Mutations of TYR and MITF Genes are Associated with Plumage Colour Phenotypes in Geese

Wang, Ye,Li, Si-Ming,Huang, Jing,Chen, Shi-Yi,Liu, Yi-Ping Asian Australasian Association of Animal Productio 2014 Animal Bioscience Vol.27 No.6

The polymorphism of microphthalmia-associated transcription factor (MITF) and tyrosinase (TYR) genes have been proposed to play a vital role in coat colour genesis in mammals, but their role remains ambiguous in geese at best. Here, we cloned and sequenced 1,397 bp coding region of MITF gene and a 588 bp fragment of TYR exon 1 for polymorphism analysis among 157 domestic geese showing three types of plumage colour. We detected a total of three SNPs (c.280T>C, c.345G>A, and c.369G>A) in TYR and six haplotypes (H1-H6). Among them, haplotypes H1, H2, H3, and H5 were significantly associated with white plumage trait of Zhedong White Geese. However, only diplotype H1H1 and H3H5 were significantly associated with white plumage trait of Zhedong White Geese (p<0.01). We only detected one SNP (c.1109C>T) for MITF gene and found that genotype CT and TT were significantly associated with white plumage trait of Zhedong White Geese. Briefly, our study suggested an association between polymorphisms of TYR and MITF genes and the plumage colour trait in domestic geese.

PXR Mediated Protection against Liver Inflammation by Ginkgolide A in Tetrachloromethane Treated Mice

Ye, Nanhui,Wang, Hang,Hong, Jing,Zhang, Tao,Lin, Chaotong,Meng, Chun The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1

The pregnane X receptor (PXR), a liver and intestine specific receptor,, has been reported to be related with the repression of inflammation as well as activation of cytochromosome P450 3A (CYP3A) expression. We examined the effect of PXR on tetrachloromethane (CCl4)-induced mouse liver inflammation in this work. Ginkgolide A, one main component of Ginkgo biloba extracts (GBE), activated PXR and enhanced PXR expression level, displayed both significant therapeutic effect and preventive effect against $CCl_4$-induced mouse hepatitis. siRNA-mediated decrease of PXR expression significantly reduced the efficacy of Ginkgolide A in treating $CCl_4$-induced inflammation in mice. Flavonoids, another important components of GBE, were shown anti-inflammatory effect in a different way from Ginkgolide A which might be independent on PXR because flavonoids significantly inhibited CYP3A11 activities in mice. The results indicated that anti-inflammatory effect of PXR might be mediated by enhancing transcription level of $I{\kappa}B{\alpha}$ through binding of $I{\kappa}B{\alpha}$. Inhibition of NF-${\kappa}B$ activity by NF-${\kappa}B$-specific suppressor $I{\kappa}B{\alpha}$ is one of the potential mechanisms of Ginkgolide A against CCl4-induced liver inflammation.

Expression and Effects of JMJD2A Histone Demethylase in Endometrial Carcinoma

Wang, Hong-Li,Liu, Mei-Mei,Ma, Xin,Fang, Lei,Zhang, Zong-Feng,Song, Tie-Fang,Gao, Jia-Yin,Kuang, Ye,Jiang, Jing,Li, Lin,Wang, Yang-Yang,Li, Pei-Ling Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.7

Previous studies have demonstrated that JMJD2A is a potential oncogene and is overexpressed in human tumors. However, its role in the endometrial carcinoma remains largely unknown. In this study, we discovered that JMJD2A was overexpressed in endometrial carcinoma, using immunohistochemistry, quantitative realtime polymerase chain reaction, and western blotting. Downregulation of JMJD2A led to reduced endometrial carcinoma RL95-2 and ISK cell proliferation, invasion and metastasis as asessed with cell counting kit-8, cell migration and invasive assays. Collectively, our results support that JMJD2A is a promoter of endometrial carcinoma cell proliferation and survival, and is a potential novel drug target.

AMPK alleviates high uric acid-induced Na+-K+-ATPase signaling impairment and cell injury in renal tubules

Jing Xiao,Sibo Zhu,Haochen Guan,Haochen Guan,Fengqin Li,Xiaoli Zhang,Hui Guo,Xiaojun Wang,Zhibin Ye 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-

One of the mechanisms in hyperuricemia (HUA)-induced renal tubular injury is the impairment of Na+-K+-ATPase (NKA) signaling, which further triggers inflammation, autophagy, and mitochondrial dysfunction and leads to cell injury. Here, we used RNA sequencing to screen the most likely regulators of NKA signaling and found that the liver kinase B1(LKB1)/adenosine monophosphate (AMP)-activated protein kinase (AMPK)/ mammalian target of rapamycin (mTOR) pathway was the most abundantly enriched pathway in HUA. AMPK is a key regulator of cell energy metabolism; hence, we examined the effect of AMPK on HUA-induced dysregulation of NKA signaling and cell injury. We first detected AMPK activation in high uric acid (UA)-stimulated proximal tubular epithelial cells (PTECs). We further found that sustained treatment with the AMPK activator 5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside (AICAR), but not the AMPK inhibitor Compound C, significantly alleviated UA-induced reductions in NKA activity and NKA α1 subunit expression on the cell membrane by reducing NKA degradation in lysosomes; sustained AICAR treatment also significantly alleviated activation of the NKA downstream molecules Src and interleukin-1β (IL-1β) in PTECs. AICAR further alleviated high UA-induced apoptosis, autophagy, and mitochondrial dysfunction. Although AMPK activation by metformin did not reduce serum UA levels in hyperuricemic rats, it significantly alleviated HUAinduced renal tubular injury and NKA signaling impairment in vivo with effects similar to those of febuxostat. Our study suggests that AMPK activation may temporarily compensate for HUA-induced renal injury. Sustained AMPK activation could reduce lysosomal NKA degradation and maintain NKA function, thus alleviating NKA downstream inflammation and protecting tubular cells from high UA-induced renal tubular injury.

Cutaneous Gnathostomiasis with Recurrent Migratory Nodule and Persistent Eosinophilia

Jing Cui,Ye Wang,Zhong Quan Wang 대한기생충학열대의학회 2013 The Korean Journal of Parasitology Vol.51 No.4

Design and performance analysis of magnetorheological grease flexible manipulator gripper

Xudan Ye,Jiqiang Dong,Wenchao Wang,Jing Lu,Jiong Wang 대한기계학회 2023 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.37 No.3

To address the issue of traditional manipulators being unable to grasp and operate objects of varying shapes or easily damaged objects in some work scenes, a new type of flexible manipulator with magnetorheological grease based on the magnetorheological effect was developed. Comsol was used to simulate the magnetic field of the flexible gripper. The results showed that as coil current increased, the magnetic induction intensity increased, the magnetic induction line began to close to the rubber capsule after the shell support was added, the magnetorheological grease solidified after the magnetic field was applied, and the object could be wrapped and grasped. Then the kinematics and grasping ability of the flexible manipulator with magnetorheological grease in the grasping process are analyzed. Finally, an experimental test platform for the magnetorheological grease flexible manipulator is built, and under different currents (0 A, 0.25 A, 0.5 A, 0.75 A, 1 A), the flexible manipulator is tested for different gripping depths (6 mm, 11 mm, 17.5 mm) and a variety of diameter wooden balls (15 mm, 40 mm, 60 mm) gripping ability. The results show that when the gripping depth is constant, the envelope angle of the flexible fingertip to the sphere decrease with the increase of the diameter of the sphere, and when the diameter of the sphere is constant, the higher the grasping depth of the flexible fingertip, the larger the envelope angle to the sphere.

Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

Zhou, Jing,Luo, Yan-Hong,Wang, Ji-Rong,Lu, Bin-Bin,Wang, Ke-Ming,Tian, Ye Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.12

Background: Gambogenic acid is a major active compound of gamboge which exudes from the Garcinia hanburyi tree. Gambogenic acid anti-cancer activity in vitro has been reported in several studies, including an A549 nude mouse model. However, the mechanisms of action remain unclear. Methods: We used nude mouse models to detect the effect of gambogenic acid on breast tumors, analyzing expression of apoptosis-related proteins in vivo by Western blotting. Effects on cell proliferation, apoptosis and apoptosis-related proteins in MDA-MB-231 cells were detected by MTT, flow cytometry and Western blotting. Inhibitors of caspase-3,-8,-9 were also used to detect effects on caspase family members. Results: We found that gambogenic acid suppressed breast tumor growth in vivo, in association with increased expression of Fas and cleaved caspase-3,-8,-9 and bax, as well as decrease in the anti-apoptotic protein bcl-2. Gambogenic acid inhibited cell proliferation and induced cell apoptosis in a concentration-dependent manner. Conclusion: Our observations suggested that Gambogenic acid suppressed breast cancer MDA-MB-231 cell growth by mediating apoptosis through death receptor and mitochondrial pathways in vivo and in vitro.

Probing the Key Binding Sequence and Improvement of the Stability of a β-Bungarotoxin-binding Aptamer in Snake Venom

Fengping Ye,Qili Mi,Ning Zhang,Xuemei Li,Jing Yu,Zhongping Gao,Ying Zheng,Quanshui Fan,Jie Wang,Jinglin Wang 대한화학회 2016 Bulletin of the Korean Chemical Society Vol.37 No.5

Chemical modifications of the nucleotides can improve the stability of aptamers against enzyme degradation in serum, but it is not clear whether these methods are effective in snake venom. In this study, a DNA aptamer, βB-1, which specifically recognize β-bungarotoxin and Bungarus multicinctus venom was chosen, and the key binding sequence of the aptamer was determined. Based on the secondary structure of the truncated aptamer, locked nucleic acids and 2′-O-methyl nucleotides were applied to modify the stem and loop sequences, respectively. In addition, a 3′-3′-thymidine cap was also adopted to block the 3′ end. It was shown that these chemical modifications can all enhance the stability of the aptamer in snake venom. Simultaneously, modified aptamer with the above modifications in one sequence exhibited a significantly elevated biostability, with the half-life improved from several minutes to 210 min while maintaining its binding affinity to the target.

Anti-VEGF Therapy with Bevacizumab - Limited Cardiovascular Toxicity

Yu, Jing,Cao, Xu-Fen,Zheng, Ye,Zhao, Rong-Cheng,Yan, Li-Qiu,Zhao, Lei,Wang, Jia-Wang Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.24

Purpose: This analysis was conducted to evaluate cardiovascular toxicity of commonly used anti-VEGF therapeutic agent, bevacizumab, in treating patients with cancer. Methods: Clinical studies evaluating the efficacy and safety of bevacizumab-based regimens on response and safety for patients with cancer were identified using a predefined search strategy, allowing cardiovascular toxicity and other side effects of treatment to be estimated. Results: In bevacizumab based regimens, 4 clinical studies including 282 patients with advanced cancer (including gliomas, cervical, breast and ovarian cancer) were considered eligible for inclusion. These bevacizumab-based regimens included docetaxel, irinitecan and carboplatin. Systematic analysis suggested that, of 282 patients treated by bevacizumab based regimens, hypertension and thrombo-embolism occurred in 2.5% (7/282), while only 3 patients reported cardiovascular events (1.1%). No treatment related death occurred in bevacizumab based treatment. Conclusion: This systemic analysis suggests that bevacizumab based regimens are associated with reasonable and accepted cardiovascular toxicity when treating patients with gliomas, cervical, breast and ovarian cancer.

Simultaneous treatment with sorafenib and glucose restriction inhibits hepatocellular carcinoma in vitro and in vivo by impairing SIAH1-mediated mitophagy

Zhou Jing,Feng Ji,Wu Yong,Dai Hui-Qi,Zhu Guang-Zhi,Chen Pan-Hong,Wang Li-Ming,Lu Guang,Liao Xi-Wen,Lu Pei-Zhi,Su Wen-Jing,Hooi Shing Chuan,Ye Xin-Pin,Shen Han-Ming,Peng Tao,Lu Guo-Dong 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Transarterial chemoembolization (TACE) is the first-line treatment for unresectable intermediate-stage hepatocellular carcinoma (HCC). It is of high clinical significance to explore the synergistic effect of TACE with antiangiogenic inhibitors and the molecular mechanisms involved. This study determined that glucose, but not other analyzed nutrients, offered significant protection against cell death induced by sorafenib, as indicated by glucose deprivation sensitizing cells to sorafenib-induced cell death. Next, this synergistic effect was found to be specific to sorafenib, not to lenvatinib or the chemotherapeutic drugs cisplatin and doxorubicin. Mechanistically, sorafenib-induced mitophagy, as indicated by PINK1 accumulation, increased the phospho-poly-ubiquitination modification, accelerated mitochondrial membrane protein and mitochondrial DNA degradation, and increased the amount of mitochondrion-localized mKeima-Red engulfed by lysosomes. Among several E3 ubiquitin ligases tested, SIAH1 was found to be essential for inducing mitophagy; that is, SIAH1 silencing markedly repressed mitophagy and sensitized cells to sorafenib-induced death. Notably, the combined treatment of glucose restriction and sorafenib abolished ATP generation and mitophagy, which led to a high cell death rate. Oligomycin and antimycin, inhibitors of electron transport chain complexes, mimicked the synergistic effect of sorafenib with glucose restriction to promote cell death mediated via mitophagy inhibition. Finally, inhibition of the glucose transporter by canagliflozin (a clinically available drug used for type-II diabetes) effectively synergized with sorafenib to induce HCC cell death in vitro and to inhibit xenograft tumor growth in vivo. This study demonstrates that simultaneous treatment with sorafenib and glucose restriction is an effective approach to treat HCC, suggesting a promising combination strategy such as transarterial sorafenib-embolization (TASE) for the treatment of unresectable HCC.