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.
Renjie Chai
Geng-Lin Li
Jian Wang
Jing Zou
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