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Articles by Y Ma
Total Records ( 14 ) for Y Ma
  Y Ma , M Ma , Y Dai and A. Hong
 

The development of rBAY, a recombinant peptide with the similar sequence of synthetic BAY55-9837, as a potential peptide therapeutic for type 2 diabetes is still a challenge mainly because of its poor stability in aqueous solution. To improve the peptide stability and bioactivity and investigate its biological effects for VPAC2-specific activation, RBAYL with 31 aa was designed based on sequence alignments of pituitary adenylate cyclase-activating peptides (PACAPs), vasoactive intestinal peptide (VIP), and related analogs and generated through site-directed mutagenesis. Stability analysis showed that the prepared RBAYL with three mutations (N9Q, V17L, and N28K) were much more stable than rBAY. rRBAYL (the recombinant RBAYL) was expressed and purified by gene-recombination technology via native thiol ligation on solid beads. As much as 27.7 mg rRBAYL peptide with purity over 98% was obtained from 1 L of LB medium without expensive high-performance liquid chromatography refinements. The bioactivity assay of rRBAYL showed that it displaced [125I]PACAP38 and [125I]VIP from VPAC2 with a half-maximal inhibitory concentration of 51 ± 6 and 50 ± 4 nM, respectively, which were similar to those of the chemically synthesized RBAYL (sRBAYL) and lower than those of Ro25-1553, an established VPAC2 agonist. rRBAYL enhances the cAMP accumulation in CHO cells expressing human VPAC2 with a half-maximal stimulatory concentration (EC50) of 0.91 nM, whereas the receptor potency of rRBAYL at human VPAC1 (EC50 of 719 nM) was only 1/790 of that at human VPAC2, and rRBAYL had no activity toward human PAC1 receptor. Western-blot assay for glucose transporter 4 (GLUT4) indicated that the rRBAYL could significantly induce GLUT4 expression more efficiently than rBAY or Ro25-1553 in adipocytes. Compared with rBAY, rRBAYL can more efficiently promote insulin release and decrease plasma glucose level in ICR mice. Our results suggested that rRBAYL is a novel recombinant VPAC2-specific agonist with high stability and bioactivity.

  B Chen , Y Ma , R Meng , Z Xiong , C Zhang , G Chen , A Zhang and Y. Dong
 

Proteasome inhibitors are involved in cell cycle control, growth and inflammatory signaling, and transcriptional regulation of mitotic cells. A recent study has suggested that specific proteasome inhibitor MG132 may suppress cardiomyocyte hypertrophy in vitro. However, the underlying molecular mechanisms are not clear. In this study, we investigated the effects of long-term MG132 treatment on cardiac hypertrophy and the related molecular mechanisms in vivo. MG132 (0.1 mg/kg/day) was intraperitoneally injected to rats with abdominal aortic banding (AAB) for 8 weeks. Results showed that treatment with MG132 significantly attenuated left ventricular (LV) myocyte area, LV weight/body weight, and lung weight/body weight ratios, decreased LV diastolic diameter and wall thickness, and increased fractional shortening in AAB rats. AAB induced the phosphorylation of ERK1/2, JNK1, and p38 in cardiac myocytes. The elevated phosphorylation levels of ERK1/2 and JNK1 in AAB rats were significantly reversed by MG132 treatment. In conclusion, our results suggested that long-term treatment with MG132 attenuates pressure-overload-induced cardiac hypertrophy and improves cardiac function in AAB rats through regulation of ERK1/2 and JNK1 signaling pathways.

  X Jin , H Mei , X Li , Y Ma , A. h Zeng , Y Wang , X Lu , F Chu , Q Wu and J. Zhu
 

We studied the apoptosis-inducing properties of the antimicrobial peptide cecropin of Musca domestica in human hepatocellular carcinoma cell line BEL-7402 and its underlying mechanism. Proliferation inhibition of the human hepatocellular carcinoma BEL-7402 cells and the human normal liver cells were determined by the MTT assay, and the cell viability was determined by trypan blue dye exclusion assay. The apoptotic tumor cells treated with cecropin were examined by transmission electron microscopy and terminal-deoxynucleotidyl transferase mediated nick end labeling. The apoptosis rate was measured by flow cytometry (FCM) with PI/Annexin-V double staining. Western blot analysis and RT-PCR were used to determine the expression levels of proteins involved in apoptosis, such as Fas, Fas-L, caspase-8, and caspase-3. The experimental results showed that Musca domestica cecropin inhibited the proliferation of human hepatocellular carcinoma BEL-7402 cells in dose-dependent and time-dependent manners, without affecting the proliferation of normal liver cells. FCM showed that the cell apoptosis rates were 5.1 ± 0.11%, 8.1 ± 0.04%, and 10.9 ± 0.15% after the treating with 100 µM cecropin for 24, 48, and 72 h, respectively. The rates of apoptosis were 5.4 ± 0.14% and 8.0 ± 0.13% after the treating with 25 and 50 µM cecropin for 72 h, respectively. Western blot analysis and RT-PCR showed that the apoptosis-related molecules including Fas, Fas-L, caspase-8 and caspase-3 were activated. This study showed that the antimicrobial peptide cecropin-inducing apoptosis in human hepatocellular carcinoma BEL-7402 cells, which might be associated with upregulation of Fas, Fas-L, and caspase-8 and caspase-3 and triggering extrinsic apoptotic pathway.

  I Sandler , T. S Ayers , J. Y Tein , S Wolchik , R Millsap , S. T Khoo , D Kaplan , Y Ma , L Luecken , E Schoenfelder and S. Coxe
 

Objective  To evaluate the efficacy of the Family Bereavement Program (FBP) to prevent mental health problems in parentally bereaved youths and their parents 6 years later.

Design  Randomized controlled trial.

Setting  Arizona State University Prevention Research Center from November 2002 to July 2005.

Participants  Two hundred eighteen bereaved youths (89.34% of 244 enrolled in the trial 6 years earlier) and 113 spousally bereaved parents.

Interventions  The FBP includes 12 group sessions for caregivers and youths; the literature control (LC) condition includes bereavement books for youths and caregivers.

Main Outcome Measures  Comparisons of youths in the FBP and LC on a measure of mental disorder diagnosis, 5 measures of mental health problems, and 4 measures of competent functioning; and comparisons of spousally bereaved parents on 2 measures of mental health problems.

Results  Youths in the FBP as compared with those in the LC had significantly lower externalizing problems as reported by caregivers and youths (adjusted mean, –0.06 vs 0.13, respectively; P = .02) and on teacher reports of externalizing problems (adjusted mean, 52.69 vs 56.27, respectively; P = .001) and internalizing problems (adjusted mean, 47.29 vs 56.27, respectively; P = .002), and they had higher self-esteem (adjusted mean, 33.93 vs 31.91, respectively; P = .005). Parents in the FBP had lower depression scores than those in the LC (adjusted mean, 5.48 vs 7.83, respectively; P = .04). A significant moderated program effect indicated that for youths with lower baseline problems, the rate of diagnosed mental disorder was lower for those in the FBP than in the LC.

Conclusion  This study demonstrates efficacy of the FBP to reduce mental health problems of bereaved youths and their parents 6 years later.

Trial Registration  clinicaltrials.gov Identifier: NCT01008189

  O. B Goodman , L. M Fink , J. T Symanowski , B Wong , B Grobaski , D Pomerantz , Y Ma , D. C Ward and N. J. Vogelzang
 

Purpose: Circulating tumor cells (CTC) have been recently accepted by the Food and Drug Administration of the United States as a prognostic tool in advanced prostate cancer. However, a number of questions remain about the use of the test. The optimal clinical cut-off has never been determined. Also, the predictive value of CTCs in the setting of low-burden advanced prostate cancer has not been evaluated. Herein we describe our experience with the CellSearch method of CTC enumeration.

Experimental Design: CTCs enumerated from 100 patients with castration-resistant prostate cancer were correlated with clinicopathologic characteristics and conventional biomarkers, such as prostate-specific antigen and lactate dehydrogenase. Patients received ongoing medical oncologic follow-up for up to 26 months, and overall survival status was documented.

Results: Forty-nine of the patients (49%) were alive at the end of the study. CTC counts correlate well with overall survival (P < 0.001) but are also tightly interrelated to other biomarkers. Threshold analysis identified 4 CTC/7.5 cc (compared with the approved value of 5) as an optimal cut-off value with respect to correlation with survival outcomes as well as predictive of metastatic disease. Univariate analysis confirmed a tight interrelationship between cut-off CTC values and biomarkers. Multivariate analysis with bootstrap sampling validation identified lactate dehydrogenase (P = 0.002) and CTCs (P = 0.001) as independently prognostically significant.

Conclusions: Baseline CTC values provide important prognostic information and specific prediction of metastatic disease. Their presence correlates with classic biomarkers. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1904–13)

  J Yin , U Vogel , Y Ma , R Qi and H. Wang
 

DNA repair genes have been proposed as candidate cancer susceptibility genes. The excision repair cross-complementing rodent repair deficiency, complementation group 2 (ERCC2)/xeroderma pigmentosum complementary group D (XPD) protein is considered to be a key enzyme in nucleotide excision repair (NER) pathway. To elucidate whether common ERCC2 variants are associated with lung cancer susceptibility, we conducted a case–control study consisting of 339 cases with primary lung cancer and 358 controls matched on age, gender and ethnicity in a Chinese population. Six haplotype tagging single-nucleotide polymorphisms (htSNPs) (rs238403, rs50871, rs3916840, rs238415, rs3916874 and rs1799787) from HapMap database were analyzed, which provide an almost complete coverage of the genetic variations in the ERCC2 gene. Although none of the six htSNPs was individually associated with lung cancer risk, we found that two ERCC2 haplotypes were associated with risk of lung cancer. Haplotype 4 defined by rs238403T-rs50871T-rs3916840C-rs238415C-rs3916874G-rs1799787C and haplotype 7 defined by rs238403C-rs50871G-rs3916840C-rs238415C-rs3916874G-rs1799787C were strongly associated with an increased risk of lung cancer [odds ratio, OR (95% confidence interval, CI) = 2.62 (1.53–4.50), P = 0.0003 for hap4; OR (95% CI) = 3.01 (1.36–6.63), P = 0.004 for hap7]. Furthermore, diplotype analyses also strengthened the significant associations of risk haplotype 4 [OR (95% CI) = 3.56 (2.12–5.87), P < 0.001] or risk haplotype 7 [OR (95% CI) = 3.38 (1.75–6.55), P < 0.001] and lung cancer. Analysis of linkage disequilibrium (LD) also confirmed that considerable LD exists between the pairs of the six htSNPs within ERCC2. These results suggested that the risk subhaplotypes cosegregate with one or more biologically functional polymorphisms. Our results provide evidence to support a role for ERCC2 in lung cancer development in a Chinese population.

  Y. M Kang , Y Ma , J. P Zheng , C Elks , S Sriramula , Z. M Yang and J. Francis
  Aims

Angiotensin II (ANG II)-induced inflammatory and oxidative stress responses contribute to the pathogenesis of hypertension. In this study, we determined whether nuclear factor-kappa B (NF-B) activation in the hypothalamic paraventricular nucleus (PVN) increases oxidative stress and contributes to the ANG II-induced hypertensive response.

Methods and results

Rats were infused intravenously with ANG II (10 ng/kg per min) or saline for 4 weeks. These rats received either vehicle or losartan (LOS, 20 µg/h), an angiotensin II type 1 receptor (AT1-R) antagonist; pyrrolidine dithiocarbamate (PDTC, 5 µg/h), a NF-B inhibitor; tempol (TEMP, 80 µg/h), a superoxide scavenger; LOS (20 µg/h), and PDTC (5 µg/h); or TEMP (80 µg/h) and PDTC (5 µg/h), given intracerebroventricularly (ICV) via osmotic minipump. ANG II infusion resulted in increased mean arterial pressure, renal sympathetic nerve activity, plasma proinflammatory cytokines (PIC), norepinephrine, and aldosterone. These rats also had higher levels of Fra-LI (an indicator of chronic neuronal activation), PIC, phosphorylated IKKβ, NF-B subunits, AT1-R, superoxide, and gp91phox (a subunit of NADP(H) oxidase) and lower levels of IB in the PVN than control animals. ICV treatment with LOS, PDTC, or TEMP attenuated these changes, and combined treatment with ICV LOS and PDTC, or ICV TEMP and PDTC prevented these ANG II-induced hypertensive responses.

Conclusion

These findings suggest that an ANG II-induced increase in the brain renin–angiotensin system activates NF-B in the PVN and contributes to sympathoexcitation in hypertension. The increased superoxide in the PVN contributes to NF-B activation and neurohumoral excitation in hypertension.

  G Weskamp , K Mendelson , S Swendeman , S Le Gall , Y Ma , S Lyman , A Hinoki , S Eguchi , V Guaiquil , K Horiuchi and C. P. Blobel
 

Rationale: Pathological neovascularization is a critical component of diseases such as proliferative retinopathies, cancer and rheumatoid arthritis, yet much remains to be learned about the underlying causes. Previous studies showed that vascular endothelial growth factor (VEGF)-A activates the membrane-anchored metalloproteinase ADAM17 (a disintegrin and metalloproteinase 17) in endothelial cells, thereby stimulating crosstalk between VEGF receptor 2 and extracellular signal-regulated kinase. These findings raised interesting questions about the role of ADAM17 in angiogenesis and neovascularization in vivo.

Objective: The objective of this study was to inactivate ADAM17 in endothelial cells or in pericytes to determine how this affects developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.

Methods and Results: We generated animals in which floxed ADAM17 was removed by Tie2-Cre in endothelial cells, or by smooth muscle (sm) Cre in smooth muscle cells and pericytes. There were no evident developmental defects in either conditional knockout strain, but pathological retinal neovascularization and growth of heterotopically injected tumor cells was reduced in Adam17flox/flox/Tie2-Cre mice, although not in Adam17flox/flox/sm-Cre mice. Moreover, lack of ADAM17 in endothelial cells decreased ex vivo chord formation, and this could be largely restored by addition of the ADAM17 substrate HB-EGF (heparin-binding epidermal growth factor–like growth factor). Finally we found that ADAM17 is important for the VEGF receptor 2 stimulated processing of several receptors with known functions in endothelial cell biology.

Conclusions: These results provide the first evidence for a role for ADAM17 in pathological neovascularization in vivo. Because ADAM17 does not appear to be required for normal developmental angiogenesis or vascular homeostasis, it could emerge as a good target for treatment of pathological neovascularization.

  J Cheng , Y Wang , Y Ma , B. T. y Chan , M Yang , A Liang , L Zhang , H Li and J. Du
  Rationale:

Mechanical stress plays an important role in proliferation of venous smooth muscle cells (SMCs) in neointima, a process of formation that contributes to failure of vein grafts. However, it is unknown what intracellular growth signal leads to proliferation of venous SMCs.

Objective:

The objective of this study is to identify mechanisms of mechanical stretch on neointima formation.

Methods and Results:

By a microarray analysis, we found that mechanical cyclic stretch (15% elongation) stimulated the transcription of SGK-1 (serum-, glucocorticoid-regulated kinase-1). Mechanical stretch–induced SGK-1 mRNA expression was blocked by actinomycin D. The mechanism for the SGK-1 expression involved MEK1 but not p38 or JNK signaling pathway. SGK-1 activation in response to stretch is blocked by insulin-like growth factor (IGF)-1 receptor inhibitor and mammalian target of rapamycin complex (mTORC)2 inhibitor (Ku-0063794) but not mTORC1 inhibitor (rapamycin). Mechanical stretch–induced bromodeoxyuridine incorporation was reduced by 83.5% in venous SMCs isolated from SGK-1 knockout mice. In contrast, inhibition of Akt, another downstream signal of PI3K resulted in only partial inhibition of mechanical stretch–induced proliferation of venous SMCs. Mechanical stretch also induced phosphorylation and nuclear exportation of p27kip1, whereas knockout of SGK-1 attenuated this effect of mechanical stretch on p27kip1. In vivo, we found that placement of a vein graft into artery increased SGK-1 expression. Knockout of SGK-1 effectively prevented neointima formation in vein graft. There is significant lower level of p27kip1 located in the nucleus of neointima cells in SGK-1 knockout mice compared with that of wild-type vein graft. In addition, we also found that wire injury of artery or growth factors in vitro increased expression of SGK-1.

Conclusions:

These results suggest that SGK-1 is an injury-responsive kinase that could mediate mechanical stretch–induced proliferation of vascular cells in vein graft, leading to neointima formation.

  Y Ling , Y Ma , W Guan , Y Cheng , Y Wang , J Han , D Jin , L Mang and H. Mahmut
 

Y chromosome acts as a single nonrecombining unit that is male specific and in effect haploid, thus ensuring the preservation of mutational events as a single haplotype via male lines. In this study, 6 Y chromosome–specific microsatellites (SSR) were tested for the patrilineal genetic variations of 573 male samples from Chinese domestic horse (30 breeds), Przewalski's horse, and donkey. All the 6 loci appeared as a haplotype block in Przewalski's horse and the domestic donkey. There were notable differences, however, at Y chromosome markers between horse and donkey. There were 2 haplotypes of Eca.YA16 in the domestic horse breeds, Haplotype A (Allele A: 156 bp) and Haplotype B (Allele B: 152 bp). Allele A was the common allele among 30 horse breeds, and Allele B was found in 11 horse breeds. This is the first description of a Y chromosome variant for horses. The 2 haplotypes of Y chromosome discovered in the domestic horse breeds in China could be helpful in unveiling their intricate genetic genealogy.

  P Katiyar , Y Ma , A Riegel , S Fan and E. M. Rosen
 

Previously, we reported that BRCA1 inhibits progesterone receptor (PR) activity and blocks progesterone-stimulated gene expression and cell proliferation. In the present manuscript, we studied the mechanism of BRCA1 inhibition of PR activity, using c-Myc as a model progesterone-regulated promoter. Here, we found that BRCA1 has little or no effect on PR ligand-binding affinity. However, BRCA1 overexpression inhibited the R5020-induced recruitment of PR to the c-Myc and mouse mammary tumor virus progesterone response elements (PREs) and blocked R5020-stimulated c-Myc expression, whereas BRCA1 underexpression did the opposite. In EMSAs, BRCA1 overexpression blocked the R5020-induced complex formation between PR and several radiolabeled PRE-containing oligonucleotides, and in vitro-translated BRCA1 blocked the interaction of full-length PR-A or a fragment containing the DNA-binding domain of PR with a radiolabeled PRE oligonucleotide. In further studies, BRCA1 overexpression inhibited the recruitment of coactivators (steroid receptor coactivator 1 and amplified in breast cancer 1) and enhanced the recruitment of a corepressor (histone deacetylase 1) to the c-Myc PRE, whereas BRCA1 knockdown increased the abundance of AIB1 and decreased the abundance of HDAC1 at the c-Myc PRE. These findings suggest that BRCA1 inhibits progestin-stimulated PR activity, in part, by preventing PR from binding to the PRE and by promoting the formation of a corepressor complex rather than a coactivator complex.

  M Jiang , Y Ma , C Chen , X Fu , S Yang , X Li , G Yu , Y Mao , Y Xie and Y. Li
 

Androgen signaling plays an important role in many biological processes. Androgen Responsive Gene Database (ARGDB) is devoted to providing integrated knowledge on androgen-controlled genes. Gene records were collected on the basis of PubMed literature collections. More than 6000 abstracts and 950 original publications were manually screened, leading to 1785 human genes, 993 mouse genes, and 583 rat genes finally included in the database. All the collected genes were experimentally proved to be regulated by androgen at the expression level or to contain androgen-responsive regions. For each gene important details of the androgen regulation experiments were collected from references, such as expression change, androgen-responsive sequence, response time, tissue/cell type, experimental method, ligand identity, and androgen amount, which will facilitate further evaluation by researchers. Furthermore, the database was integrated with multiple annotation resources, including National Center for Biotechnology Information, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes pathway, to reveal the biological characteristics and significance of androgen-regulated genes. The ARGDB web site is mainly composed of the Browse, Search, Element Scan, and Submission modules. It is user friendly and freely accessible at http://argdb.fudan.edu.cn. Preliminary analysis of the collected data was performed. Many disease pathways, such as prostate carcinogenesis, were found to be enriched in androgen-regulated genes. The discovered androgen-response motifs were similar to those in previous reports. The analysis results are displayed in the web site. In conclusion, ARGDB provides a unified gateway to storage, retrieval, and update of information on androgen-regulated genes.

  Y Ma , S Fan , C Hu , Q Meng , S. A Fuqua , R. G Pestell , Y. A Tomita and E. M. Rosen
 

Inherited mutations of the breast cancer susceptibility gene BRCA1 confer a high risk for breast cancer development. The 300RXKK and 266KXK motifs have been identified previously as sites for acetylation of the estrogen receptor- (ER-), and 302K was also found to be a site for BRCA1-mediated mono-ubiquitination of ER- in vitro. Here we show that ER- proteins with single or double lysine mutations of these motifs (including K303R, a cancer-associated mutant) are resistant to inhibition by BRCA1, even though the mutant ER- proteins retain the ability to bind to BRCA1. We also found that BRCA1 overexpression reduced and knockdown increased the level of acetylated wild-type ER-, without changing the total ER- protein level. Increased acetylation of ER- due to BRCA1 small interfering RNA was dependent upon phosphatidylinositol 3-kinase/Akt signaling and on up-regulation of the coactivator p300. In addition, using an in vitro acetylation assay, we found that in vitro-translated wild-type BRCA1 but not a cancer-associated point mutant (C61G) inhibited p300-mediated acetylation of ER-. Furthermore, BRCA1 overexpression increased the levels of mono-ubiquitinated ER- protein, and a BRCA1 mutant that is defective for ubiquitin ligase activity but retains other BRCA1 functions (I26A) did not ubiquitinate ER- or repress its activity in vivo. Finally, ER- proteins with mutations of the 300RXKK or 266KXK motifs showed modest or no BRCA1-induced ubiquitination. We propose a model in which BRCA1 represses ER- activity, in part, by regulating the relative degree of acetylation vs. ubiquitination of ER-.

 
 
 
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