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Articles by Q Cheng
Total Records ( 4 ) for Q Cheng
  Q Cheng , R Harrison and A. Zelikovsky
 

Summary: The accumulation of high-throughput genomic, proteomic and metabolical data allows for increasingly accurate modeling and reconstruction of metabolic networks. Alignment of the reconstructed networks can help to catch model inconsistencies and infer missing elements. In this note, we present the web service tool MetNetAligner which aligns metabolic networks, taking in account the similarity of network topology and the enzymes' functions. It can be used for predicting unknown pathways, comparing and finding conserved patterns and resolving ambiguous identification of enzymes. The tool supports several alignment options including allowing or forbidding enzyme deletion and insertion. It is based on a novel scoring scheme which measures enzyme-to-enzyme functional similarity and a fast algorithm which efficiently finds optimal mappings from a directed graph with restricted cyclic structure to an arbitrary directed graph.

  A. V Finn , M John , G Nakazawa , R Polavarapu , V Karmali , X Xu , Q Cheng , T Davis , C Raghunathan , E Acampado , T Ezell , S Lajoie , M Eppihimer , F. D Kolodgie , R Virmani and H. K. Gold
 

Rationale: Sirolimus-eluting coronary stents (SESs) and paclitaxel-eluting coronary stents (PESs) are used to reduce restenosis but have different sites of action. The molecular targets of sirolimus overlap with those of the peroxisome proliferator-activated receptor (PPAR) agonist rosiglitazone (RSG) but the consequence of this interaction on endothelialization is unknown.

Objective: Using the New Zealand white rabbit iliac model of stenting, we examined the effects of RSG on SESs, PESs, and bare metal stents endothelialization.

Methods and Results: Animals receiving SESs, PESs, or bare metal stents and either RSG (3 mg/kg per day) or placebo were euthanized at 28 days, and arteries were evaluated by scanning electron microscopy. Fourteen-day organ culture and Western blotting of iliac arteries and tissue culture experiments were conducted. Endothelialization was significantly reduced by RSG in SESs but not in PESs or bare metal stents. Organ culture revealed reduced vascular endothelial growth factor in SESs receiving RSG compared to RSG animals receiving bare metal stent or PESs. Quantitative polymerase chain reaction in human aortic endothelial cells (HAECs) revealed that sirolimus (but not paclitaxel) inhibited RSG-induced vascular endothelial growth factor transcription. Western blotting demonstrated that inhibition of molecular signaling in SES+RSG–treated arteries was similar to findings in HAECs treated with RSG and small interfering RNA to PPAR, suggesting that sirolimus inhibits PPAR. Transfection of HAECs with mTOR (mammalian target of rapamycin) short hairpin RNA and with Akt2 small interfering RNA significantly inhibited RSG-mediated transcriptional upregulation of heme oxygenase-1, a PPAR target gene. Chromatin immunoprecipitation assay demonstrated sirolimus interferes with binding of PPAR to its response elements in heme oxygenase-1 promoter.

Conclusions: mTOR/Akt2 is required for optimal PPAR activation. Patients who receive SESs during concomitant RSG treatment may be at risk for delayed stent healing.

  J He , Q Cheng and W. Xie
 

Steroid hormones are essential in normal physiology whereas disruptions in hormonal homeostasis represent an important etiological factor for many human diseases. Steroid hormones exert most of their functions through the binding and activation of nuclear hormone receptors (NRs or NHRs), a superfamily of DNA-binding and often ligand-dependent transcription factors. In recent years, accumulating evidence has suggested that NRs can also regulate the biosynthesis and metabolism of steroid hormones. This review will focus on the recent progress in our understanding of the regulatory role of NRs in hormonal homeostasis and the implications of this regulation in physiology and diseases.

  M Aldakkak , D. F Stowe , Q Cheng , W. M Kwok and A. K. S. Camara
 

Large-conductance Ca2+-activated K+ channels (BKCa) in the inner mitochondrial membrane may play a role in protecting against cardiac ischemia-reperfusion injury. NS1619 (30 µM), an activator of BKCa channels, was shown to increase respiration and to stimulate reactive oxygen species generation in isolated cardiac mitochondria energized with succinate. Here, we tested effects of NS1619 to alter matrix K+, H+, and swelling in mitochondria isolated from guinea pig hearts. We found that 30 µM NS1619 did not change matrix K+, H+, and swelling, but that 50 and 100 µM NS1619 caused a concentration-dependent increase in matrix K+ influx (PBFI fluorescence) only when quinine was present to block K+/H+ exchange (KHE); this was accompanied by increased mitochondrial matrix volume (light scattering). Matrix pH (BCECF fluorescence) was decreased slightly by 50 and 100 µM NS1619 but markedly more so when quinine was present. NS1619 (100 µM) caused a significant leak in lipid bilayers, and this was enhanced in the presence of quinine. The K+ ionophore valinomycin (0.25 nM), which like NS1619 increased matrix volume and increased K+ influx in the presence of quinine, caused matrix alkalinization followed by acidification when quinine was absent, and only alkalinization when quinine was present. If K+ is exchanged instantly by H+ through activated KHE, then matrix K+ influx should stimulate H+ influx through KHE and cause matrix acidification. Our results indicate that KHE is not activated immediately by NS1619-induced K+ influx, that NS1619 induces matrix K+ and H+ influx through a nonspecific transport mechanism, and that enhancement with quinine is not due to the blocking of KHE, but to a nonspecific effect of quinine to enhance current leak by NS1619.

 
 
 
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