KCNA1 and TRPC6 ion channels and NHE1 exchanger operate the biological outcome of HGF/scatter factor in renal tubular cells

Teresa Rampino, Marilena Gregorini, Cristina Guidetti, Massimo Broggini, Sergio Marchini, Riccardo Bonomi, Milena Maggio, Elisabetta Roscini, Grazia Soccio, Renza Tiboldo, Antonio Dal Canton

Research output: Contribution to journalArticlepeer-review

Abstract

Hepatocyte growth factor (HGF) is a glycoprotein that induces in vitro epithelial tubular cell growth, motility, scattering and branching morphogenesis. The cell machineries that account for HGF biological effects are still unclear. In previous study, we found that HGF upregulated in epithelial tubular cell line (HK2) 3 genes: potassium channel KCNA1, calcium channel (transient receptor potential channel, subfamily C, member 6, TRPC6) and Na+/H+ exchanger-1 (NHE1). In this study, we validated these results with reverse transcription PCR and WB analysis. To investigate whether KCNA1, TRPC6, NHE1 mediate the changes induced by HGF in HK2, we studied the effects of their inhibitors: 4-aminopyridine, charybdotoxin, dendrotoxin K inhibitors of KCNA1, lanthanum, N-(p-amylcinnamoyl) anthranilic acid inhibitors of TRPC6, 5-(N-ethyl-N-isopropyl)amiloride, cariporide inhibitors of NHE1. The inhibitors prevented HGF-induced growth, migration, cytoskeletal reorganization and tubulogenesis in HK2. These results indicate that KCNA1, TRPC6 and NHE1 are cell machineries that are exploited by HGF to effect its biological outcome in renal tubular cells.

Original languageEnglish
Pages (from-to)382-391
Number of pages10
JournalGrowth Factors
Volume25
Issue number6
DOIs
Publication statusPublished - Dec 2007

Keywords

  • Calcium channel
  • Na/H exchanger-1
  • Potassium channel

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Endocrinology
  • Cell Biology

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