The Endolymphatic Sac: A Scanning and Transmission Electron Microscopy Study

Qvortrup, Klaus; Bretlau, P

doi:10.1159/000057792

Cited by 4 publications

(4 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One may definitely speculate on a possible endocrine function, as suggested in previous papers, maybe as a local function involving the mitochondria‐rich cells, as a response to altered endolymph volume or changes in intracranial pressure. The presence of fenestrated capillaries supports the hypothesis of a potential endocrine function and is consistent with ultrastructural observations in animal studies . These observations could indicate the existence of a hormonal feedback system, which also was suggested in a recent animal study, in which the hormone angiotensinogen was found in the rat ES .…”

Section: Discussionsupporting

confidence: 90%

“…These studies overall show evidence of transcellular water transport through several different aquaporin channels located in the epithelial cells, potentially initiated by vasopressin, through its receptor located in the ES epithelium. Previously described mitochondria‐rich cells in the ES are speculated to have a key role in water transport, possibly driving the sodium‐potassium adenosine triphosphatases (Na + , K + ‐ATPases), the Na + ‐H + exchanger, as well as the two Na + ‐K + 2Cl cotransporters recently demonstrated in the human ES . In addition, the ES has been proposed to synthesize a natriuretic compound, and ultrastructural analysis has previously demonstrated morphology compatible with an endocrine activity .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxygenated fixation demonstrates novel and improved ultrastructural features of the human endolymphatic sac

2013

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Oxygenated fixation demonstrates novel and improved ultrastructural features of the human endolymphatic sac

2013

Self Cite

View full text Add to dashboard Cite

show abstract

“…The FORE cell, here genetically defined, has many similarities with a morphologically identified cell type called 'mitochondria-rich' cell. (Qvortrup and Bretlau, 2002). We would like to speculate that the FORE cell could prove to play a role in diseases characterized by altered endolymph turnover/composition, e.g.…”

Section: Discussionmentioning

confidence: 99%

Lack of pendrin expression leads to deafness and expansion of the endolymphatic compartment in inner ears ofFoxi1null mutant mice

et al. 2003

View full text Add to dashboard Cite

Mice that lack the winged helix/forkhead gene Foxi1 (also known as Fkh10) are deaf and display shaker/waltzer behavior, an indication of disturbed balance. While Foxi1 is expressed in the entire otic vesicle at E9.5, it becomes gradually restricted to the endolymphatic duct/sac epithelium and at E16.5 Foxi1 expression in the inner ear is confined to this epithelium. Histological sections, paintfill experiments and whole-mount hybridizations reveal no abnormality in inner ear development of Foxi1 -/-mice before E13.5. Between E13.5 and E16.5 the membranous labyrinth of inner ears from null mutants starts to expand as can be seen in histological sections, paint-fill experiments and three-dimensional reconstruction. Postnatally, inner ears of Foxi1 -/-mice are extremely expanded, and large irregular cavities, compressing the cerebellum and the otherwise normal middle ear, have replaced the delicate compartments of the wild-type inner ear. This phenotype resembles that of the human sensorineural deafness syndrome Pendred syndrome, caused by mutations in the PDS gene. In situ hybridization of Foxi1 -/-endolymphatic duct/sac epithelium shows a complete lack of the transcript encoding the chloride/iodide transporter pendrin. Based on this, we would like to suggest that Foxi1 is an upstream regulator of pendrin and that the phenotype seen in Foxi1 null mice is, at least in part, due to defective pendrinmediated chloride ion resorption in the endolymphatic duct/sac epithelium. We show that this regulation could be mediated by absence of a specific endolymphatic cell type -FORE (forkhead related) cells -expressing Foxi1, Pds, Coch and Jag1. Thus, mutations in FOXI1 could prove to cause a Pendred syndrome-like human deafness.

show abstract

“…These macromolecules are taken up and degraded by free-floating cells such as luminal macrophages and lymphoid cells. The ES is believed to play an important role in maintaining homeostasis in the inner ear, by the absorption and secretion of endolymph (Kimura and Schuknecht, 1965;Lundquist, 1965;Friberg et al, 1986;Erwall et al, 1988;Rask-Andersen et al, 1999), pressure regulation in the endolymphatic compartment (Rask-Andersen et al, 1987), immunodefense of the inner ear (Rask-Andersen and Stahle, 1980;Tomiyama and Harris, 1986), the removal of waste products and foreign materials from the endolymphatic space (Fukazawa et al, 1991), and endocrine function (Qvortrup and Bretlau, 2002).…”

Section: Introductionmentioning

confidence: 99%

Soluble Megalin Is Accumulated in the Lumen of the Rat Endolymphatic Sac

Ishida

Hatae

Nishi

et al. 2006

Cell Struct. Funct.

View full text Add to dashboard Cite

ABSTRACT. The endolymphatic sac (ES) is believed to play an important role in maintaining homeostasis in the inner ear by the absorption and endocytosis of endolymph. Megalin is a 600-kDa multiligand endocytic receptor expressed in certain types of absorptive epithelia including kidney proximal tubules. We analyzed the immunoreactivity for megalin in rat ES by immunofluorescence, immunogold electron microscopy, and immunoblotting. With immunostaining, the luminal substances of the ES were strongly stained for megalin. Megalin was also localized in luminal macrophage-like cells and both types of epithelial cell (mitochondria-rich cells and ribosomerich cells). In these cells, the megalin was localized in the lumen of endosomes, but was not membrane associated. This localization pattern indicates that the megalin in these cells is not a membrane receptor, but merely one of the constituents that are endocytosed from the lumen of the ES. Immunoblotting indicated that the megalin in the ES is a 210-kDa molecule lacking a cytoplasmic domain. This suggests that the megalin in the ES may be a soluble form, different from the 600-kDa membrane-bound receptor expressed in kidneys. Taken together, it is likely that the megalin in the ES lumen is a soluble component and may be endocytosed by the ES epithelial cells. Furthermore, we found that the tectorial membrane, an acellular structure in the cochlea, gave a strong megalin immunoreaction. Since the cochlea is connected to the ES, the megalin may be transported alone or with the components of the tectorial membrane from the cochlea to the ES lumen through longitudinal flow.

show abstract

The Endolymphatic Sac: A Scanning and Transmission Electron Microscopy Study

Cited by 4 publications

References 18 publications

Oxygenated fixation demonstrates novel and improved ultrastructural features of the human endolymphatic sac

Oxygenated fixation demonstrates novel and improved ultrastructural features of the human endolymphatic sac

Lack of pendrin expression leads to deafness and expansion of the endolymphatic compartment in inner ears ofFoxi1null mutant mice

Soluble Megalin Is Accumulated in the Lumen of the Rat Endolymphatic Sac

Contact Info

Product

Resources

About