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Articles by G Yang
Total Records ( 12 ) for G Yang
  Y Xu , G Yang and G. Hu

Interferon-induced transmembrane protein 1 (IFITM1) is an essential mediator of interferon--induced anti-proliferation. Here, we reported the interaction between IFITM1 and caveolin-1 (CAV-1), and their inhibitory regulatory function on extracellular signal-regulated kinase (ERK). The immunofluorescence staining result showed that IFITM1 localized in caveolae of the plasma membrane and could interact with CAV-1. Deletion mutagenesis clearly revealed that the hydrophobic transmembrane domains were responsible for the interaction between IFITM1 and CAV-1. It has been reported that CAV-1 has inhibitory effect on the phosphorylation of ERK, and subsequently ERK-mediated transcription. Our study showed the interaction of IFITM1- and CAV-1-enhanced CAV-1's inhibitory effect on ERK activation, whereas the IFITM1 did not activate ERK directly. This inhibitory effect was further confirmed by knocking down the endogenous CAV-1 using RNA interference. These results revealed that the interaction between IFITM1 and CAV-1 could enhance the inhibitory effect of CAV-1 on ERK activation.

  H Zhao , Y Wang , Y Wu , X Li , G Yang , X Ma , R Zhao and H. Liu

Hyperlipidemia is regarded as an independent risk factor in the development of ischemic heart disease, and it can increase the myocardial susceptibility to ischemia/reperfusion (I/R) injury. Ischemic postconditioning (Postcon) has been demonstrated to attenuate the myocardial injury induced by I/R in normal conditions. But the effect of ischemic Postcon on hyperlipidemic animals is unknown. Hypoxia inducible factor-1 (HIF-1) has been demonstrated to play a central role in the cardioprotection by preconditioning, which is one of the protective strategies except for Postcon. The aim of this study was to determine whether Postcon could reduce myocardial injury in hyperlipidemic animals and to assess whether HIF-1 was involved in Postcon mechanisms. Male Wistar rats underwent the left anterior descending coronary occlusion for 30 min followed by 180 min of reperfusion with or without Postcon after fed with high fat diet or normal diet for 8 weeks. The detrimental indices induced by the I/R insult included infarct size, plasma creatine kinase activity and caspase-3 activity. Results showed that hyperlipidemia remarkably enhanced the myocardial injury induced by I/R, while Postcon significantly decreased the myocardial injury in both normolipidemic and hyperlipidemic rats. Moreover, both hyperlipidemia and I/R promoted the HIF-1 expression. Most importantly, we have for the first time demonstrated that Postcon further induced a significant increase in HIF-1 protein level not only in normolipidemic but also in hyperlipidemic conditions. Thus, Postcon reduces the myocardial injury induced by I/R in normal and hyperlipidemic animals, and HIF-1 upregulation may involve in the Postcon-mediated cardioprotective mechanisms.

  S. A Lee , X. O Shu , H Li , G Yang , H Cai , W Wen , B. T Ji , J Gao , Y. T Gao and W. Zheng

Background: Soy food is a rich source of isoflavones—a class of phytoestrogens that has both antiestrogenic and anticarcinogenic properties.

Objective: The objective was to evaluate the association of adolescent and adult soy food intake with breast cancer risk in a cohort of 73,223 Chinese women who participated in the Shanghai Women's Health Study.

Design: A validated food-frequency questionnaire was used to assess usual dietary intake during adulthood and adolescence. After a mean follow-up of 7.4 y, 592 incident cases of breast cancer were identified for longitudinal analyses by using Cox regressions.

Results: Adult soy food consumption, measured either by soy protein or isoflavone intake, was inversely associated with the risk of premenopausal breast cancer, and the association was highly statistically significant (P for trend < 0.001). The multivariate-adjusted relative risks (RRs) for the upper intake quintile compared with the lowest quintile were 0.41 (95% CI: 0.25, 0.70) for soy protein intake and 0.44 (95% CI: 0.26, 0.73) for isoflavone intake. High intake of soy foods during adolescence was also associated with a reduced risk of premenopausal breast cancer (RR: 0.57; 95% CI: 0.34, 0.97). Women who consumed a high amount of soy foods consistently during adolescence and adulthood had a substantially reduced risk of breast cancer. No significant association with soy food consumption was found for postmenopausal breast cancer.

Conclusion: This large, population-based, prospective cohort study provides strong evidence of a protective effect of soy food intake against premenopausal breast cancer.

  K Matsumoto , J Huang , N Viswakarma , L Bai , Y Jia , Y. T Zhu , G Yang , J Borensztajn , M.S Rao , Y. J Zhu and J. K. Reddy

Nuclear receptor coactivator [peroxisome proliferator-activated receptor-binding protein (PBP)/mediator subunit 1 (MED1)] is a critical component of the mediator transcription complex. Disruption of this gene in the mouse results in embryonic lethality. Using the PBP/MED1 liver conditional null (PBP/MED1Liv) mice, we reported that PBP/MED1 is essential for liver regeneration and the peroxisome proliferator-activated receptor ligand Wy-14,643-induced receptor-mediated hepatocarcinogenesis. We now examined the role of PBP/MED1 in genotoxic chemical carcinogen diethylnitrosamine (DEN)-induced and phenobarbital-promoted hepatocarcinogenesis. The carcinogenic process was initiated by a single intraperitoneal injection of DEN at 14 days of age and initiated cells were promoted with phenobarbital (PB) (0.05%) in drinking water. PBP/MED1Liv mice, killed at 1, 4 and 12 weeks, revealed a striking proliferative response of few residual PBP/MED1-positive hepatocytes that escaped Cre-mediated deletion of PBP/MED1 gene. No proliferative expansion of PBP/MED1 null hepatocytes was noted in the PBP/MED1Liv mouse livers. Multiple hepatocellular carcinomas (HCCs) developed in the DEN-initiated PBP/MED1fl/fl and PBP/MED1Liv mice, 1 year after the PB promotion. Of interest is that all HCC developing in PBP/MED1Liv mice were PBP/MED1 positive. None of the tumors was PBP/MED1 negative implying that hepatocytes deficient in PBP/MED1 are not susceptible to neoplastic conversion. HCC that developed in PBP/MED1Liv mouse livers were transplantable in athymic nude mice and these maintained PBP/MED1fl/fl genotype. PBP/MED1fl/fl HCC cell line derived from these tumors expressed PBP/MED1 and deletion of PBP/MED1fl/fl allele by adeno-Cre injection into tumors caused necrosis of tumor cells. These results indicate that PBP/MED1 is essential for the development of HCC in the mouse.

  R. F Klie , W Walkosz , G Yang and Y. Zhao

Many fundamental problems in materials science, physics, and particular nanotechnology rely on the direct determination and characterization of atomic arrangements and electronic environments of individual interfaces or defects. In this paper, we will show how aberration-corrected Z-contrast imaging in combination with electron energy-loss spectroscopy can be used to directly measure the local atomic and electronic structures of dislocation cores in low-angle SrTiO [001] tilt grain boundaries. In particular, we will study two types of dislocation cores in a 3 tilt grain boundary, a pure edge dislocation, and a dissociated dislocation core. While it is energetically favorable for an edge dislocation to dissociate into two partial dislocations in such a low-angle grain boundary, we can find pure edge dislocations that show a higher O vacancy concentration than the dissociated cores. We suggest that the increased oxygen vacancy concentration might help stabilizing the pure edge dislocations in 3° tilt grain boundaries of SrTiO .

  M Zhang , X. W Fei , Y. L He , G Yang and Y. A. Mei

Bradykinin (BK) is an endogenous peptide with diverse biological actions and is considered to be an important mediator of the inflammatory response in both the peripheral and the central nervous systems. BK has attracted recent interest as a potential mediator of K+ conductance, Cl channels, and Ca2+-activated K+ channels. However, few reports have associated BK with the voltage-gated K+ current. In this study, we demonstrated that BK suppressed the transient outward potassium current (IA) in mouse Schwann cells using whole cell recording techniques. At a concentration of 0.1 µM to 5 µM, BK reversibly inhibited IA in a dose-dependent manner with the modulation of steady-state activation and inactivation properties. The effect of BK on IA current was abolished after preincubation with a B2 receptor antagonist but could not be eliminated by B1 receptor antagonist. Intracellular application of GTP-S induced an irreversible decrease in IA, and the inhibition of Gs using NF449 provoked a gradual augmentation in IA and eliminated the BK-induced effect on IA, while the Gi/o antagonist NF023 did not. The application of forskolin or dibutyryl-cAMP mimicked the inhibitory effect of BK on IA and abolished the BK-induced effect on IA. H-89, an inhibitor of PKA, augmented IA amplitude and completely eliminated the BK-induced inhibitory effect on IA. In contrast, activation of PKC by PMA augmented IA amplitude. A cAMP assay revealed that BK significantly increased intracellular cAMP level. It is therefore concluded that BK inhibits the IA current in Schwann cells by cAMP/PKA-dependent pathways via activation of the B2 receptor.

  F Yokoi , G Yang , J Li , M. P DeAndrade , T Zhou and Y. Li

DYT1 early-onset generalized torsion dystonia is an inherited movement disorder caused by mutations in DYT1 coding for torsinA with ~30% penetrance. Most of the DYT1 dystonia patients exhibit symptoms during childhood and adolescence. On the other hand, DYT1 mutation carriers without symptoms during these periods mostly do not exhibit symptoms later in their life. Little is known about what controls the timing of the onset, a critical issue for DYT1 mutation carriers. DYT11 myoclonus-dystonia is caused by mutations in SGCE coding for -sarcoglycan. Two dystonia patients from a single family with double mutations in DYT1 and SGCE exhibited more severe symptoms. A recent study suggested that torsinA contributes to the quality control of -sarcoglycan. Here, we derived mice carrying mutations in both Dyt1 and Sgce and found that these double mutant mice showed earlier onset of motor deficits in beam-walking test. A novel monoclonal antibody against mouse -sarcoglycan was developed by using Sgce knock-out mice to avoid the immune tolerance. Western blot analysis suggested that functional deficits of torsinA and -sarcoglycan may independently cause motor deficits. Examining additional mutations in other dystonia genes may be beneficial to predict the onset in DYT1 mutation carriers.

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