Organization of cell junctions and cytoskeleton in the reticular lamina in normal and ototoxically damaged organ of Corti

Леонова, Е. В.; Raphael, Yehoash

doi:10.1016/s0378-5955(97)00130-5

Cited by 87 publications

(77 citation statements)

References 44 publications

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“…By using methanol fixation, we were able to show that N-and E-cadherin persist at the hair cellsupporting cell junctions at P6 and beyond (see Fig. S7 in the supplementary material), thereby confirming earlier observations in the guinea pig (Leonova and Raphael, 1997). Moreover, we found that E-cadherin was nearly homogeneously distributed all along the apical circumference of OHCs and remained so during the reshaping period.…”

Section: Myosin II Myosin Viia Shroom2 and F-actin Redistribute Asysupporting

confidence: 89%

Cochlear outer hair cells undergo an apical circumference remodeling constrained by the hair bundle shape

et al. 2010

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SUMMARYEpithelial cells acquire diverse shapes relating to their different functions. This is particularly relevant for the cochlear outer hair cells (OHCs), whose apical and basolateral shapes accommodate the functioning of these cells as mechano-electrical and electromechanical transducers, respectively. We uncovered a circumferential shape transition of the apical junctional complex (AJC) of OHCs, which occurs during the early postnatal period in the mouse, prior to hearing onset. Geometric analysis of the OHC apical circumference using immunostaining of the AJC protein ZO1 and Fourier-interpolated contour detection characterizes this transition as a switch from a rounded-hexagon to a non-convex circumference delineating two lateral lobes at the neural side of the cell, with a negative curvature in between. This shape tightly correlates with the 'V'-configuration of the OHC hair bundle, the apical mechanosensitive organelle that converts sound-evoked vibrations into variations in cell membrane potential. The OHC apical circumference remodeling failed or was incomplete in all the mouse mutants affected in hair bundle morphogenesis that we tested. During the normal shape transition, myosin VIIa and myosin II (A and B isoforms) displayed polarized redistributions into and out of the developing lobes, respectively, while Shroom2 and F-actin transiently accumulated in the lobes. Defects in these redistributions were observed in the mutants, paralleling their apical circumference abnormalities. Our results point to a pivotal role for actomyosin cytoskeleton tensions in the reshaping of the OHC apical circumference. We propose that this remodeling contributes to optimize the mechanical coupling between the basal and apical poles of mature OHCs.

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Section: Myosin II Myosin Viia Shroom2 and F-actin Redistribute Asysupporting

confidence: 89%

Cochlear outer hair cells undergo an apical circumference remodeling constrained by the hair bundle shape

et al. 2010

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“…Following trauma-induced OHC loss, epithelial surface is closed by apical extensions and new F-actin belts of DCs, as shown in prior TEM studies (Forge 1985;Raphael and Altschuler 1991;Leonova and Raphael 1997). Our SBEM data bring novel insights into F-actin dynamics in this process.…”

Section: Discussionsupporting

confidence: 67%

“…In the organ of Corti, apical extensions and new Factin belts of DCs reseal the places of lost OHCs through a process referred as scar formation (Forge 1985;Raphael and Altschuler 1991;Leonova and Raphael 1997). The current SBEM analysis revealed that DC apical extensions undergo dynamic reorganization at the acute lesion site, leading to more uniform shape of scars (Fig.…”

Section: Apical Surface Closure Is Reinforced By New F-actin Beltsmentioning

confidence: 71%

How to Bury the Dead: Elimination of Apoptotic Hair Cells from the Hearing Organ of the Mouse

Anttonen

Belevich

Kirjavainen

et al. 2014

JARO

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Hair cell death is a major cause of hearing impairment. Preservation of surface barrier upon hair cell loss is critical to prevent leakage of potassium-rich endolymph into the organ of Corti and to prevent expansion of cellular damage. Understanding of wound healing in this cytoarchitecturally complex organ requires ultrastructural 3D visualization. Powered by the serial block-face scanning electron microscopy, we penetrate into the cell biological mechanisms in the acute response of outer hair cells and glial-like Deiters' cells to ototoxic trauma in vivo. We show that Deiters' cells function as phagocytes. Upon trauma, their phalangeal processes swell and the resulting close cellular contacts allow engulfment of apoptotic cell debris. Apical domains of dying hair cells are eliminated from the inner ear sensory epithelia, an event thought to depend on supporting cells' actomyosin contractile activity. We show that in the case of apoptotic outer hair cells of the organ of Corti, elimination of their apices is preceded by strong cell body shrinkage, emphasizing the role of the dying cell itself in the cleavage. Our data reveal that the resealing of epithelial surface by junctional extensions of Deiters' cells is dynamically reinforced by newly polymerized F-actin belts. By analyzing Cdc42-inactivated Deiters' cells with defects in actin dynamics and surface closure, we show that compromised barrier integrity shifts hair cell death from apoptosis to necrosis and leads to expanded hair cell and nerve fiber damage. Our results have implications concerning therapeutic protective and regenerative interventions, because both interventions should maintain barrier integrity.

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“…It is important to note that the concentrations of aminoglycoside and loop diuretic used in this study are several times higher than those used for guinea pigs and rats (e.g., Leonova and Raphael 1997;Li et al 1999), and that the damage observed in these other species progresses and is more severe (degrades to a monolayer) than that seen here. The increased resistance of mice to aminoglycoside-induced damage is not a kanamycin-specific phenomenon, as it has also been observed when either amikacin or gentamicin is administered instead of kanamycin .…”

Section: Absence Of Transition To a Monolayermentioning

confidence: 66%

Supporting Cell Characteristics in Long-deafened Aged Mouse Ears

Oesterle

Campbell

2009

JARO

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Significant sensory hair cell loss leads to irreversible hearing and balance deficits in humans and other mammals. Future therapeutic strategies to repair damaged mammalian auditory epithelium may involve inserting stem cells into the damaged epithelium, inducing non-sensory cells remaining in the epithelium to transdifferentiate into replacement hair cells via gene therapy, or applying growth factors. Little is currently known regarding the status and characteristics of the non-sensory cells that remain in the deafened auditory epithelium, yet this information is integral to the development of therapeutic treatments. A single high-dose injection of the aminoglycoside kanamycin coupled with a single injection of the loop diuretic furosemide was used to kill hair cells in adult mice, and the mice were examined 1 year after the drug insult. Outer hair cells are lost throughout the entire length of the cochlea and less than a third of the inner hair cells remain in the apical turn. Over 20% and 55% of apical organ of Corti support cells and spiral ganglion cells are lost, respectively. We examined the expression of several known support cell markers to investigate for possible support cell dedifferentiation in the damaged ears. The support cell markers investigated included the microtubule protein acetylated tubulin, the transcription factor Sox2, and the Notch signaling ligand Jagged1. Non-sensory epithelial cells remaining in the organ of Corti retain acetylated tubulin, Sox2 and Jagged1 expression, even when the epithelium has a monolayer-like appearance. These results suggest a lack of marked SC dedifferentiation in these aged and badly damaged ears.

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Organization of cell junctions and cytoskeleton in the reticular lamina in normal and ototoxically damaged organ of Corti

Cited by 87 publications

References 44 publications

Cochlear outer hair cells undergo an apical circumference remodeling constrained by the hair bundle shape

Cochlear outer hair cells undergo an apical circumference remodeling constrained by the hair bundle shape

How to Bury the Dead: Elimination of Apoptotic Hair Cells from the Hearing Organ of the Mouse

Supporting Cell Characteristics in Long-deafened Aged Mouse Ears

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