Literature DB >> 19299496

Airway delivery of low-dose miglustat normalizes nasal potential difference in F508del cystic fibrosis mice.

Bob Lubamba1, Jean Lebacq, Patrick Lebecque, Rita Vanbever, Anissa Leonard, Pierre Wallemacq, Teresinha Leal.   

Abstract

RATIONALE: N-butyldeoxynojyrimicin (NB-DNJ, miglustat [Zavesca]) an approved drug for treating Gaucher disease, was reported to be able to correct the defective trafficking of the F508del-CFTR protein.
OBJECTIVES: To evaluate the efficacy of in vivo airway delivery of miglustat for restoring ion transport in cystic fibrosis (CF).
METHODS: We used nasal transepithelial potential difference (PD) as a measure of sodium and chloride transport. The effect of nasal instillation of a single dose of miglustat was investigated in F508del, cftr knockout and normal homozygous mice. The galactose iminosugar analog N-butyldeoxygalactonojirimycin (NB-DGJ) was used as a placebo.
MEASUREMENTS AND MAIN RESULTS: In F508del mice, sodium conductance (evaluated by basal hyperpolarization) and chloride conductance (evaluated by perfusing the nasal mucosa with chloride-free solution in the presence of amiloride and forskolin) were normalized 1 hour after an intranasal dose of 50 picomoles of miglustat. Chloride conductance in the presence of 200 microM 4-4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), an inhibitor of alternative chloride channels, was much higher after miglustat than after placebo. In cftr knockout mice, a normalizing effect was observed on sodium but not on chloride conductance.
CONCLUSIONS: Our results provide clear evidence that nasal delivery of miglustat, at picomolar doses, normalizes sodium and Cftr-dependent chloride transport in F508del transgenic mice; they highlight the potential of topical miglustat as a therapy for CF.

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Year:  2009        PMID: 19299496     DOI: 10.1164/rccm.200901-0049OC

Source DB:  PubMed          Journal:  Am J Respir Crit Care Med        ISSN: 1073-449X            Impact factor:   21.405


  14 in total

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2.  Roscovitine is a proteostasis regulator that corrects the trafficking defect of F508del-CFTR by a CDK-independent mechanism.

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4.  Nasal Potential Difference to Quantify Trans-epithelial Ion Transport in Mice.

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7.  Correction of chloride transport and mislocalization of CFTR protein by vardenafil in the gastrointestinal tract of cystic fibrosis mice.

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Review 9.  Cystic fibrosis transmembrane conductance regulator modulators in cystic fibrosis: current perspectives.

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10.  Characterization of nasal potential difference in cftr knockout and F508del-CFTR mice.

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