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Articles by Y Tu
Total Records ( 6 ) for Y Tu
  S. J Matkovich , W Wang , Y Tu , W. H Eschenbacher , L. E Dorn , G Condorelli , A Diwan , J. M Nerbonne and G. W. Dorn

Rationale: MicroRNA (miR)-133a regulates cardiac and skeletal muscle differentiation and plays an important role in cardiac development. Because miR-133a levels decrease during reactive cardiac hypertrophy, some have considered that restoring miR-133a levels could suppress hypertrophic remodeling.

Objective: To prevent the "normal" downregulation of miR-133a induced by an acute hypertrophic stimulus in the adult heart.

Methods and Results: miR-133a is downregulated in transverse aortic constriction (TAC) and isoproterenol-induced hypertrophy, but not in 2 genetic hypertrophy models. Using MYH6 promoter-directed expression of a miR-133a genomic precursor, increased cardiomyocyte miR-133a had no effect on postnatal cardiac development assessed by measures of structure, function, and mRNA profile. However, increased miR-133a levels increased QT intervals in surface electrocardiographic recordings and action potential durations in isolated ventricular myocytes, with a decrease in the fast component of the transient outward K+ current, Ito,f, at baseline. Transgenic expression of miR-133a prevented TAC-associated miR-133a downregulation and improved myocardial fibrosis and diastolic function without affecting the extent of hypertrophy. Ito,f downregulation normally observed post-TAC was prevented in miR-133a transgenic mice, although action potential duration and QT intervals did not reflect this benefit. miR-133a transgenic hearts had no significant alterations of basal or post-TAC mRNA expression profiles, although decreased mRNA and protein levels were observed for the Ito,f auxiliary KChIP2 subunit, which is not a predicted target.

Conclusions: These results reveal striking differences between in vitro and in vivo phenotypes of miR expression, and further suggest that mRNA signatures do not reliably predict either direct miR targets or major miR effects.

  H Ding , Y Xu , X Wang , Q Wang , L Zhang , Y Tu , J Yan , W Wang , R Hui , C. Y Wang and D. W. Wang

Background— Recent studies on genome-wide association have identified common variants on chromosome 9p21 associated with coronary artery disease (CAD). Given that ischemic stroke and CAD share several aspects of etiology and pathogenesis, we investigated the association of variants on chromosome 9p21 with ischemic stroke and CAD in the Chinese Han population by capturing the majority of diversity in this locus using haplotype-tagging single-nucleotide polymorphisms.

Methods and Results— We performed a shared control-cases study using 15 tagging single-nucleotide polymorphisms and 2 previously reported susceptibility single-nucleotide polymorphisms spanning 58 kb of the chromosome of 9p21 in a set of 558 patients with ischemic stroke, 510 patients with CAD, and 557 unaffected participants (controls) in the Chinese Han population. The association analyses were performed at both SNP and haplotype levels. We further verified our findings in an independent cohort of 442 ischemic stroke cases and 502 control subjects. In the first study, rs2383206, rs1004638, and rs10757278 in block 3 were significantly associated with CAD but not with ischemic stroke independent of traditional cardiovascular risk factors in additive model (P=0.002 to 0.0001, q=0.026 to 0.004). Analysis from all blocks revealed that haplotype profiles of block 3 on 9p21 were significantly different between shared control and cases of CAD (P=1.3x10–10, q=1.2x10–9) and ischemic stroke (P=1.7x10–6, q=7.7x10–6). In the expanded second case-control study, block 3 on 9p21 remained associated with ischemic stroke (P=2.6x10–4, q=6.3x10–4).

Conclusions— Our results suggest for the first time that 9p21 is a shared susceptibility locus, strongly for CAD and weakly for ischemic stroke, in a Chinese Han population.

  C Liu , G Tian , Y Tu , J Fu , C Lan and N. Wu

Bone morphogenetic protein-2 (BMP-2) is normally expressed in the embryo promoting the development of several organs. Aberrant expression of BMP-2 occurs in various tumors. However, a correlation between BMP-2 expression in human gliomas and patients' prognosis has not been reported. To address this question, this study was to investigate the BMP-2 expression pattern in human gliomas and to evaluate its prognostic relevance.


We analyzed the expression of the BMP-2 antigen in a series of 98 gliomas of various grade and histology by immunohistochemistry on paraffin-embedded sections. Then, the correlation of BMP-2 expression pattern with clinical–pathological features of patients and its prognostic relevance were determined.


Immunohistochemical analysis with anti-BMP-2 antibody revealed dense and spotty staining in the tumor cells and its expression levels became significantly higher as the gliomas' grade advanced (P < 0.001). The median survival of patients with intensively positive BMP-2 expression was significantly shorter than that with negative expression (318 vs. 1197 days, P < 0.0001). The Kaplan–Meier survival curves showed that the BMP-2 expression was not only a significant predictor of survival in high-grade gliomas (grade IV, P = 0.02), but also in lower-grade gliomas (grades II and III, P < 0.001).


These results indicate that BMP-2 is a highly sensitive marker for gliomas prognosis and suggest that the expression level of BMP-2 may be a potent tool for the clinical prognosis of gliomas patients.

  Y Tu , J Lu , J Fu , Y Cao , G Fu , R Kang , X Tian and B. Wang

Neuroepithelial-transforming protein 1 is a member of the guanine nucleotide exchange factor family, a group of proteins which are known to activate and thereby regulate Rho family members. Deregulation of neuroepithelial-transforming protein 1 expression has been found in certain types of human tumors. To investigate its prognostic value in human gliomas, which is currently unknown, we examined the correlation between neuroepithelial-transforming protein 1 expression and prognosis in patients with gliomas.


Immunohistochemical staining was performed to detect neuroepithelial-transforming protein 1 expression patterns in the biopsies from 96 patients with primary gliomas. Kaplan–Meier survival and Cox's regression analyses were performed to evaluate the prognosis of patients.


Immunohistochemical analysis with anti-neuroepithelial-transforming protein 1 antibody revealed that neuroepithelial-transforming protein 1 was significantly associated with the Karnofsky performance scale score and World Health Organization grades of patients with gliomas. Especially, the positive expression rates of neuroepithelial-transforming protein 1 were significantly higher in patients with higher grade (P = 0.001) and lower Karnofsky's performance scale score (P = 0.005). The median survival of patients with high neuroepithelial-transforming protein 1 expression was significantly shorter than that with low expression and without expression (316, 892 and 1180 days, respectively). Cox's multifactor analysis showed that the Karnofsky performance scale (P = 0.01), World Health Organization grade (P = 0.008) and neuroepithelial-transforming protein 1 (P = 0.006) were independent prognosis factors for human glioma.


Taken together, our study indicates for the first time that neuroepithelial-transforming protein 1 status may be a highly sensitive marker for glioma prognosis and suggest that the expression patterns of neuroepithelial-transforming protein 1 might be a potent tool for predicting the clinical prognosis of glioma patients.

  L Kang , X Zhang , Y Xie , Y Tu , D Wang , Z Liu and Z. Y. Wang

Accumulating evidence suggested that an orphan G protein-coupled receptor (GPR)30, mediates nongenomic responses to estrogen. The present study was performed to investigate the molecular mechanisms underlying GPR30 function. We found that knockdown of GPR30 expression in breast cancer SK-BR-3 cells down-regulated the expression levels of estrogen receptor (ER)-36, a variant of ER-. Introduction of a GPR30 expression vector into GPR30 nonexpressing cells induced endogenous ER-36 expression, and cotransfection assay demonstrated that GPR30 activated the promoter activity of ER-36 via an activator protein 1 binding site. Both 17β-estradiol (E2) and G1, a compound reported to be a selective GPR30 agonist, increased the phosphorylation levels of the MAPK/ERK1/2 in SK-BR-3 cells, which could be blocked by an anti-ER-36-specific antibody against its ligand-binding domain. G1 induced activities mediated by ER-36, such as transcription activation activity of a VP16-ER-36 fusion protein and activation of the MAPK/ERK1/2 in ER-36-expressing cells. ER-36-expressing cells, but not the nonexpressing cells, displayed high-affinity, specific E2 and G1 binding, and E2- and G1-induced intracellular Ca2+ mobilization only in ER-36 expressing cells. Taken together, our results demonstrated that previously reported activities of GPR30 in response to estrogen were through its ability to induce ER-36 expression. The selective G protein-coupled receptor (GPR)30 agonist G1 actually interacts with ER-36. Thus, the ER- variant ER-36, not GPR30, is involved in nongenomic estrogen signaling.

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