By a News Reporter-Staff News Editor at Gene Therapy Weekly -- Investigators discuss new findings in Biotechnology. According to news originating from Shanghai, People's Republic of China, by NewsRx correspondents, research stated, "Mutations in GJB2, which codes for the gap junction (GJ) protein connexin26 (Cx26), are the most common causes of human nonsyndromic hereditary deafness. We inoculated modified adeno-associated viral (AAV) vectors into the scala media of early postnatal conditional Gjb2 knockout mice to drive exogenous Cx26 expression."
Our news journalists obtained a quote from the research from Fudan University, "We found extensive virally expressed Cx26 in cells lining the scala media, and intercellular GJ network was re-established in the organ of Corti of mutant mouse cochlea. Widespread ectopic Cx26 expression neither formed ectopic GJs nor affected normal hearing thresholds in wild-type (WT) mice, suggesting that autonomous cellular mechanisms regulate proper membrane trafficking of exogenously expressed Cx26 and govern the functional manifestation of them. Functional recovery of GJ-mediated coupling among the supporting cells was observed. We found that both cell death in the organ of Corti and degeneration of spiral ganglion neurons in the cochlea of mutant mice were substantially reduced, although auditory brainstem responses did not show significant hearing improvement. This is the first report demonstrating that virally mediated gene therapy restored extensive GJ intercellular network among cochlear non-sensory cells in vivo."
According to the news editors, the research concluded: "Such a treatment performed at early postnatal stages resulted in a partial rescue of disease phenotypes in the cochlea of the mutant mice."
For more information on this research see: Virally expressed connexin26 restores gap junction function in the cochlea of conditional Gjb2 knockout mice. Gene Therapy, 2014;21(1):71-80. Gene Therapy can be contacted at: Nature Publishing Group, Macmillan Building, 4 Crinan St, London N1 9XW, England. (Nature Publishing Group - www.nature.com/; Gene Therapy - www.nature.com/gt/)
The news correspondents report that additional information may be obtained from Q. Yu, Fudan University, Dept. of Otolaryngol, Eye & ENT Hosp, Shanghai 200433, People's Republic of China. Additional authors for this research include Y. Wang, Q. Chang, J. Wang, S. Gong, H. Li and X. Lin (see also Biotechnology).
Keywords for this news article include: Asia, Biotechnology, Shanghai, Gene Therapy, Bioengineering, People's Republic of China
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