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Articles by P Wang
Total Records ( 21 ) for P Wang
  W Gu , K. A Winters , A. S Motani , R Komorowski , Y Zhang , Q Liu , X Wu , I. C Rulifson , G Sivits , M Graham , H Yan , P Wang , S Moore , T Meng , R. A Lindberg and M. M. Veniant

Antagonism of the glucagon receptor (GCGR) is associated with increased circulating levels of glucagon-like peptide-1 (GLP-1). To investigate the contribution of GLP-1 to the antidiabetic actions of GCGR antagonism, we administered an anti-GCGR monoclonal antibody (mAb B) to wild-type mice and GLP-1 receptor knockout (GLP-1R KO) mice. Treatment of wild-type mice with mAb B lowered fasting blood glucose, improved glucose tolerance, and enhanced glucose-stimulated insulin secretion during an intraperitoneal glucose tolerance test (ipGTT). In contrast, treatment of GLP-1R KO mice with mAb B had little efficacy during an ipGTT. Furthermore, pretreatment with the GLP-1R antagonist exendin-(9–39) diminished the antihyperglycemic effects of mAb B in wild-type mice. To determine the mechanism whereby mAb B improves glucose tolerance, we generated a monoclonal antibody that specifically antagonizes the human GLP-1R. Using a human islet transplanted mouse model, we demonstrated that pancreatic islet GLP-1R signaling is required for the full efficacy of the GCGR antagonist. To identify the source of the elevated GLP-1 observed in GCGR mAb-treated mice, we measured active GLP-1 content in pancreas and intestine from db/db mice treated with anti-GCGR mAb for 8 wk. Elevated GLP-1 in GCGR mAb-treated mice was predominantly derived from increased pancreatic GLP-1 synthesis and processing. All together, these data show that pancreatic GLP-1 is a significant contributor to the glucose-lowering effects observed in response to GCGR antagonist treatment.

  V Kolla , L. W Gonzales , N. A Bailey , P Wang , S Angampalli , M. H Godinez , M Madesh and P. L. Ballard

Carcinoembryonic cell adhesion molecule 6 (CEACAM6) is a glycosylated, glycosylphosphatidylinositol (GPI)-anchored protein expressed in epithelial cells of various human tissues. It binds gram-negative bacteria and is overexpressed in cancers, where it is antiapoptotic and promotes metastases. To characterize CEACAM6 expression in developing lung, we cultured human fetal lung epithelial cells and examined responses to differentiation-promoting hormones, adenovirus expressing thyroid transcription factor-1 (TTF-1), and silencing of TTF-1 with small inhibitory RNA. Glucocorticoid and cAMP had additive stimulatory effects on CEACAM6 content, and combined treatment maximally increased transcription rate, mRNA, and protein ~10-fold. Knockdown of TTF-1 reduced hormone induction of CEACAM6 by 80%, and expression of recombinant TTF-1 increased CEACAM6 in a dose-dependent fashion. CEACAM6 content of lung tissue increased during the third trimester and postnatally. By immunostaining, CEACAM6 was present in fetal type II cells, but not mesenchymal cells, and localized to both the plasma membrane and within surfactant-containing lamellar bodies. CEACAM6 was secreted from cultured type II cells and was present in both surfactant and supernatant fractions of infant tracheal aspirates. In functional studies, CEACAM6 reduced inhibition of surfactant surface properties by proteins in vitro and blocked apoptosis of electroporated cultured cells. We conclude that CEACAM6 in fetal lung epithelial cells is developmentally and hormonally regulated and a target protein for TTF-1. Because CEACAM6 acts as an antiapoptotic factor and stabilizes surfactant function, in addition to a putative role in innate defense against bacteria, we propose that it is a multifunctional alveolar protein.

  X Guo , X Xiao , S Li , P Wang , X Jia and Q. Zhang

Objective  To identify the genetic locus for X-linked nonsyndromic high myopia in a large Chinese family.

Methods  Phenotypic information and DNA samples were collected from 19 individuals in a Chinese family; 7 had high myopia and 12 were unaffected. We performed a linkage scan on the X chromosome and sequenced several candidate genes.

Results  High myopia in this family, presenting since early childhood and ranging from –6.00 to –15.00 diopters of sphere, is consistent with an X-linked recessive trait. The presence of a normal optic disc and the absence of color visual defects and other systemic abnormalities indicated that high myopia in this family is nonsyndromic. Our linkage analysis mapped the disease locus to Xq28, a 6.1-cM region between DXS8069 and Xqter, with 2-point logarithm of odds scores greater than 2.0 for 5 markers and a maximum logarithm of odds score of 3.59 at  = 0 for 2 markers. Sequence analysis of coding and adjacent intronic regions of GPR50, PRRG3, CNGA2, and BGN did not identify any potential causative mutation.

Conclusions  Nonsyndromic high myopia in a Chinese family was mapped to the MYP1 region, which confirmed and refined this region for high myopia. In addition, our results suggest that color visual defects and optic disc hypoplasia are not necessary signs of high myopia attributed to the MYP1 region.

Clinical Relevance  MYP1 is a common and the best locus for positional cloning of the gene responsible for high myopia. Our results suggest that MYP1 is also responsible for nonsyndromic high myopia.

  Z Tian , T Ye , X Zhang , E Liu , W Wang , P Wang , G Liu , X Yang , G Hu and Z. Yu

Objective  To investigate the association between sleep duration and risk of hyperglycemia among preschool Chinese children.

Design  A population-based cross-sectional study.

Setting  Seventy-one randomly selected kindergartens in Tianjin, China.

Participants  Six hundred nineteen obese (body mass index z score ≥1.65) and 617 nonobese (body mass index z score <1.65) children aged 3 to 6 years were recruited and matched by age.

Main Exposure  Sleep duration.

Main Outcome Measures  Hyperglycemia, defined as a fasting glucose level of 100 mg/dL or higher.

Results  Obese children were more likely to have shorter sleep duration (≤8 hours) compared with their nonobese counterparts (P < .001). Compared with those who slept for 9 or 10 hours per night, those who slept for 8 hours or less had a significantly higher likelihood of having hyperglycemia, controlling for age and sex (odds ratio [OR], 1.65; 95% confidence interval [CI], 1.12-2.45). After further adjustment for other potential confounders, the association still remained statistically significant (OR, 1.64; 95% CI, 1.09-2.46). In the stratified multivariable analyses, those who were obese and slept for 8 hours or less had an increased risk of having hyperglycemia (OR, 2.12; 95% CI, 1.06-4.21) compared with those who were nonobese and slept for 9 hours or more.

Conclusions  Shorter sleep duration is associated with an increased risk of having hyperglycemia among preschool Chinese children. Whether adequate sleep may help maintain euglycemia among children, especially for those who are overweight or obese, warrants further investigation.

  P Wang , W. J Aronson , M Huang , Y Zhang , R. P Lee , D Heber and S. M. Henning

Epidemiologic, preclinical, and clinical trials suggest that green tea consumption may prevent prostate cancer through the action of green tea polyphenols including (–)-epigallocatechin-3-gallate (EGCG). To study the metabolism and bioactivity of green tea polyphenols in human prostate tissue, men with clinically localized prostate cancer consumed six cups of green tea (n = 8) daily or water (n = 9) for 3 to 6 weeks before undergoing radical prostatectomy. Using high-performance liquid chromatography, 4''-O-methyl EGCG (4''-MeEGCG) and EGCG were identified in comparable amounts, and (–)-epicatechin-3-gallate was identified in lower amounts in prostatectomy tissue from men consuming green tea (38.9 ± 19.5, 42.1 ± 32.4, and 17.8 ± 10.1 pmol/g tissue, respectively). The majority of EGCG and other green tea polyphenols were not conjugated. Green tea polyphenols were not detected in prostate tissue or urine from men consuming water preoperatively. In the urine of men consuming green tea, 50% to 60% of both (–)-epigallocatechin and (–)-epicatechin were present in methylated form with 4'-O-MeEGC being the major methylated form of (–)-epigallocatechin. When incubated with EGCG, LNCaP prostate cancer cells were able to methylate EGCG to 4''-MeEGCG. The capacity of 4''-MeEGCG to inhibit proliferation and NF-B activation and induce apoptosis in LNCaP cells was decreased significantly compared with EGCG. In summary, methylated and nonmethylated forms of EGCG are detectable in prostate tissue following a short-term green tea intervention, and the methylation status of EGCG may potentially modulate its preventive effect on prostate cancer, possibly based on genetic polymorphisms of catechol O-methyltransferase. Cancer Prev Res; 3(8); 985–93. ©2010 AACR.

  P Wang , Z Chen , Z. Q Meng , J Fan , J. M Luo , W Liang , J. H Lin , Z. H Zhou , H Chen , K Wang , Y. H Shen , Z. D Xu and L. M. Liu

Ski used to be defined as an oncogene that contributes to the resistance of tumor cells to transforming growth factor-β (TGF-β)-induced growth arrest. As TGF-β has a dual effect on tumor growth with both tumor-suppressing and -promoting activity depending on the stage of carcinogenesis and the cell type, the precise role of Ski in carcinogenesis remains unclear. In this study, we show that downregulation of Ski through lentivirus-mediated RNA interference decreases tumor growth both in vitro and in vivo, yet promotes cell invasiveness in vitro, and lung metastasis in vivo in the pancreatic cancer cell line SW1990, which contain wild-type Smad4 expression, and the BxPC3 cell line, which is Smad4 deficient. We also show that the downregulation of Ski increases TGF-β-induced transcriptional activity, which is associated with increased TGF-β-dependent Smad2/3 phosphorylation, and results in an altered expression profile of TGF-β-inducible genes involved in metastasis, angiogenesis and cell proliferation and epithelial–mesenchymal transition. Immunohistochemical analysis of specimens from 71 patients with pancreatic adenocarcinoma showed a significant association between overexpression of Ski and decreased patient survival time (P = 0.0024). Our results suggest that Ski may act as a tumor proliferation-promoting factor or as a metastatic suppressor in human pancreatic cancer.

  J. M Predmore , P Wang , F Davis , S Bartolone , M. V Westfall , D. B Dyke , F Pagani , S. R Powell and S. M. Day

Background— The ubiquitin proteasome system maintains a dynamic equilibrium of proteins and prevents accumulation of damaged and misfolded proteins, yet its role in human cardiac dysfunction is not well understood. The present study evaluated ubiquitin proteasome system function in human heart failure and hypertrophic cardiomyopathy (HCM).

Methods and Results— Proteasome function was studied in human nonfailing donor hearts, explanted failing hearts, and myectomy samples from patients with HCM. Proteasome proteolytic activities were markedly reduced in failing and HCM hearts compared with nonfailing hearts (P<0.01). This activity was partially restored after mechanical unloading in failing hearts (P<0.01) and was significantly lower in HCM hearts with pathogenic sarcomere mutations than in those lacking these mutations (P<0.05). There were no changes in the protein content of ubiquitin proteasome system subunits (ie, 11S, 20S, and 19S) or in active-site labeling of the 20S proteolytic subunit β-5 among groups to explain decreased ubiquitin proteasome system activity in HCM and failing hearts. Examination of protein oxidation revealed that total protein carbonyls, 4-hydroxynonenylated proteins, and oxidative modification to 19S ATPase subunit Rpt 5 were increased in failing compared with nonfailing hearts.

Conclusions— Proteasome activity in HCM and failing human hearts is impaired in the absence of changes in proteasome protein content or availability of proteolytic active sites. These data provide strong evidence that posttranslational modifications to the proteasome may account for defective protein degradation in human cardiomyopathies.

  L Di Biase , J. D Burkhardt , P Mohanty , J Sanchez , S Mohanty , R Horton , G. J Gallinghouse , S. M Bailey , J. D Zagrodzky , P Santangeli , S Hao , R Hongo , S Beheiry , S Themistoclakis , A Bonso , A Rossillo , A Corrado , A Raviele , A Al Ahmad , P Wang , J. E Cummings , R. A Schweikert , G Pelargonio , A Dello Russo , M Casella , P Santarelli , W. R Lewis and A. Natale

Background— Together with pulmonary veins, many extrapulmonary vein areas may be the source of initiation and maintenance of atrial fibrillation. The left atrial appendage (LAA) is an underestimated site of initiation of atrial fibrillation. Here, we report the prevalence of triggers from the LAA and the best strategy for successful ablation.

Methods and Results— Nine hundred eighty-seven consecutive patients (29% paroxysmal, 71% nonparoxysmal) undergoing redo catheter ablation for atrial fibrillation were enrolled. Two hundred sixty-six patients (27%) showed firing from the LAA and became the study population. In 86 of 987 patients (8.7%; 5 paroxysmal, 81 nonparoxysmal), the LAA was found to be the only source of arrhythmia with no pulmonary veins or other extrapulmonary vein site reconnection. Ablation was performed either with focal lesion (n=56; group 2) or to achieve LAA isolation by placement of the circular catheter at the ostium of the LAA guided by intracardiac echocardiography (167 patients; group 3). In the remaining patients, LAA firing was not ablated (n=43; group 1). At the 12±3-month follow-up, 32 patients (74%) in group 1 had recurrence compared with 38 (68%) in group 2 and 25 (15%) in group 3 (P<0.001).

Conclusions— The LAA appears to be responsible for arrhythmias in 27% of patients presenting for repeat procedures. Isolation of the LAA could achieve freedom from atrial fibrillation in patients presenting for a repeat procedure when arrhythmias initiating from this structure are demonstrated.

  P Wang , J Liu , Y Li , S Wu , J Luo , H Yang , R Subbiah , J Chatham , O Zhelyabovska and Q. Yang

Rationale: Peroxisome proliferator-activated receptors (PPARs) (, , and /β) are nuclear hormone receptors and ligand-activated transcription factors that serve as key determinants of myocardial fatty acid metabolism. Long-term cardiomyocyte-restricted PPAR deficiency in mice leads to depressed myocardial fatty acid oxidation, bioenergetics, and premature death with lipotoxic cardiomyopathy.

Objective: To explore the essential role of PPAR in the adult heart.

Methods and Results: We investigated the consequences of inducible short-term PPAR knockout in the adult mouse heart. In addition to a substantial transcriptional downregulation of lipid metabolic proteins, short-term PPAR knockout in the adult mouse heart attenuated cardiac expression of both Cu/Zn superoxide dismutase and manganese superoxide dismutase, leading to increased oxidative damage to the heart. Moreover, expression of key mitochondrial biogenesis determinants such as PPAR coactivator-1 were substantially decreased in the short-term PPAR deficient heart, concomitant with a decreased mitochondrial DNA copy number. Rates of palmitate and glucose oxidation were markedly depressed in cardiomyocytes of PPAR knockout hearts. Consequently, PPAR deficiency in the adult heart led to depressed cardiac performance and cardiac hypertrophy.

Conclusions: PPAR is an essential regulator of cardiac mitochondrial protection and biogenesis and PPAR activation can be a potential therapeutic target for cardiac disorders.

  L Di Biase , C. S Elayi , T. S Fahmy , D. O Martin , C. K Ching , C Barrett , R Bai , D Patel , Y Khaykin , R Hongo , S Hao , S Beheiry , G Pelargonio , A. D Russo , M Casella , P Santarelli , D Potenza , R Fanelli , R Massaro , P Wang , A Al Ahmad , M Arruda , S Themistoclakis , A Bonso , A Rossillo , A Raviele , R. A Schweikert , D. J Burkhardt and A. Natale

Background— Whether different ablation strategies affect paroxysmal atrial fibrillation (AF) long-term freedom from AF/atrial tachyarrhythmia is unclear. We sought to compare the effect of 3 different ablation approaches on the long-term success in patients with paroxysmal AF.

Methods and Results— One hundred three consecutive patients with paroxysmal AF scheduled for ablation and presenting in the electrophysiology laboratory in AF were selected for this study. Patients were randomized to pulmonary vein antrum isolation (PVAI; n=35) versus biatrial ablation of the complex fractionated atrial electrograms (CFAEs; n=34) versus PVAI followed by CFAEs (n=34). Patients were given event recorders and followed up at 3, 6, 9, 12, and 15 months postablation. There was no statistical significant difference between the groups in term of sex, age, AF duration, left atrial size, and ejection fraction. At 1 year follow-up, freedom from AF/atrial tachyarrhythmia was documented in 89% of patients in the PVAI group, 91% in the PVAI plus CFAEs group, and 23% in the CFAEs group (P<0.001) after a single procedure and with antiarrhythmic drugs.

Conclusion— No difference in terms of success rate was seen between PVAI alone and PVAI associated with defragmentation. CFAEs ablation alone had the smallest impact on AF recurrences at 1-year follow-up. These results suggest that antral isolation is sufficient to treat most patients with paroxysmal AF.

  D Patel , P Mohanty , L Di Biase , M Shaheen , W. R Lewis , K Quan , J. E Cummings , P Wang , A Al Ahmad , P Venkatraman , E Nashawati , D Lakkireddy , R Schweikert , R Horton , J Sanchez , J Gallinghouse , S Hao , S Beheiry , D. S Cardinal , J Zagrodzky , R Canby , S Bailey , J. D Burkhardt and A. Natale

Obstructive sleep apnea (OSA) may be associated with pulmonary vein antrum isolation (PVAI) failure. The aim of the present study was to investigate if treatment with continuous positive airway pressure (CPAP) improved PVAI success rates.

Methods and Results—

From January 2004 to December 2007, 3000 consecutive patients underwent PVAI. Patients were screened for OSA and CPAP use. Six hundred forty (21.3%) patients had OSA. Patients with OSA had more procedural failures (P=0.024) and hematomas (P<0.001). Eight percent of the non-OSA paroxysmal atrial fibrillation patients had nonpulmonary vein antrum triggers (non-PV triggers) and posterior wall firing versus 20% of the OSA group (P<0.001). Nineteen percent of the non-OSA nonparoxysmal atrial fibrillation population had non-PV triggers versus 31% in the OSA group (P=0.001). At the end of the follow-up period (32±14 months), 79% of the non-CPAP and 68% of the CPAP group were free of atrial fibrillation (P=0.003). Not using CPAP in addition to having non-PV triggers strongly predicted procedural failure (hazard ratio, 8.81; P<0.001).


OSA was an independent predictor for PVAI failure. Treatment with CPAP improved PVAI success rates. Patients not treated with CPAP in addition to having higher prevalence of non-PV triggers were 8 times more likely to fail the procedure.

  V. W Tsai , J Cooper , H Garan , A Natale , L. M Ptaszek , P. T Ellinor , K Hickey , R Downey , P Zei , H Hsia , P Wang , S Hunt , F Haddad and A. Al Ahmad

Background— Sudden cardiac death among orthotopic heart transplant recipients is an important mechanism of death after cardiac transplantation. The role for implantable cardioverter-defibrillators (ICDs) in this population is not well established. This study sought to determine whether ICDs are effective in preventing Sudden cardiac death in high-risk heart transplant recipients.

Methods and Results— We retrospectively analyzed the records of all orthotopic heart transplant patients who had ICD implantation between January 1995 and December 2005 at 5 heart transplant centers. Thirty-six patients were considered high risk for sudden cardiac death. The mean age at orthotopic heart transplant was 44±14 years, the majority being male (n=29). The mean age at ICD implantation was 52±14 years, whereas the average time from orthotopic heart transplant to ICD implant was 8 years ±6 years. The main indications for ICD implantation were severe allograft vasculopathy (n=12), unexplained syncope (n=9), history of cardiac arrest (n=8), and severe left ventricular dysfunction (n=7). Twenty-two shocks were delivered to 10 patients (28%), of whom 8 (80%) received 12 appropriate shocks for either rapid ventricular tachycardia or ventricular fibrillation. The shocks were effective in terminating the ventricular arrhythmias in all cases. Three (8%) patients received 10 inappropriate shocks. Underlying allograft vasculopathy was present in 100% (8 of 8) of patients who received appropriate ICD therapy.

Conclusions— Use of ICDs after heart transplantation may be appropriate in selected high-risk patients. Further studies are needed to establish an appropriate prevention strategy in this population.

  P Wang , N Dharmaraj , M. J Brayman and D. D. Carson

Mucin 1 (MUC1) is a type I transmembrane glycoprotein abundantly expressed on nearly all epithelial tissues and overexpressed by many cancer cells. Previous studies from our lab showed that progesterone receptor (PR)B is a strong stimulator of MUC1 gene expression. It is reported that liganded peroxisome proliferator-activated receptor (PPAR) stimulates Muc1 expression in murine trophoblast. Here, we demonstrate that although the PPAR ligand, rosiglitazone, stimulates the murine Muc1 promoter in HEC1A, a human uterine epithelial cell line, rosiglitazone alone, has no significant effect on basal human MUC1 promoter activity. In fact, rosiglitazone treatment antagonizes progesterone-stimulated human MUC1 promoter activity and protein expression in two human uterine epithelial cell lines and T47D human breast cancer cells. This response is antagonized by the PPAR antagonist, GW9662, as well as a dominant-negative form of PPAR, demonstrating the response is mediated by PPAR. Additional studies indicate that PPAR activation does not change PR binding to the MUC1 promoter but generally antagonizes progesterone activity by stimulating PRB degradation and inhibiting progesterone-induced PRB phosphorylation. Collectively, these studies indicate that PPAR activation inhibits PRB activity through both acute (phosphorylation) and long-term (PRB degradation) pathways.

  N Dharmaraj , P Wang and D. D. Carson

Mucin 1 (MUC1), a transmembrane mucin expressed at the apical surface of uterine epithelia, is a barrier to microbial infection and enzymatic attack. MUC1 loss at implantation sites appears to be required to permit embryo attachment and implantation in most species. MUC1 expression is regulated by progesterone (P) and proinflammatory cytokines, including TNF and interferon (IFN). TNF and IFN are highly expressed in uterine tissues under conditions where MUC1 expression is also high and activate MUC1 expression via their downstream transcription factors, nuclear factor (NF) B and signal transducers and activators of transcription. P receptor (PR) regulates MUC1 gene expression in a PR isoform-specific fashion. Here we demonstrate that interactions among PR isoforms and cytokine-activated transcription factors cooperatively regulate MUC1 expression in a human uterine epithelial cell line, HES. Low doses of IFN and TNF synergistically stimulate MUC1 promoter activity, enhance PRB stimulation of MUC1 promoter activity and cooperate with PRA to stimulate MUC1 promoter activity. Cooperative stimulation of MUC1 promoter activity requires the DNA-binding domain of the PR isoforms. MUC1 mRNA and protein expression is increased by cytokine and P treatment in HES cells stably expressing PRB. Using chromatin immunoprecipitation assays, we demonstrate efficient recruitment of NFB, p300, SRC3 (steroid receptor coactivator 3), and PR to the MUC1 promoter. Collectively, our studies indicate a dynamic interplay among cytokine-activated transcription factors, PR isoforms and transcriptional coregulators in modulating MUC1 expression. This interplay may have important consequences in both normal and pathological contexts, e.g. implantation failure and recurrent miscarriages.

  P Wang , F Zhu and K. Konstantopoulos

Elevated levels of prostaglandin (PG)E2 and interleukin (IL)-6 have been reported in the cartilage and synovial fluid from patients with arthritic disorders. PGE2 regulates IL-6 production in numerous different cells including macrophages and synovial fibroblasts. Although PGE2 stimulates IL-6 expression in human chondrocytes, the underlying signaling pathway of this process has yet to be delineated. Here, we investigate the mechanism of IL-6 induction in human T/C-28a2 chondrocytes treated with exogenously added PGE2. PGE2 induces IL-6 mRNA and protein expression via a cAMP-dependent pathway, reaching maximal levels after 60 min of stimulation before declining to baseline levels at 6 h. Forskolin, an adenylyl cyclase activator, also stimulates IL-6 expression in human chondrocytes in a dose- and time-dependent fashion. Inhibition of downstream effectors of cAMP activity such as protein kinase A (PKA) or phosphatidylinositol 3 kinase (PI3K) blocks PGE2- and forskolin-induced IL-6 upregulation. Simultaneous inhibition of PKA and PI3K reduces IL-6 expression in stimulated chondrocytes well below the basal levels of untreated cells. Gel shift, supershift, and chromatin immunoprecipitation assays reveal the activation and binding of the nuclear factor (NF)-B p65 subunit to the IL-6 promoter, which is markedly suppressed by selective PI3K or PKA pharmacological inhibitors. p65 knockdown completely abrogates IL-6 mRNA synthesis in PGE2- and forskolin-primed chondrocytes. Cumulatively, our data show that PGE2 and forskolin induce IL-6 expression in human chondrocytes via cAMP/PKA and PI3K-dependent pathways, which in turn regulate the activation and binding of p65 to the IL-6 promoter.

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