American Journal of Clinical and Experimental Medicine
Volume 3, Issue 5, September 2015, Pages: 279-282
Received: Nov. 20, 2015;
Published: Nov. 20, 2015
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Changjoon Lee, Department of Otolaryngology-Head and Neck Surgery, Chonnam National University Hospital, Gwang-ju, Republic of Korea
Hyong-Ho Cho, Department of Otolaryngology-Head and Neck Surgery, Chonnam National University Hospital, Gwang-ju, Republic of Korea
Sungsu Lee, Department of Otolaryngology-Head and Neck Surgery, Chonnam National University Hospital, Gwang-ju, Republic of Korea
An altered vascular function may be related with several inner ear diseases such as Meniere’s disease, sudden deafness, and noise-induced hearing loss. The present study was aimed to visualize the cochlear blood-labyrinth barrier and to analyze angiogenic molecules in the cochlear vasculature. Murine cochlea was obtained and its bony shell was removed. Whole mount immunostaining of endothelial cell markers, PECAM-1 and VE-cadherin, was done. There were pericytes and vascular smooth muscle cells shown. Angiogenic molecules including VEGFR2, VEGFR3, Sox17 and Dll4 were expressed. Precapillary arterioles, stria vascularis, and postcapillary venules were shown in the cochlear vasculature. The components of blood-labyrinth barrier were observed from basal turn to apical turn of the cochlea. The endothelial expression of VEGFR3, VEGFR2, and Sox17 denotes that the cochlea is not in a static, but in an active state. The robust expression of claudin-5 suggests its important role in blood-labyrinth barrier. The expression of α-SMA represents its need for vascular contraction. Visualizing cochlear vessels and determining angiogenic molecules could help to understand the pathophysiology of hearing loss ailments.
Expression of Angiogenic Molecules in Cochlear Vasculature, American Journal of Clinical and Experimental Medicine.
Vol. 3, No. 5,
2015, pp. 279-282.
K.R. Koehler, A.M. Mikosz, A.I. Molosh, D. Patel, E. Hashino, “Generation of inner ear sensory epithelia from pluripotent stem cells in 3D culture.” Nature, 2013, 500(7461), pp. 217-221.
K. Mizutari, M. Fujioka, M. Hosoya, N. Bramhall, H.J. Okano, H. Okano, A.S.B. Edge, “Notch inhibition induces cochlear hair cell regeneration and recovery of hearing after acoustic trauma,” Neuron, 2013, Vol. 77, pp.58-69.
J.P. Vasama, F.H. Linthicum, “Meniere's disease and endolymphatic hydrops without Meniere's symptoms: temporal bone histopathology,” Acta oto-laryngologica, 1999, vol. 119, pp.297-301.
F. Ihler, M. Bertlich, K. Sharaf, S. Strieth, M. Strupp, M. Canis, “Betahistine exerts a dose-dependent effect on cochlear stria vascularis blood flow in guinea pigs in vivo,” PloS one, 2012, vol.7, pp.e39086.
E.G. Nelson, R. Hinojosa, “Presbycusis: a human temporal bone study of individuals with downward sloping audiometric patterns of hearing loss and review of the literature,” The Laryngoscope, 2006, vol. 116, pp.1-12.
J.N. Brown, J.M. Miller, A.L. Nuttal, “Age-related changes in cochlear vascular conductance in mice,“ Hearing research, 1995, vol. 86, pp.189-194.
M. M. Ciccone, F. Cortese, M. Pinto, “Endothelial function and cardiovascular risk in patients with idiopathic sudden sensorineural hearing loss,” Atherosclerosis, 2012, vol.225, pp.511-516.
C. Aimoni, C. Bianchini, M. Borin, “Diabetes, cardiovascular risk factors and idiopathic sudden sensorineural hearing loss: a case-control study,” Audiology & neuro-otology, 2010, vol.15, pp.111-115.
W. Arpornchayanon, M. Canis, M. Suckfuell, F. Ihler, B. Olzowy, S. Strieth, “Modeling the measurements of cochlear microcirculation and hearing function after loud noise,” Otolaryngology--head and neck surgery, 2011, vol.145, pp.463-469.
S.H. Lee, S. Lee, H. Yang, S. Song, K. Kim, T.L. Saunders, J.K. Yoon, G.Y. Koh, I. Kim, Circulation Research, 2014, Vol115(2), pp.215-226.
N. Ferrara, H.P. Gerber, J. LeCouter, “The biology of VEGF and its receptors,” Nature Medicine, 2003, vol.9(6), pp.669-676.
M. Hellstrom, L.K. Phng, J.J. Hofmann, E. Wallgard, L. Coultas, P. Lindblom, J. Alva, A.K. Nilsson, L. Karlsson, N. Gaiano, K. Yoon, J. Rossant, M.K. Iruela-Arispe, M. Kalén, H. Gerhardt, C. Betsholtz, “Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis, “ Nature, 2007, vol445(7129), pp.776-780.
T. Tammela, G. Zarkada, H. Nurmi, L. Jakobsson, K. Heinolainen, D. Tvorogov, W. Zheng, C.A. Franco, A. Murtomäki, E. Aranda, N. Miura, S. Ylä-Herttuala, M. Fruttiger, T. Mäkinen, A. Eichmann, J.W. Pollard, H. Gerhardt, K. Alitalo.
R. Benedito, S.F. Rocha, M. Zamykal, F. Radtke, O. Casanovas, A. Duarte, B. Pytowski, R.H. Adams, “Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling,” Nature, 2012, vol.484(7392), pp.110-114.