Faculty Opinions recommendation of Intrinsic regenerative potential of murine cochlear supporting cells.

2011 ◽  
Author(s):  
Andy Groves
Keyword(s):  
Supporting Cells ◽  
Cochlear Supporting Cells

scholarly journals Partial Hearing Restoration after ERBB2 Induction in Deafened Adult Mice

2019 ◽  
Author(s):  
Jingyuan Zhang ◽  
Daxiang Na ◽  
Miriam Dilts ◽  
Kenneth S. Henry ◽  
Patricia M. White
Keyword(s):  
Cell Proliferation ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Supporting Cell ◽  
Supporting Cells ◽  
Adult Mice ◽  
Hearing Thresholds ◽  
Brainstem Response ◽  
Noise Damage ◽  
Cochlear Supporting Cells

AbstractNoise induced hearing loss (NIHL) affects over ten million adults in the United States, and there is no biological treatment to restore endogenous function after damage. We hypothesized that activation of signaling from ERBB2 receptors in cochlear supporting cells could mitigate NIHL damage. We used the Tet-On genetic expression system to drive a constitutively active variant of ERBB2 (CA-ERBB2) in cochlear supporting cells three days after permanent noise damage in young adult mice. Hearing thresholds were assessed with auditory brainstem response tests prior to noise damage, and hearing recovery was assessed over a three month period. We evaluated supporting cell proliferation, inner and outer hair cell (IHC and OHC) survival, synaptic preservation, and IHC cytoskeletal alterations with histological techniques. Mice harboring CA-ERBB2 capability had similar hearing thresholds to control littermates prior to and immediately after noise exposure, and incurred similar levels of permanent hearing loss. Two and three months after noise exposure, CA-ERBB2+ mice demonstrated a partial but significant reversal of NIHL threshold shifts at the lowest frequency tested, out of five frequencies (n=19 total mice, p=0.0015, ANOVA). We also observed improved IHC and OHC survival (n=7 total cochleae, p=5 × 10−5, Kruskal-Wallis rank sum test). There was no evidence for sustained supporting cell proliferation. Some mortality was associated with doxycycline and furosemide treatments to induce the Tet-ON system. These data suggest that ERBB2 signaling in supporting cells promotes HC repair and some functional recovery. Funded by NIH R01 DC014261, and grants from the Schmitt Foundation and UR Ventures.

ATP-sensitive K+ channels (Kir6.1/SUR1) regulate gap junctional coupling in cochlear-supporting cells

2016 ◽  
Vol 468 (7) ◽  
pp. 1215-1222 ◽  
Author(s):  
Alexander Blödow ◽  
Daniela Begandt ◽  
Almke Bader ◽  
Annegret Becker ◽  
Alice Burghard ◽  
...  
Keyword(s):  
Supporting Cells ◽  
K Channels ◽  
Junctional Coupling ◽  
Cochlear Supporting Cells ◽  
Gap Junctional ◽  
Gap Junctional Coupling

scholarly journals Purinergic signaling in cochlear supporting cells reduces hair cell excitability by increasing the extracellular space

2019 ◽  
Author(s):  
Travis A. Babola ◽  
Calvin J. Kersbergen ◽  
Han Chin Wang ◽  
Dwight E. Bergles
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Extracellular Space ◽  
Molecular Mechanisms ◽  
Purinergic Signaling ◽  
Burst Firing ◽  
Supporting Cells ◽  
Cell Excitability ◽  
Sensory Pathways ◽  
Cochlear Supporting Cells

AbstractNeurons in developing sensory pathways exhibit spontaneous bursts of electrical activity that are critical for survival, maturation and circuit refinement. In the auditory system, intrinsically generated activity arises within the cochlea, but the molecular mechanisms that initiate this activity remain poorly understood. We show that burst firing of mouse inner hair cells prior to hearing onset requires P2RY1 autoreceptors expressed by inner supporting cells. P2RY1 activation triggers K+ efflux and depolarization of hair cells, as well as osmotic shrinkage of supporting cells that dramatically increased the extracellular space and speed of K+ redistribution. Pharmacological inhibition or genetic disruption of P2RY1 suppressed neuronal burst firing by reducing K+ release, but unexpectedly enhanced their tonic firing, as water resorption by supporting cells reduced the extracellular space, slowing K+ clearance. These studies indicate that purinergic signaling in supporting cells regulates hair cell excitability by controlling the volume of the extracellular space.

Mammalian cochlear supporting cells can divide and trans-differentiate into hair cells

Nature ◽  
2006 ◽  
Vol 441 (7096) ◽  
pp. 984-987 ◽  
Author(s):  
Patricia M. White ◽  
Angelika Doetzlhofer ◽  
Yun Shain Lee ◽  
Andrew K. Groves ◽  
Neil Segil
Keyword(s):  
Hair Cells ◽  
Supporting Cells ◽  
Cochlear Supporting Cells

Localization of Glucocorticoid Receptors in the Murine Inner Ear

2002 ◽  
Vol 111 (12) ◽  
pp. 1133-1138 ◽  
Author(s):  
Toshiki Shimazaki ◽  
Masashi Suzuki ◽  
Issei Ichimiya ◽  
Goro Mogi
Keyword(s):  
Inner Ear ◽  
Glucocorticoid Receptors ◽  
Spiral Ligament ◽  
Supporting Cells ◽  
Cochlear Hair Cells ◽  
Sensory Epithelia ◽  
Vestibular Sensory Epithelia ◽  
Cochlear Supporting Cells ◽  
Spiral Ganglia

We performed an immunohistochemical investigation of the distribution of glucocorticoid receptors (GRs) in the murine inner ear and found that GRs were expressed extensively, but with various degrees of immunoreactivity in different regions. We observed the strongest GR expression in the type III fibrocytes of the spiral ligament. Although the immunoreactivity of the cochlear hair cells and of the vestibular sensory epithelia was weak, the neighboring cochlear supporting cells and the subepithelial regions of the vestibular sensory epithelia were immunostained. Staining for GRs was also positive in the spiral ganglia and vestibular ganglia, as well as in the endolymphatic sac. The role of GRs in the inner ear is discussed.

scholarly journals Cochlear supporting cells function as macrophage-like cells and protect audiosensory receptor hair cells from pathogens

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yushi Hayashi ◽  
Hidenori Suzuki ◽  
Wataru Nakajima ◽  
Ikuno Uehara ◽  
Atsuko Tanimura ◽  
...  
Keyword(s):  
Hair Cells ◽  
Supporting Cells ◽  
Cochlear Supporting Cells
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