Expression patterns of aquaporins in the inner ear: evidence for concerted actions of multiple types of aquaporins to facilitate water transport in the cochlea

Huang, Daixin; Chen, Ping; Chen, Shanping; Nagura, Mitsuyoshi; Lim, David J.; Lin, Xiaobo

doi:10.1016/s0378-5955(02)00288-5

Cited by 77 publications

(67 citation statements)

References 23 publications

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“…1Fii, G). Aquaporin-1 (aqp1) has been reported as a marker of type III fibrocytes in guinea pigs (Stankovic et al 1995), mice (Li andVerkman 2001;Huang et al 2002), and rats (Sawada et al 2003). In agreement with these observations, an anti-aqp1 antibody labeled type III fibrocytes, mesenchymal cells lining scala tympani, and mesenchymal cells underlying the basilar membrane of guinea pig cochlea ( Fig.…”

Section: Expression Of Type III Fibrocyte Markers In Cells Derived Frsupporting

confidence: 65%

“…Most notably, these included the presence of prominent stress fibers (Henson et al 1985;Kuhn and Vater 1997) that we determined contained αsma both in vivo and in vitro. The cells also expressed recognized type III fibrocyte markers such as nmII (Henson et al 1985), aqp1 (Stankovic et al 1995;Li and Verkman 2001;Huang et al 2002;Sawada et al 2003), andcx43 (Forge et al 2003). The cells could generate prolonged contractility within a collagenous substrate, assumed to be a primary property of type III fibrocytes in vivo (Henson et al 1984;Naidu and Mountain 2007).…”

Section: Contractile Type III Fibrocytes Can Be Derived From the Cultmentioning

confidence: 99%

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Contractility in Type III Cochlear Fibrocytes Is Dependent on Non-muscle Myosin II and Intercellular Gap Junctional Coupling

Kelly

Forge

Jagger

2012

JARO

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The cochlear spiral ligament is a connective tissue that plays diverse roles in normal hearing. Spiral ligament fibrocytes are classified into functional subtypes that are proposed to carry out specialized roles in fluid homeostasis, the mediation of inflammatory responses to trauma, and the fine tuning of cochlear mechanics. We derived a secondary sub-culture from guinea pig spiral ligament, in which the cells expressed protein markers of type III or "tension" fibrocytes, including non-muscle myosin II (nmII), α-smooth muscle actin (αsma), vimentin, connexin43 (cx43), and aquaporin-1. The cells formed extensive stress fibers containing αsma, which were also associated intimately with nmII expression, and the cells displayed the mechanically contractile phenotype predicted by earlier modeling studies. cx43 immunofluorescence was evident within intercellular plaques, and the cells were coupled via dye-permeable gap junctions. Coupling was blocked by meclofenamic acid (MFA), an inhibitor of cx43-containing channels. The contraction of collagen lattice gels mediated by the cells could be prevented reversibly by blebbistatin, an inhibitor of nmII function. MFA also reduced the gel contraction, suggesting that intercellular coupling modulates contractility. The results demonstrate that these cells can impart nmII-dependent contractile force on a collagenous substrate, and support the hypothesis that type III fibrocytes regulate tension in the spiral ligament-basilar membrane complex, thereby determining auditory sensitivity.

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Section: Expression Of Type III Fibrocyte Markers In Cells Derived Frsupporting

confidence: 65%

Section: Contractile Type III Fibrocytes Can Be Derived From the Cultmentioning

confidence: 99%

Contractility in Type III Cochlear Fibrocytes Is Dependent on Non-muscle Myosin II and Intercellular Gap Junctional Coupling

Kelly

Forge

Jagger

2012

JARO

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“…Gap junction coupling could provide extensive spatial buffering, as seen in astrocytes (Leis et al, 2005) and retinal Müller cells (Karwoski et al, 1989). The widespread localization of gap junction channels, K/Cl cotransporters (Boettger et al, 2002), and aquaporins (Huang et al, 2002) could provide a passive mechanism of K ϩ buffering and osmotic homeostasis. In the brain, comparable energy-independent mechanisms ensure rapid siphoning and redistribution of K ϩ .…”

Section: Discussionmentioning

confidence: 99%

Compartmentalized and Signal-Selective Gap Junctional Coupling in the Hearing Cochlea

Jagger¹,

Forge²

2006

J. Neurosci.

102

114

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“…The signal intensities of spots were extracted from the scanned images by using CodeLink Expression Analysis Software (version 4.1; GE Healthcare) and imported into GeneSpring 7.3 (Silicon Genetics, Redwood City, CA) for further data analyses. Details of real-time PCR amplifications were given in our previous publication (22). The starting amount of mRNA in samples was quantified relatively by setting the threshold cycle (C t ) at a linear increasing phase of PCR amplifications.…”

mentioning

confidence: 99%

Restoration of connexin26 protein level in the cochlea completely rescues hearing in a mouse model of human connexin30-linked deafness

Ahmad

Tang²,

Chang³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

117

132

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Mutations in genes coding for connexin26 (Cx26) and/or Cx30 are linked to approximately half of all cases of human autosomal nonsyndromic prelingual deafness. Cx26 and Cx30 are the two major Cx isoforms found in the cochlea, and they coassemble to form hybrid (heteromeric and heterotypic) gap junctions (GJs). This molecular arrangement implies that homomeric GJs would remain in the cochlea if one of the coassembly partners were mutated resulting in null expression. We generated mice in which extra copies of the Cx26 gene were transgenically expressed from a modified bacterial artificial chromosome in a Cx30 ؊/؊ background. In the absence of the Cx30 gene, Cx26 expressed from extra alleles completely restored hearing sensitivity and prevented hair cell death in deaf Cx30 ؊/؊ mice. The results indicated that hybrid GJs consisting of Cx26 and Cx30 were not essential for normal hearing in mice and suggested that up-regulation of Cx26 or slowing down its protein degradation might be a therapeutic strategy to prevent and treat deafness caused by Cx30 mutations.gap junction ͉ hearing rescue ͉ hereditary deafness

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Expression patterns of aquaporins in the inner ear: evidence for concerted actions of multiple types of aquaporins to facilitate water transport in the cochlea

Cited by 77 publications

References 23 publications

Contractility in Type III Cochlear Fibrocytes Is Dependent on Non-muscle Myosin II and Intercellular Gap Junctional Coupling

Contractility in Type III Cochlear Fibrocytes Is Dependent on Non-muscle Myosin II and Intercellular Gap Junctional Coupling

Compartmentalized and Signal-Selective Gap Junctional Coupling in the Hearing Cochlea

Restoration of connexin26 protein level in the cochlea completely rescues hearing in a mouse model of human connexin30-linked deafness

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