Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.48 (transcriptase)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the effect of intensive statins therapy on the outcome of small-diameter vascular prosthesis, we investigated whether atorvastatin treatment (30 mg/d) could accelerate the re-endothelialization process and improve the patency rate in a canine infrarenal abdominal aorta-expanded polytetrafluoroethylene (ePTFE) bypass model. Furthermore, we also evaluated the effect of atorvastatin on the migratory and adherent capacity of circulating endothelial progenitor cells (EPCs) in vitro. Improved patency was confirmed by Doppler sonography and arteriography. Histological and scanning electron microscopy illustrated enhanced re-endothelialization process. Treatment with atorvastatin enhanced the circulating pool of EPCs with fortified migratory and adherent capacity. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that atorvastatin treatment increased endothelial nitric oxide synthase (eNOS) and kinase insert domain receptor (KDR) messenger RNA (mRNA) expression in cultured EPCs and neointima. In conclusion, intensive statin therapy could be considered a favorable option to improve small-diameter vascular graft patency.
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PMID:Intensive statin therapy: a favorable adjunct to the improvement of small-diameter vascular grafts. 2039 33

Peritoneal dialysis requires large solution volumes that increase abdominal girth and stretch the mesothelial cells of the abdominal wall. To address the hypothesis that stretch stimulates those cells to increase synthesis and production of inflammatory cytokines, we grew MeT-5A human mesothelial cells to confluence and placed the cells in growth arrest on BioFlex Collagen membranes (Flexcell International Corporation, Hillsborough, NC, U.S.A.). After 48 hours, cells were either left stationary (STA) or cycled using a 3000T system (Flexcell International Corporation) with a sinusoidal stretch (STR) frequency of 10 cycles per minute and an amplitude of 30%. The supernatant and cells of individual wells were removed at 0, 4, 12, 24, 48, 72, and 96 hours. Supernatant was assayed by ELISA for transforming growth factor beta (TGF-beta), interleukin 6 (IL-6), and vascular endothelial growth factor (VEGF). After trypsinization, the total number of viable cells in each well was estimated from the lack of trypan blue staining. Total RNA from the cells was extracted, and real-time reverse-transcriptase polymerase chain reaction was used to determine messenger RNA (mRNA) for IL-6, TGF-beta, VEGF, TGF-beta receptors 2 and 3 (TGF-beta-R2, -R3), kinase insert domain receptor (KDR), and FMS-related tyrosine kinase 1 (Flt1). Because of decline of cell numbers and viability, results for STR were compared with those for STA at each time interval up to 72 hours. The mRNA for TGF-beta, VEGF, TGF-beta-R3, and KDR were significantly higher in the STR group throughout the 72 hours, and STR IL-6 mRNA declined nonsignificantly. Normalized to the number of viable cells, supernatant IL-6, TGF-beta, and VEGF were not significantly different between the groups. We conclude that mechanical stress from mesothelial stretch does not enhance mesothelial cell secretion oflL-6, TGF-f, or VEGF, but does increase expression ofTGF-P, VEGF, and their corresponding cell receptors TGF-f-R3 and KDR.
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PMID:Stretch of human mesothelial cells increases cytokine expression. 2331 Dec 5


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