Hearing Loss: Reestablish the Neural Plasticity in Regenerated Spiral Ganglion Neurons and Sensory Hair Cells

Edi o ial Hea ing Loss: Rees ablish he Neu al Plas ici y in Regene a ed Spi al Ganglion Neu ons and Senso y Hai Cells Renjie Chai,1,2 Geng-Lin Li,3Jian Wang,4and Jing Zou5,6 1MOE Key Labo a o y o De elopmen al Genes and Human Disease, Ins i u e o Li e Sciences, Sou heas Uni e si y, Nanjing 210096, China 2Co-Inno a ion Cen e o Neu o egene a ion, Nan ong Uni e si y, Nan ong 226001, China 3Biology Depa men , Uni e si y o Massachuse s Amhe s , Amhe s , MA 01003, USA 4School o Human Communica ion Diso de s, Dalhousie Uni e si y, 1256 Ba ing on S ee , Hali ax, NS, Canada B3J1Y6 5Depa men o O ola yngology-Head and Neck Su ge y, Changhai Hospi al, Second Mili a y Medical Uni e si y, Shanghai 200433, China 6Hea ing and Balance Resea ch Uni , School o Medicine, Uni e si y o Tampe e, L¨ a¨ ak¨ a inka u 1, Room E222, 33520 Tampe e, Finland Co espondence should be add essed o Renjie Chai; en[email p o ec ed].cn Recei ed 29 Janua y 2017; Accep ed 29 Janua y 2017; Published 20 Feb ua y 2017 Copy igh © 2017 Renjie Chai e al. This is an open access a icle dis ibu ed unde he C ea i e Commons A ibu ion License, which pe mi s un es ic ed use, dis ibu ion, and ep oduc ion in any medium, p o ided he o iginal wo k is p ope ly ci ed. Hea ing loss is conside ed as he mos common senso y diso de in human popula ion ha occu s a all ages wo ld- widely and senso ineu al hea ing loss (SNHL) is he mos common ype o hea ing loss. Va ious insul s could induce SNHL, including acous ic auma, ea and b ain umo s, aging, noise exposu e, o o o oxic medica ions o chemicals. SNHL is caused by i e e sible loss o senso y hai cells and/o degene a ion o spi al ganglion neu ons. SNHL is no ye cu able due o he lack o au oma ic egene a ion o hai cells and spi al ganglion neu ons in he cochlea. In ecen yea s, exci ing animal s udies on signaling pa hway manipula ion, gene he apy, and s em cell ansplan a ion as well as pha maceu ical agen s ha e demons a ed ha hai cells and spi al ganglion neu ons could be igge ed o egene a e, sugges ing ha hea ing loss migh be cu able e en ually in he u u e. Neu al plas ici y is he key ea u e o hai cells and spi al ganglion neu ons, and i is especially impo an o he newly egene a ed hai cells and spi al ganglion neu ons o be unc ionally in eg a ed in o audi o y pa hways. In his special issue on neu al plas ici y o hai cells and spi al ganglion neu ons, we a e pleased o p esen a se ies o a icles ha ep esen he la es ad ances in hai cell de elopmen , p o ec ion and egene a ion, spi al ganglion neu on de elopmen and p o ec ion, and inhe i ed hea ing loss. Hai Cell De elopmen . J. Hang e al. (“Synch onized P og es- sion o P es in Exp ession and Audi o y B ains em Response du ing Pos na al De elopmen in Ra s”) epo ha he onse ime o hea ing may equi e he exp ession o p es in and is de e mined by he unc ional ma u a ion o ou e hai cells. H. Nie e al. (“Plasma Memb ane Ta ge ing o P o ocadhe in 15 Is Regula ed by he Golgi-Associa ed Chape one P o ein PIST”) epo ha PIST egula es he in acellula a icking and memb ane a ge ing o he ip-link p o eins CDH23 and PCDH15 in hai cells. Hai Cell Damage and Hai Cell P o ec ion.X.Liue al. (“Analysiso heDamageMechanismRela ed oCO 2Lase Cochleos omy on Guinea Pig Cochlea”) epo ha enhanced cell-cell adhesion and ac i a ion o 𝛽-ca enin- ela ed canon- ical Wn signaling pa hway may play a ole in he p o ec ion o he cochlea om u he damage. M. Fu e al. (“The E ec s o U e hane on Ra Ou e Hai Cells”) epo ha u e hane anes hesia is expec ed o dec ease he esponses o ou e hai cells,whe eas he equencyselec i i yo he cochlea emains unchanged. X. Fu e al. (“Loss o Myh14 Inc eases Suscep ibili y o Noise-Induced Hea ing loss in CBA/CaJ Mice”) epo ha Myh14 may play a bene icial ole in he p o ec ion o he cochlea a e acous ic o e s imula ion in CBA/CaJ mice. L. Shi e al. (“Cochlea Synap opa hy Hindawi Neu al Plas ici y Volume 2017, A icle ID 1807581, 2 pages h ps://doi.o g/10.1155/2017/1807581 2Neu al Plas ici y and Noise-Induced Hidden Hea ing Loss”) p o ide a b ie e iew o add ess se e al c i ical issues ela ed o NIHHL: mechanisms o noise-induced synap ic damage, e e sibili y o synap ic damage, unc ional de ici s in NIHHL animal models, e idence o NIHHL in human subjec s, and pe iph- e al and cen al con ibu ions o NIHHL. Hai Cell Regene a ion. Y. Shu e al. (“Adeno i us Vec o s Ta ge Se e al Cell Sub ypes o Mammalian Inne Ea In Vi o”) epo ha adeno i us ec o s a e capable o e icien ly and speci ically ans ec ing di e en cell ypes in he mam- malian cochlea and he e o e p o ide use ul ools o s udy inne ea gene unc ions and e alua e gene he apies o ea ing hea ing loss and es ibula dys unc ion. X. Lu e al. (“Mammalian Cochlea Hai Cell Regene a ion and Ribbon Synapse Re o ma ion”) e iew ecen esea ch p og ess in hai cell egene a ion, synap ic plas ici y, and einne a ion o new egene a ed hai cells in he mammalian cochlea. C. Wang e al. (“E alua ion o he Hai Cell Regene a ion in Zeb a ish La ae by Measu ing and Quan i ying he S a le Responses”) epo he capabili y o a beha io al assay in nonin asi ely e alua ing hai cell unc ions o ish la ae and i s po en ial as a high- h oughpu sc eening ool o audi o y- ela ed gene and d ug disco e y. Spi al Ganglion Neu on De elopmen and P o ec ion.P.Chen e al. (“NLRP3 Is Exp essed in he Spi al Ganglion Neu ons and Associa ed wi h Bo h Synd omic and Nonsynd omic Senso ineu al Dea ness”) epo ha NLRP3 may ha e spe- ci ic unc ions in spi al ganglion neu ons ha a e al e ed in bo h synd omic and nonsynd omic senso ineu al dea ness. X.Baie al.(“P o ec i eE ec o Eda a oneonGlu ama e- Induced Neu o oxici y in Spi al Ganglion Neu ons”) in es i- ga ed he oxici y o glu ama e in spi al ganglion neu ons and hey ound ha he p o ec ion o eda a one is ela ed o he PI3K pa hway and Bcl-2 p o ein amily. Inhe i ed Hea ing Loss. X. Gu e al. (“Massi ely Pa allel Sequencing o a Chinese Family wi h DFNA9 Iden i ied a No el Missense Mu a ion in he LCCL Domain o COCH”) iden i iedamissensemu a ionin heLCCLdomaino COCH ha is absen in 100 no mal hea ing con ols and coseg ega ed wi h impai ed hea ing. J. Chen e al. (“Iden- i ica ion o a No el ENU-Induced Mu a ion in Mouse Tbx1 Linked o Human DiGeo ge Synd ome”) con i m he pa hogenic basis o Tbx1 in DGS, poin ou he c ucial ole o DNA binding ac i i y o Tbx1 o heea unc ion,and p o ide addi ional animal model o s udying mechanisms unde lying he DGS disease. Y. Guo e al. (“The Rela i e Weigh o Tempo al En elope Cues in Di e en F equency Regions o Manda in Sen ence Recogni ion”) epo ha , o Manda in Chinese, a onal language, he empo al E cues o F equency Region 1 (80–502 Hz) and Region 3 (1,022– 1,913 Hz) con ibu e mo e o he in elligence o sen ence ecogni ion han o he egions, pa icula ly he egion o 80– 502 Hz, which con ains undamen al equency (F0) in o - ma ion. L. He e al. (“Mu a ion in he Hai Cell Speci ic Gene POU4F3 Is a Common Cause o Au osomal Dominan Nonsynd omic Hea ing Loss in Chinese Hans”) epo ha mu a ions in POU4F3 a e a ela i ely common cause (3/16) o ADNSHL in Chinese Hans, which should be ou inely sc eened in such cases du ing gene ic es ing. C. Zhang e al. (“A No el Nonsense Mu a ion o POU4F3 GeneCausesAu o- somal Dominan Hea ing Loss”) epo he i s nonsense mu a ion o POU4F3 associa ed wi h p og essi e hea ing loss and explo ed he possible unde lying mechanism. The a icles in his special issue p o ide aluable insigh s in o de elopmen , p o ec ion, and egene a ion o hai cells and spi al ganglion neu ons. By highligh ing indings in hese a icles, we hope his special issue will p o ide no only new pe spec i es o u u e di ec ions in hea ing esea ch bu also po en ial he apeu ic s a egies o ea ing hea ing loss. 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