Isoproterenol induces mitogenesis in MCT and LLC-PK1 tubular cells

Gunter Wolf*, Eric G. Neilson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


This study assessed the effects of exogenous isoproterenol on the proliferation of the proximal tubular cell lines MCT and LLC-PK1. Both cell lines express β-adrenergic receptors as demonstrated by Scatchard analysis of binding data, receptor-cross linking studies, and mRNA expression for β2-adrenergic receptors, Isoproterenol (10-7 M) for 15 min stimulated the formation of intracellular cAMP in MCT cells (controls, 8.0 ± 0.7; isoproterenol, 12.6 ± 0.89 fmol of cAMP/μg of protein; P < 0.01). This effect was blocked by the β-receptor antagonist propranolol (10-6 M). Isoproterenol, in a dose-dependent manner, also induced proliferation in MCT and LLC-PK1 cells, as measured by (3H)thymidine incorporation and direct cell counts. Time-course experiments demonstrated maximal mitogenesis 48 h after a single dose of 10-7 M isoproterenol. This mitogenic effect was mimicked by a stable cAMP analog or cholera toxin, but not by a cGMP analog, indicating that the isoproterenol-mediated growth effects are likely caused by cAMP. These results provide evidence that isoproterenol is a mitogenic growth factor for cultured proximal tubular cells. These findings may be important in the growth mechanisms involved in the proliferative remodeling of injured tubules after acute renal failure.

Original languageEnglish (US)
Pages (from-to)1995-2002
Number of pages8
JournalJournal of the American Society of Nephrology
Issue number12
StatePublished - Jun 1994


  • Mitogenesis
  • Propranolol
  • Tubular cells
  • cAMP
  • β-receptors

ASJC Scopus subject areas

  • General Medicine


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