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Chemical Compound Review

Aminonucleoside     (2R,3R,4S,5R)-4-amino-2-(6...

Synonyms: ARDMA, SureCN346679, CHEMBL1233071, CHEBI:42839, AC1L1LML, ...
 
 
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Disease relevance of Puromycin aminonucleoside

  • During phase II, PA rats exhibited spontaneous resolution of proteinuria, impaired function, and morphologic abnormalities [1].
  • During phase I, PA rats exhibited overt nephrotic syndrome and impaired glomerular filtration, primarily due to a reduction in the glomerular capillary ultrafiltration coefficient [1].
  • In PA rats, prior glomerular hypertension was associated with development of recurrent proteinuria and extensive glomerular sclerosis, whereas concurrent CEI administration limited these parameters to values comparable to those in sham rats [1].
  • This study shows that maneuvers that modulate the glomerular macrophage number are also associated with corresponding changes in the number of proliferating cells within the mesangium, suggesting a paracrine growth stimulation by the infiltrating macrophage during acute PA nephrosis [2].
  • In contrast to the PA-HC group with hypercholesterolemia, the PA-normal group did not show hypercholesterolemia from week 16 onwards [3].
 

High impact information on Puromycin aminonucleoside

  • To test this, three maneuvers to either raise or lower the glomerular macrophage number during acute PA nephrosis (2 weeks after PA) were employed: 1) an essential fatty acid-deficient (EFAD) diet; 2) a cholesterol-supplemented diet (CSD); and 3) a single dose (600 rad) whole-body X-irradiation (XI) given to CSD-fed PA rats [2].
  • The proximity of infiltrating glomerular macrophages to the contractile mesangial cells during acute puromycin aminonucleoside (PA) nephrosis suggests the possibility of a paracrine effect on mesangial cell growth [2].
  • The EFAD diet significantly reduced both the glomerular macrophage and PCNA/cyclin-positive cell number at 2 weeks after PA with a positive correlation (r = 0.89, P < 0.05) [2].
  • METHODS: To address these questions, we analyzed the effect of the polycation, protamine sulfate (PS), and puromycin aminonucleoside (PA) on the morphology, cytoskeleton, and tyrosine phosphorylation of differentiated process-bearing cultured podocytes [4].
  • RESULTS: PS and PA induced similar profound morphological alterations, including retraction and detachment of podocyte processes from the extracellular matrix (ECM) [4].
 

Chemical compound and disease context of Puromycin aminonucleoside

  • In the present study we examined whether lipid-soluble antioxidants, probucol and vitamin E, could inhibit renal injury in rats with chronic puromycin aminonucleoside (PA) nephrosis and dietary hypercholesterolemia by protecting lipoproteins from oxidation [3].
  • The effect of the nephrotic syndrome induced by puromycin aminonucleoside (PA) in rats on specific antibody responses to 2,4 dinitrophenyl (DNP) conjugated to either spider crab haemocyanin (MSH), a T cell-dependent antigen, or hydroxyethyl starch (HES), a T cell-independent type 2 antigen were studied [5].
  • Measurement of plasma corticosterone and serum interleukin-6 revealed that these circulating factors were not involved in the elevation of plasma angiotensinogen in rats with PA-induced nephrosis [6].
  • We investigated the effects of lovastatin on glomerular MCP-1 expression and macrophage infiltration in rats with puromycin aminonucleoside (PA) nephrosis, an experimental model of renal disease characterized by early macrophage infiltration [7].
 

Biological context of Puromycin aminonucleoside

 

Anatomical context of Puromycin aminonucleoside

 

Associations of Puromycin aminonucleoside with other chemical compounds

  • To test the effects of PA on capillary wall permeability, plasma elimination rates were determined for tritium-labeled tracers of different-sized Ficolls, negatively charged Ficolls, and (14)C-labeled tracer of albumin in control and PA-treated Sprague-Dawley rats [13].
 

Gene context of Puromycin aminonucleoside

  • In the present study, gp38P, a protein homologous to rat podoplanin was cloned from mouse glomerular epithelial cells and was found to be down-regulated by PA [8].
  • Only at final PA concentrations of less than 5 microgram/ml did PHA induce normal blastogenesis [12].
  • We measured proteinuria, urine renin, and urine angiotensinogen daily, for 11 days after PA injection [14].
  • Thus, there is an attenuated natriuretic and diuretic response to ANF in rats with AMN-induced nephrotic syndrome [9].
 

Analytical, diagnostic and therapeutic context of Puromycin aminonucleoside

References

  1. Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome. Anderson, S., Diamond, J.R., Karnovsky, M.J., Brenner, B.M. J. Clin. Invest. (1988) [Pubmed]
  2. Glomerular macrophages and the mesangial proliferative response in the experimental nephrotic syndrome. Diamond, J.R., Ding, G., Frye, J., Diamond, I.P. Am. J. Pathol. (1992) [Pubmed]
  3. Dietary antioxidant inhibits lipoprotein oxidation and renal injury in experimental focal segmental glomerulosclerosis. Lee, H.S., Jeong, J.Y., Kim, B.C., Kim, Y.S., Zhang, Y.Z., Chung, H.K. Kidney Int. (1997) [Pubmed]
  4. Regulation of mouse podocyte process dynamics by protein tyrosine phosphatases rapid communication. Reiser, J., Pixley, F.J., Hug, A., Kriz, W., Smoyer, W.E., Stanley, E.R., Mundel, P. Kidney Int. (2000) [Pubmed]
  5. Hypogammaglobulinaemia in nephrotic rats is attributable to hypercatabolism of IgG. Beaman, M., Oldfield, S., MacLennan, I.C., Michael, J., Adu, D. Clin. Exp. Immunol. (1988) [Pubmed]
  6. Elevation of plasma angiotensinogen in rats with experimentally induced nephrosis. Yayama, K., Konishi, K., Ohta, A., Takano, M., Ohtani, R., Itoh, N., Okamoto, H. Nephron (1993) [Pubmed]
  7. Lovastatin reduces glomerular macrophage influx and expression of monocyte chemoattractant protein-1 mRNA in nephrotic rats. Park, Y.S., Guijarro, C., Kim, Y., Massy, Z.A., Kasiske, B.L., Keane, W.F., O'Donnell, M.P. Am. J. Kidney Dis. (1998) [Pubmed]
  8. Cloning and expression of the mouse glomerular podoplanin homologue gp38P. Boucherot, A., Schreiber, R., Pavenstädt, H., Kunzelmann, K. Nephrol. Dial. Transplant. (2002) [Pubmed]
  9. Effect of atrial natriuretic factor on renal function in rats with nephrotic syndrome. Hildebrandt, D.A., Banks, R.O. Am. J. Physiol. (1988) [Pubmed]
  10. Transforming growth factor-beta expression in macrophages during hypercholesterolemic states. Ding, G., van Goor, H., Frye, J., Diamond, J.R. Am. J. Physiol. (1994) [Pubmed]
  11. Experimental focal segmental glomerulosclerosis: correlation with protein excretion, glomerular filtration rate, and renal plasma flow. Chandra, M., Susin, M., Teichberg, S., McVicar, M. Pediatr. Res. (1984) [Pubmed]
  12. Experimental nephrosis: interassociation of proteinuria with impaired lymphocyte blastogenesis. Minchin, M.A., Bower, G.D., Turner, K.J. Clin. Exp. Immunol. (1981) [Pubmed]
  13. Mechanism of hypoalbuminemia in rodents. Koltun, M., Nikolovski, J., Strong, K., Nikolic-Paterson, D., Comper, W.D. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
  14. Urinary excretion of renin and angiotensinogen in nephrotic rats. Pedraza-Chaverrí, J., Cruz, C., Ibarra-Rubio, M.E., Hernández, C., Tapia, E., Peña, J.C. Nephron (1991) [Pubmed]
  15. Elevation of urinary IL-1beta levels during transplant associated nephropathy in rat model of the nephrotic syndrome. Higuchi, A., Fujisawa, M., Ueno, K., Kamidono, S. Urol. Res. (2002) [Pubmed]
 
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