The stria vascularis (SV) is a highly vascularized tissue lining the lateral wall of the cochlea. The SV maintains cochlear fluid homeostasis, generating the endocochlear potential that is required for sound transduction. In addition, the SV acts as an important blood-labyrinth barrier, tightly regulating the passage of molecules from the blood into the cochlea. A healthy SV is therefore vital for hearing function. Degeneration of the SV is a leading cause of age-related hearing loss, and has been associated with several hearing disorders, including Norrie disease, Meniere’s disease, Alport syndrome, Waardenburg syndrome, and Cytomegalovirus-induced hearing loss. Despite the SV’s important role in hearing, there is still much that remains to be discovered, including cell-specific function within the SV, mechanisms of SV degeneration, and potential protective or regenerative therapies. In this review, we discuss recent discoveries elucidating the molecular regulatory networks of SV function, mechanisms underlying degeneration of the SV, and otoprotective strategies for preventing drug-induced SV damage. We also highlight recent clinical developments for treating SV-related hearing loss and discuss future research trajectories in the field.
The pale summer sedge caddisfly, Limnephilus hyalinus Hagen, 1861 (Limnephilidae, the Northern Caddisflies), is widespread in North America. Genome skimming by Illumina sequencing allowed assembly of a complete 15,168 bp circular mitogenome from L. hyalinus consisting of 78.0% AT nucleotides, 22 tRNAs, 13 protein-coding genes, two rRNAs and a control region in the ancestral insect gene order. Limnephilus hyalinus COX1 features an atypical CGA start codon while ATP8, NAD1, NAD5, and NAD6 exhibit incomplete stop codons. The mtTERM binding site is conserved between the Trichoptera and the Lepidoptera. Phylogenetic reconstruction reveals a monophyletic Order Trichoptera, Family Limnephilidae, and genus Limnephilus.
Myelin‐associated glycoprotein (MAG) and Nogo inhibit neurite outgrowth by binding to receptors such as NgR1, PirB and LRP1, and they have also been shown to induce phosphorylation of Smad2, a key intermediate in the transforming growth factor β (TGFβ) signalling pathway. In this study, we determined that MAG and Nogo do not transactivate the TGFβ receptor through their canonical receptors or discoidin domain receptor 1, which we identified as a novel receptor for MAG and Nogo. Instead, MAG and Nogo promoted Smad2 phosphorylation by stimulating secretion of TGFβ. Proteomic analysis of the neuronal secretome revealed that MAG also regulated the secretion of proteins that affect central nervous system plasticity—inducing the secretion of S100A6, septin‐7 and neurofascin 186, while inhibiting the secretion of frataxin, MAP6, syntenin‐1 and GAP‐43. This represents a novel function for MAG that has broad implications for the treatment for spinal cord injury.
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