoS CC Cited Count: 6 SCOPUS Cited Count: 6
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In human mutant BRAF melanoma cells, the stemness transcription factor FOXD3 is rapidly induced by inhibition of ERK1/2 signaling and mediates adaptive resistance to RAF inhibitors. However, the mechanism underlying ERK signaling control of FOXD3 expression remains unknown. Here we show that SOX10 is both necessary and sufficient for RAF inhibitor-induced expression of FOXD3 in mutant BRAF melanoma cells. SOX10 activates the transcription of FOXD3 by binding to a regulatory element in FOXD3 promoter. Phosphorylation of SOX10 by ERK inhibits its transcription activity toward multiple target genes by interfering with the sumoylation of SOX10 at K55, which is essential for its transcription activity. Finally, depletion of SOX10 sensitizes mutant BRAF melanoma cells to RAF inhibitors in vitro and in vivo. Thus, our work discovers a novel phosphorylation-dependent regulatory mechanism of SOX10 transcription activity and completes an ERK1/2/SOX10/FOXD3/ERBB3 axis that mediates adaptive resistance to RAF inhibitors in mutant BRAF melanoma cells.

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GB/T 7714 Han, Shujun , Ren, Yibo , He, Wangxiao et al. ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma [J]. | NATURE COMMUNICATIONS , 2018 , 9 .
MLA Han, Shujun et al. "ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma" . | NATURE COMMUNICATIONS 9 (2018) .
APA Han, Shujun , Ren, Yibo , He, Wangxiao , Liu, Huadong , Zhi, Zhe , Zhu, Xinliang et al. ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma . | NATURE COMMUNICATIONS , 2018 , 9 .
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SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress SCIE PubMed Scopus
期刊论文 | 2018 , 25 (2) , 229-240 | CELL DEATH AND DIFFERENTIATION
WoS CC Cited Count: 8 SCOPUS Cited Count: 8
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Recent studies have revealed robust metabolic changes during cell differentiation. Mitochondria, the organelles where many vital metabolic reactions occur, may play an important role. Here, we report the involvement of SIRT3-regulated mitochondrial stress in osteoblast differentiation and bone formation. In both the osteoblast cell line MC3T3-E1 and primary calvarial osteoblasts, robust mitochondrial biogenesis and supercomplex formation were observed during differentiation, accompanied by increased ATP production and decreased mitochondrial stress. Inhibition of mitochondrial activity or an increase in mitochondrial superoxide production significantly suppressed osteoblast differentiation. During differentiation, SOD2 was specifically induced to eliminate excess mitochondrial superoxide and protein oxidation, whereas SIRT3 expression was increased to enhance SOD2 activity through deacetylation of K68. Both SOD2 and SIRT3 knockdown resulted in suppression of differentiation. Meanwhile, mice deficient in SIRT3 exhibited obvious osteopenia accompanied by osteoblast dysfunction, whereas overexpression of SOD2 or SIRT3 improved the differentiation capability of primary osteoblasts derived from SIRT3-deficient mice. These results suggest that SIRT3/SOD2 is required for regulating mitochondrial stress and plays a vital role in osteoblast differentiation and bone formation.

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GB/T 7714 Gao, Jing , Feng, Zhihui , Wang, Xueqiang et al. SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress [J]. | CELL DEATH AND DIFFERENTIATION , 2018 , 25 (2) : 229-240 .
MLA Gao, Jing et al. "SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress" . | CELL DEATH AND DIFFERENTIATION 25 . 2 (2018) : 229-240 .
APA Gao, Jing , Feng, Zhihui , Wang, Xueqiang , Zeng, Mengqi , Liu, Jing , Han, Shujun et al. SIRT3/SOD2 maintains osteoblast differentiation and bone formation by regulating mitochondrial stress . | CELL DEATH AND DIFFERENTIATION , 2018 , 25 (2) , 229-240 .
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ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma (vol 9, 28, 2018) SCIE PubMed Scopus
期刊论文 | 2018 , 9 | NATURE COMMUNICATIONS
WoS CC Cited Count: 1
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GB/T 7714 Han, Shujun , Ren, Yibo , He, Wangxiao et al. ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma (vol 9, 28, 2018) [J]. | NATURE COMMUNICATIONS , 2018 , 9 .
MLA Han, Shujun et al. "ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma (vol 9, 28, 2018)" . | NATURE COMMUNICATIONS 9 (2018) .
APA Han, Shujun , Ren, Yibo , He, Wangxiao , Liu, Huadong , Zhi, Zhe , Zhu, Xinliang et al. ERK-mediated phosphorylation regulates SOX10 sumoylation and targets expression in mutant BRAF melanoma (vol 9, 28, 2018) . | NATURE COMMUNICATIONS , 2018 , 9 .
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C10orf99 contributes to the development of psoriasis by promoting the proliferation of keratinocytes SCIE PubMed Scopus
期刊论文 | 2018 , 8 | SCIENTIFIC REPORTS
WoS CC Cited Count: 1
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Psoriasis is a chronic, relapsing inflammatory skin disease. The pathogenesis of psoriasis is complex and has not been fully understood. C10orf99 was a recently identified human antimicrobial peptide whose mRNA expression is elevated in psoriatic human skin samples. In this study, we investigated the functional roles of C10orf99 in epidermal proliferation under inflammatory condition. We showed that C10orf99 protein was significantly up-regulated in psoriatic skin samples from patients and the ortholog gene expression levels were up-regulated in imiquimod (IMQ)-induced psoriasis-like skin lesions in mice. Using M5-stimulated HaCaT cell line model of inflammation and a combinational approach of knockdown and overexpression of C10orf99, we demonstrated that C10orf99 could promote keratinocyte proliferation by facilitating the G1/S transition, and the pro-proliferation effect of C10orf99 was associated with the activation of the ERK1/2 and NF-kappa B but not the AKT pathways. Local depletion of C10orf99 by lentiviral vectors expressing C10orf99 shRNA effectively ameliorated IMQ-induced dermatitis. Taken together, these results indicate that C10orf99 plays a contributive role in psoriasis pathogenesis and may serve as a new target for psoriasis treatment.

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GB/T 7714 Chen, Caifeng , Wu, Na , Duan, Qiqi et al. C10orf99 contributes to the development of psoriasis by promoting the proliferation of keratinocytes [J]. | SCIENTIFIC REPORTS , 2018 , 8 .
MLA Chen, Caifeng et al. "C10orf99 contributes to the development of psoriasis by promoting the proliferation of keratinocytes" . | SCIENTIFIC REPORTS 8 (2018) .
APA Chen, Caifeng , Wu, Na , Duan, Qiqi , Yang, Huizi , Wang, Xin , Yang, Peiwen et al. C10orf99 contributes to the development of psoriasis by promoting the proliferation of keratinocytes . | SCIENTIFIC REPORTS , 2018 , 8 .
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Human Enteric alpha-Defensin 5 Promotes Shigella Infection by Enhancing Bacterial Adhesion and Invasion SCIE PubMed Scopus
期刊论文 | 2018 , 48 (6) , 1233-+ | IMMUNITY
WoS CC Cited Count: 1 SCOPUS Cited Count: 1
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Shigella is a Gram-negative bacterium that causes bacillary dysentery worldwide. It invades the intestinal epithelium to elicit intense inflammation and tissue damage, yet the underlying mechanisms of its host selectivity and low infectious inoculum remain perplexing. Here, we report that Shigella coopts human alpha-defensin 5 (HD5), a host defense peptide important for intestinal homeostasis and innate immunity, to enhance its adhesion to and invasion of mucosal tissues. HD5 promoted Shigella infection in vitro in a structure-dependent manner. Shigella, commonly devoid of an effective host-adhesion apparatus, preferentially targeted HD5 to augment its ability to colonize the intestinal epithelium through interactions with multiple bacterial membrane proteins. HD5 exacerbated infectivity and Shigella-induced pathology in a culture of human colorectal tissues and three animal models. Our findings illuminate how Shigella exploits innate immunity by turning HD5 into a virulence factor for infection, unveiling a mechanism of action for this highly proficient human pathogen.

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GB/T 7714 Xu, Dan , Liao, Chongbing , Zhang, Bing et al. Human Enteric alpha-Defensin 5 Promotes Shigella Infection by Enhancing Bacterial Adhesion and Invasion [J]. | IMMUNITY , 2018 , 48 (6) : 1233-+ .
MLA Xu, Dan et al. "Human Enteric alpha-Defensin 5 Promotes Shigella Infection by Enhancing Bacterial Adhesion and Invasion" . | IMMUNITY 48 . 6 (2018) : 1233-+ .
APA Xu, Dan , Liao, Chongbing , Zhang, Bing , Tolbert, W. David , He, Wangxiao , Dai, Zhijun et al. Human Enteric alpha-Defensin 5 Promotes Shigella Infection by Enhancing Bacterial Adhesion and Invasion . | IMMUNITY , 2018 , 48 (6) , 1233-+ .
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