Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1832588 (PSS)
 2,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four sulfonic acid polymers [poly(4-styrenesulfonic acid)(PSS), poly(anetholesulfonic acid)(PAS), poly(vinylsulfonic acid)(PVS), poly(2-acrylamido-2-methyl-1-propanesulfonic acid)(PAMPS)] have been found to inhibit the cytopathicity of HIV-1 and HIV-2 in MT-4 cells at concentrations that are not toxic to the host cells. The sulfonic acid polymers also inhibited syncytium formation in co-cultures of MOLT-4 cells with HIV-1- or HIV-2-infected HUT-78 cells. They also inhibited binding of anti-gp120 mAb to HIV-1 gp120 and blocked adsorption of HIV-1 virions to MT-4 cells. PSS and PAS, but not PVS and PAMPS, interfered with the binding of OKT4A/Leu3a to the CD4 receptor. The anti-HIV activity of these polyanionic compounds can be ascribed to inhibition of the gp120-CD4 interaction. Sulfonic acid polymers represent a lead of anti-HIV compounds that warrant further evaluation of their therapeutic potential.
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PMID:Sulfonic acid polymers as a new class of human immunodeficiency virus inhibitors. 138 28

The sulfonic acid polymers poly(2-acrylamido-2-methyl-1-propanesulfonic acid) (PAMPS), poly(4-styrenesulfonic acid) (PSS), and poly(anetholesulfonic acid) (PAS) proved to be highly potent inhibitors of angiogenesis in the chick chorioallantoic membrane (CAM) assay. PAMPS was found to achieve a dose-dependent inhibition of microvessel formation in the CAM assay ranging from 57 +/- 16% inhibition at 10 micrograms/disc to 72 +/- 15% at 150 micrograms/ disc. Also, PSS and PAS caused a strong inhibition of angiogenesis (55 +/- 19% and 48 +/- 16%, respectively, at 50 micrograms/disc), whereas poly(vinylsulfonic acid) (PVS) was found to be inactive at this dose. The compounds proved to be nontoxic for the developing chick embryo at these doses. Suramin, which was included as a reference compound, caused only a slight inhibition of vascular density, at a dose of 150 micrograms/disc, whereas pentosan polysulfate (PPS) was found to be toxic. PAMPS, PAS, and PSS, but not PVS, inhibited microvessel formation in the rat aorta-ring assay. In addition, the increased [3H-methyl]dThd uptake in endothelial cells in vitro upon stimulation with basic fibroblast growth factor (bFGF) was inhibited by PAMPS, PAS, and PSS at 20 micrograms/ml. A strong correlation (r = 0.95) was found between the antiangiogenic effect of the sulfonic acid polymers in the CAM assay and their inhibition of the bFGF-induced mitogenic response, indicating that bFGF is the target for these sulfonic acid polymers. These results suggest that sulfonic acid polymers, and in particular PAMPS, may be considered as specific, nontoxic angiogenesis inhibitors.
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PMID:The sulfonic acid polymers PAMPS [poly(2-acrylamido-2-methyl-1-propanesulfonic acid)] and related analogues are highly potent inhibitors of angiogenesis. 926 88

Basic fibroblast growth factor (FGF-2) interacts with high-affinity tyrosine-kinase fibroblast growth factor receptors (FGFRs) and low-affinity heparan sulfate proteoglycans (HSPGs) in target cells. Both interactions are required for FGF-2-mediated biological responses. Here we report the FGF-2 antagonist activity of novel synthetic sulfonic acid polymers with distinct chemical structures and molecular masses (MMs). PAMPS [poly(2-acrylamido-2-methyl-1-propanesulfonic acid)], (MM approximately 7,000-10,000), PAS [poly(anetholesulfonic acid)], (MM approximately 9,000-11,000), PSS [poly(4-styrenesulfonic acid)], (MM = 70,000), and poly(vinylsulfonic acid) (MM = 2,000), inhibited FGF-2 binding to HSPGs and FGFRs in fetal bovine aortic endothelial GM 7373 cells. They also abrogated the formation of the HSPG/FGF-2/FGFR ternary complex, as evidenced by their capacity to prevent FGF-2-mediated cell-cell attachment of FGFR-1-overexpressing, HSPG-deficient Chinese hamster ovary cells to wild-type HSPG-bearing cells. Direct interaction of the polysulfonates with FGF-2 was demonstrated by their ability to protect the growth factor from proteolytic cleavage. Accordingly, molecular modeling, based on the crystal structure of the interaction of FGF-2 with a heparin hexamer, showed the feasibility of docking PAMPS into the heparin-binding domain of FGF-2. In agreement with their FGF-2-binding capacity, PSS, PAS, and PAMPS inhibited FGF-2-induced cell proliferation in GM 7373 cells and murine brain microvascular endothelial cells. The antiproliferative activity of these compounds was associated with the abrogation of FGF-2-induced tyrosine phosphorylation of FGFR-1. Moreover, the polysulfonates PSS and PAS inhibited FGF-2-induced activation of mitogen-activated protein kinase-1/2, involved in FGF-2 signal transduction. In conclusion, sulfonic acid polymers bind FGF-2 by mimicking heparin interaction. These compounds may provide a tool to inhibit FGF-2-induced endothelial cell proliferation in angiogenesis and tumor growth.
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PMID:Modulation of fibroblast growth factor-2 receptor binding, signaling, and mitogenic activity by heparin-mimicking polysulfonated compounds. 1038 2

Polyelectrolyte multilayers (PEMs) are now widely used for bioanalytical applications. In this work, a bilayer of poly(diallydimethylammonium chloride) (PDDA) and poly(sodium 4-styrenesulfonate) (PSS) is consecutively adsorbed on 3-mercapto-1-propanesulfonic acid modified Au electrode surfaces, forming stable, ultrathin multilayer films. Subsequently, Prussian blue nanoparticles protected by PDDA (denoted as P-PB) and negatively charged glucose oxidase (GOx) are consecutively adsorbed onto the PSS-terminated bilayer. The growth of each of the P-PB/GOx bilayers is followed quantitatively using UV-visible absorption spectroscopy and the electrochemical method. The P-PB nanoparticles can catalyze the electroreduction of hydrogen peroxide formed from enzymatic reaction at lower potential and inhibit the responses of interferents, such as ascorbic acid (AA) and uric acid (UA). Performance of the multilayer films can be tailored by controlling the number of bilayers. Under optimal conditions, a linear range of 0.10 to 11.0 mM and a detection limit of 10 microM were achieved. The glucose biosensor has good stability and reproducibility.
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PMID:Multilayer membranes via layer-by-layer deposition of organic polymer protected Prussian blue nanoparticles and glucose oxidase for glucose biosensing. 1620 46

Novel flexible NH(3) gas sensors were formed by the in situ self-assembly of polypyrrole (PPy) on plastic substrates. A negatively charged substrate was prepared by the formation of an organic monolayer (3-mercapto-1-propanesulfonic acid sodium salt-MPS) on a polyester (PET) substrate using a pair of comb-like Au electrodes. Two-cycle poly(4-styrenesulfonic acid) sodium salt/poly(allylamine hydrochloride) (PSS/PAH) bilayers (precursor layer) were then layer-by-layer (LBL) deposited on an MPS-modified substrate. Finally, a monolayer of PPy self-assembled in situ and PPy multilayer thin films self-assembled LBL in situ on a (PSS/PAH)(2)/MPS/Au/Cr/PET substrate. The thin films were analyzed by atomic force microscopy (AFM). The effects of the precursor layer (PSS), the deposition time of the monolayer of PPy and the number of PPy multilayers on the gas sensing properties (response) and the flexibility of the sensors were investigated to optimize the fabrication of the film. Additionally, other sensing properties such as sensing linearity, reproducibility, response and recovery times, as well as cross-sensitivity effects were studied. The flexible NH(3) gas sensor exhibited a strong response that was comparable to or even greater than that of sensors that were fabricated on rigid substrate at room temperature.
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PMID:Flexible NH3 sensors fabricated by in situ self-assembly of polypyrrole. 1983 49