Format

Send to

Choose Destination
Dev Biol. 2011 Nov 1;359(1):95-107. doi: 10.1016/j.ydbio.2011.08.030. Epub 2011 Sep 9.

Impaired stria vascularis integrity upon loss of E-cadherin in basal cells.

Author information

1
Institut für Molekularbiologie, OE5250, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany.
2
Dept. of Experimental Otology, ENT Clinics & Inst. of Audioneurotechnology (VIANNA), Medical University Hannover, Germany.
3
Abteilung für Elektronenmikroskopie, Zentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, 20251 Hamburg, Germany.
4
Institut für Molekularbiologie, OE5250, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. Electronic address: kispert.andreas@mh-hannover.de.

Abstract

In the cochlea, sensory transduction depends on the endocochlear potential (EP) and the unique composition of the endolymph, both of which are maintained by a highly specialized epithelium at the cochlear lateral wall, the stria vascularis. The generation of the EP by the stria vascularis, in turn, relies on the insulation of an intrastrial extracellular compartment by epithelial basal cells. Despite the physiological importance of basal cells, their cellular origin and the molecular pathways that lead to their differentiation are unclear. Here, we show by genetic lineage tracing in the mouse that basal cells exclusively derive from the otic mesenchyme. Conditional deletion of E-cadherin in the otic mesenchyme and its descendants does not abrogate the transition from mesenchymal precursors to epithelial basal cells. Rather, dedifferentiation of intermediate cells, altered morphology of basal and marginal cells and hearing impairment due to decreased EP in E-cadherin mutant mice demonstrate an essential role of E-cadherin in terminal basal cell differentiation and their interaction with other strial cell types to establish and maintain the functional architecture of the stria vascularis.

PMID:
21925491
DOI:
10.1016/j.ydbio.2011.08.030
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center