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Related Experiment Videos

Role of cyclic AMP in idiopathic nephrotic syndrome: a pathway involving a decrease in glomerular cell heparan

B Birmelé1, A De Agostini, E P Girardin

  • 1Départment of Pediatrics, University Hospital of Geneva, Switzerland.

Journal of Cellular Biochemistry
|June 22, 2000
PubMed
Summary

Idiopathic nephrotic syndrome involves a plasma factor that decreases heparan sulfate (HS) in kidney cells. This study reveals that cyclic adenosine monophosphate (cAMP) mediates this HS reduction, offering new insights into disease mechanisms.

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Area of Science:

  • Nephrology
  • Cellular Biology
  • Biochemistry

Background:

  • Idiopathic nephrotic syndrome (INS) is characterized by a circulating plasma factor that reduces heparan sulfate (HS) in the glomerular basement membrane.
  • Previous in vitro studies show that patient plasma decreases glomerular cell HS.

Purpose of the Study:

  • To investigate the role of cyclic adenosine monophosphate (cAMP) in the interaction between the INS plasma factor and mesangial cell HS.
  • To determine if modulation of cAMP levels affects mesangial cell HS.

Main Methods:

  • Incubation of mesangial cells with plasma from INS patients and control plasma.
  • Measurement of cellular cAMP levels.
  • Metabolic labeling to determine mesangial cell HS levels after modifying cAMP with forskolin, IBMX, or dideoxyadenosine (ddAdo).

Related Experiment Videos

  • Assessment of the effect of ddAdo preincubation on plasma-induced HS reduction.

    • Main Results:

    • Plasma from INS patients significantly increased mesangial cell cAMP levels compared to control plasma (+77%, P = 0.01).
    • Agents that increased cAMP (forskolin, IBMX) decreased HS levels, while an agent that decreased cAMP (ddAdo) increased HS levels.
    • Plasma from INS patients reduced glomerular cell HS (-34 +/- 8%, P < 0.05), an effect abolished by ddAdo preincubation.

    Conclusions:

    • In mesangial cells, plasma from INS patients elevates cAMP levels.
    • cAMP mediates the decrease in HS levels induced by the plasma factor.
    • Preventing cAMP increase inhibits the detrimental effect of the plasma factor on mesangial cell HS, suggesting cAMP's instrumental role in INS pathophysiology.