Lack of pendrin HCO3 transport elevates vestibular endolymphatic [Ca ] by inhibition of acid-sensitive TRPV5 and TRPV6 channels

نویسندگان

  • Kazuhiro Nakaya
  • Donald G. Harbidge
  • Philine Wangemann
  • Bruce D. Schultz
  • Eric D. Green
  • Susan M. Wall
  • Daniel C. Marcus
چکیده

Kazuhiro Nakaya, Donald G. Harbidge, Philine Wangemann, Bruce D. Schultz, Eric D. Green, Susan M. Wall, and Daniel C. Marcus Cellular Biophysics Laboratory, Cell Physiology Laboratory, and Epithelial Cell Biology Laboratory, Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas; Department of Otolaryngology-Head and Neck Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan; Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland; and Renal Division, Emory University School of Medicine, Atlanta, Georgia

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منابع مشابه

Lack of pendrin HCO3- transport elevates vestibular endolymphatic [Ca2+] by inhibition of acid-sensitive TRPV5 and TRPV6 channels.

The low Ca(2+) concentration ([Ca(2+)]) of mammalian endolymph in the inner ear is required for normal hearing and balance. We reported (Yamauchi et al., Biochem Biophys Res Commun 331: 1353-1357, 2005) that the epithelial Ca(2+) channels TRPV5 and TRPV6 (transient receptor potential types 5 and 6) are expressed in the vestibular system and that TRPV5 expression is stimulated by 1,25-dihydroxyv...

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Loss of cochlear HCO3 secretion causes deafness via endolymphatic acidification and inhibition of Ca reabsorption in a Pendred syndrome mouse model

Wangemann P, Nakaya K, Wu T, Maganti RJ, Itza EM, Sanneman JD, Harbidge DG, Billings S, Marcus DC. Loss of cochlear HCO3 secretion causes deafness via endolymphatic acidification and inhibition of Ca reabsorption in a Pendred syndrome mouse model. Am J Physiol Renal Physiol 292: F1345–F1353, 2007. First published February 13, 2007; doi:10.1152/ajprenal.00487.2006.— Pendred syndrome, characteriz...

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Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model.

Pendred syndrome, characterized by childhood deafness and postpuberty goiter, is caused by mutations of SLC26A4, which codes for the anion exchanger pendrin. The goal of the present study was to determine how loss of pendrin leads to hair cell degeneration and deafness. We evaluated pendrin function by ratiometric microfluorometry, hearing by auditory brain stem recordings, and expression of K(...

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Direct Interaction with Rab11a Targets the Epithelial Ca Channels TRPV5 and TRPV6 to the Plasma Membrane

TRPV5 and TRPV6 are the most Ca -selective members of the transient receptor potential (TRP) family of cation channels and play a pivotal role in the maintenance of Ca balance in the body. However, little is known about the mechanisms controlling the plasma membrane abundance of these channels to regulate epithelial Ca transport. In this study, we demonstrated the direct and specific interactio...

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Expression of transient receptor potential vanilloid channels TRPV5 and TRPV6 in retinal pigment epithelium

PURPOSE Hydration and ionic composition of the subretinal space (SRS) is modulated by the retinal pigment epithelium (RPE). In particular calcium concentration (Ca(2+)) in the SRS varies with light exposure, and although this change is regulated by RPE transport activity, the specific transport proteins involved have yet to be defined. Two members of the transient receptor potential vanilloid f...

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تاریخ انتشار 2007