• 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:刘健康

Refining:

Source

Submit Unfold

Co-Author

Submit Unfold

Language

Submit

Clean All

Export Sort by:
Default
  • Default
  • Title
  • Year
  • WOS Cited Count
  • Impact factor
  • Ascending
  • Descending
< Page ,Total 17 >
Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats. PubMed SCIE
期刊论文 | 2019 , 128 , 26-37 | Journal of molecular and cellular cardiology
Abstract&Keyword Cite

Abstract :

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

Cite:

Copy from the list or Export to your reference management。

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 .
Export to NoteExpress RIS BibTex
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
WoS CC Cited Count: 1
Abstract&Keyword Cite

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

Cite:

Copy from the list or Export to your reference management。

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 .
Export to NoteExpress RIS BibTex
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
WoS CC Cited Count: 2 SCOPUS Cited Count: 2
Abstract&Keyword Cite

Abstract :

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

Cite:

Copy from the list or Export to your reference management。

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 .
Export to NoteExpress RIS BibTex
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
WoS CC Cited Count: 1 SCOPUS Cited Count: 1
Abstract&Keyword Cite

Abstract :

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.

Cite:

Copy from the list or Export to your reference management。

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 .
Export to NoteExpress RIS BibTex
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)
Abstract&Keyword Cite

Cite:

Copy from the list or Export to your reference management。

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 .
Export to NoteExpress RIS BibTex
The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria SCIE
期刊论文 | 2018 , 45 (12) , 1240-1249 | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS
Abstract&Keyword Cite

Abstract :

Phytosterols are a type of bioactive substances widely found in plants and have broad application prospects in food, medicine, cosmetics and other fields. Phytosterols, as cholesterol analogues, can inhibit the absorption of cholesterol in the intestine and decrease serum cholesterol level and thus reduce the risk of cardiovascular diseases. In addition, phytosterols have many other functions such as cancer suppression, anti-inflammation or anti-fever, anti-oxidation and hormone-like effects. In-depth exploration of the subcellular and molecular mechanism of phytosterols' biological functions contributes to the full development of the application value of phytosterols. Mitochondria are the most important sites for cellular energy metabolism. Cholesterol metabolism, cancer cell proliferation and apoptosis, oxidative stress, and inflammatory response are all closely related to mitochondrial function. Recent studies have suggested that phytosterols can regulate mitochondrial function in various models, which potentially may be a pivotal mechanism underlying phytosterols' various biological functions. This article will first summarize the biological functions of phytosterols and then discuss its mitochondria-related regulatory mechanisms in detail, hoping to provide frontier insights and progress report for researchers in the field as well as to provide reference for the application of phytosterols.

Keyword :

antioxidase anticancer beta-sitosterol LDL-C mitochondrial membrane potential

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Lou Jing , Cui Ya-Juan , Liu Jian-Kang et al. The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria [J]. | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS , 2018 , 45 (12) : 1240-1249 .
MLA Lou Jing et al. "The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria" . | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS 45 . 12 (2018) : 1240-1249 .
APA Lou Jing , Cui Ya-Juan , Liu Jian-Kang , Zhao Lin . The Physiological Functions of Phytosterols and Their Underlying Mechanism of Regulating Mitochondria . | PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS , 2018 , 45 (12) , 1240-1249 .
Export to NoteExpress RIS BibTex
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: 5 SCOPUS Cited Count: 4
Abstract&Keyword Cite

Abstract :

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.

Cite:

Copy from the list or Export to your reference management。

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-+ .
Export to NoteExpress RIS BibTex
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 SCOPUS Cited Count: 1
Abstract&Keyword Cite

Cite:

Copy from the list or Export to your reference management。

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 .
Export to NoteExpress RIS BibTex
Benefits of the soluble and insoluble fractions of bitter gourd in mice fed a high-fat diet SCIE Scopus
期刊论文 | 2018 , 42 , 216-223 | JOURNAL OF FUNCTIONAL FOODS
WoS CC Cited Count: 2 SCOPUS Cited Count: 1
Abstract&Keyword Cite

Abstract :

Background Bitter gourd (BG) fruit powder was previously showed to prevent high-fat diet (HFD)-induced metabolic disorders in mice. In current study, we investigated the beneficial difference of the water soluble (SBG) and insoluble fractions (IS-BG) of bitter gourd. Results: Compared to normal chow diet, the HFD induced greater body weight gain and increased fat mass accompanied by impaired insulin sensitivity, elevated serum lipids and inflammation. Supplementation of BG, SBG, and IS-BG showed similar beneficial effects and restored the metabolic changes in mice. Interestingly, BG showed no effect on fat mass, which was decreased by both S-BG and IS-BG. Additionally, S-BG and IS-BG inhibited the SREBP-1/FAS pathway, thereby decreasing liver cholesterol accumulation, while only BG showed improvement on mitochondrial activity. Conclusion: These results further support the position that bitter gourd has multiple active ingredients and that both fractions have beneficial effects on metabolic disorders.

Keyword :

High-fat diet Obesity Metabolic disorder Bitter gourd

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Xu, Jie , Cao, Ke , Feng, Zhihui et al. Benefits of the soluble and insoluble fractions of bitter gourd in mice fed a high-fat diet [J]. | JOURNAL OF FUNCTIONAL FOODS , 2018 , 42 : 216-223 .
MLA Xu, Jie et al. "Benefits of the soluble and insoluble fractions of bitter gourd in mice fed a high-fat diet" . | JOURNAL OF FUNCTIONAL FOODS 42 (2018) : 216-223 .
APA Xu, Jie , Cao, Ke , Feng, Zhihui , Liu, Jiankang . Benefits of the soluble and insoluble fractions of bitter gourd in mice fed a high-fat diet . | JOURNAL OF FUNCTIONAL FOODS , 2018 , 42 , 216-223 .
Export to NoteExpress RIS BibTex
Yes-associated protein promotes the abnormal proliferation of psoriatic keratinocytes via an amphiregulin dependent pathway SCIE PubMed Scopus
期刊论文 | 2018 , 8 | SCIENTIFIC REPORTS
WoS CC Cited Count: 1
Abstract&Keyword Cite

Abstract :

Psoriasis is a chronic inflammatory skin disease with high morbidity, poor treatment methods and high rates of relapse. Keratinocyte hyperproliferation and shortened cell cycles are important pathophysiological features of psoriasis. As a known oncogene, Yes-associated protein (YAP) plays a role in promoting cell proliferation and inhibiting cell apoptosis; however, whether YAP is involved in the pathogenesis of psoriasis remains to be determined. Amphiregulin (AREG), a transcriptional target of YAP, was found to be upregulated in psoriasis, and overexpression of AREG promoted keratinocyte proliferation. In the present study, immunohistochemistry showed that YAP expression was elevated in the skin of psoriasis patients and in the Imiquimod (IMQ) mouse model of psoriasis. Knockdown of YAP in HaCaT cells inhibited cell proliferation, caused cell cycle arrest in G0/G1 phase and promoted apoptosis. These changes in YAP-knockdown HaCaT cells were related to changes in AREG expression. We concluded that YAP may play an important role in the regulation of abnormal keratinocyte proliferation via an AREG-dependent pathway and that YAP could be a new target in the treatment of psoriasis.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Jia, Jinjing , Li, Changji , Yang, Jiao et al. Yes-associated protein promotes the abnormal proliferation of psoriatic keratinocytes via an amphiregulin dependent pathway [J]. | SCIENTIFIC REPORTS , 2018 , 8 .
MLA Jia, Jinjing et al. "Yes-associated protein promotes the abnormal proliferation of psoriatic keratinocytes via an amphiregulin dependent pathway" . | SCIENTIFIC REPORTS 8 (2018) .
APA Jia, Jinjing , Li, Changji , Yang, Jiao , Wang, Xin , Li, Ruilian , Luo, Suju et al. Yes-associated protein promotes the abnormal proliferation of psoriatic keratinocytes via an amphiregulin dependent pathway . | SCIENTIFIC REPORTS , 2018 , 8 .
Export to NoteExpress RIS BibTex
10| 20| 50 per page
< Page ,Total 17 >

Export

Results:

Selected

to

Format:
FAQ| About| Online/Total:2556/65149090
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.