Expression of transforming growth factor-beta 1 in rat embryohic cochlea

doi:10.3969/j.issn.2095-4344.2013.46.004

Abstract

Abstract:

BACKGROUND: Many researches on the development of cochlea have been made, but mainly depend on the pathological conditions and developmental deformity, while the researches on the development process of normal embryonic cochlea and expression of related factors are rare.
OBJECTIVE: To investigate the expression of transforming growth factor β1 in rat embryonic cochlea.
METHODS: Fifty-six Sprague Dawley rats were selected and the rats were pregnancy, and the embryos were obtained from the rats, trimmed the inner ear specimens under the anatomical microscope, and then the specimens were treated with dehydration, decalcification, directly paraffin embedding and slicing processing. The morphology evolution of inner cochlea was observed under light microscope after hematoxylin-eosin staining. The expression of transforming growth factor β1 in rat embryonic cochlea was observed by immunohistochemical streptavidin biotin-peroxidase complex method.
RESULTS AND CONCLUSION: The development of rat inner ear began in ectoderm thickening area of E8 phase, otocyst and the emergency of the mesenchymal could be seen in E9 phase, otocyst and ossicular chain began to develop in E9.5 phase, formation of cochlear duct anlage could be seen in E12.5 phase, cochlea tube development was completed in E18.5 phase and Corti’s formation could be seen in E16 phase. The structure and function of the inner ear could be fully developed after birth. The expression of transforming growth factor β1 could be seen in E12.5-E19 phases, and the expression was changed from weak to strong and then weakened further, and strongest in E14.5 phase. This suggested that transforming growth factor β1 may be involved during the development of rat cochlear epithelium.

Key words: transforming growth factor beta, cochlea, embryonic development, rats, Sprague-Dawley

CLC Number:

R318

Li Cui-e, Shi Yan-li. Expression of transforming growth factor-beta 1 in rat embryohic cochlea[J]. Chinese Journal of Tissue Engineering Research, 2013, 17(46): 8000-8003.

Figures/Tables 2

References

[1]赵玉林,董明敏,李晓萍,等.小鼠耳蜗发育的形态学研究[J].解剖学杂志,2000,23(1):69-72.
[2]Romand R, Dollé P, Hashino E. Retinoid signaling in inner ear development. J Neurobiol. 2006;66(7):687-704.
[3]Liu J, Johnson K, Li J,et al. Regenerative phenotype in mice with a point mutation in transforming growth factor beta type I receptor (TGFBR1). Proc Natl Acad Sci U S A. 2011;108(35): 14560-14565.
[4]Matsunobu T, Torigoe K, Ishikawa M,et al. Critical roles of the TGF-beta type I receptor ALK5 in perichondrial formation and function, cartilage integrity, and osteoblast differentiation during growth plate development. Dev Biol. 2009;332(2): 325-338.
[5]Yang SM, Hou ZH, Yang G,et al. Chondrocyte-specific Smad4 gene conditional knockout results in hearing loss and inner ear malformation in mice. Dev Dyn. 2009;238(8):1897-1908.
[6]Li XS, Sun JJ, Jiang W,et al. Effect on cochlea function of guinea pig after controlled release recombinant human bone morphogenetic protein 2. Chin Med J (Engl). 2010;123(1): 84-88.
[7]Liu X, Chen Q, Kuang C,et al. A 4.3 kb Smad7 promoter is able to specify gene expression during mouse development. Biochim Biophys Acta. 2007;1769(2):149-152.
[8]Mukherjee A, Dong SS, Clemens T,et al. Co-ordination of TGF-beta and FGF signaling pathways in bone organ cultures. Mech Dev. 2005;122(4):557-571.
[9]Teng Y, Kanasaki K, Bardeesy N,et al. Deletion of Smad4 in fibroblasts leads to defective chondrocyte maturation and cartilage production in a TGFβ type II receptor independent manner. Biochem Biophys Res Commun. 2011;407(4): 633-639.
[10]Martinez-Alvernia EA, Mankarious LA. Matrix metalloproteinases 2 and 9 are concentrated in the luminal aspect of the cricoid cartilage, diminish with loss of perichondrium, and are reinstated by transforming growth factor beta 3. Ann Otol Rhinol Laryngol. 2008;117(12): 925-930.
[11]Kryger ZB, Sisco M, Roy NK,et al. Temporal expression of the transforming growth factor-Beta pathway in the rabbit ear model of wound healing and scarring. J Am Coll Surg. 2007; 205(1):78-88.
[12]Anderson CF, Lira R, Kamhawi S,et al. IL-10 and TGF-beta control the establishment of persistent and transmissible infections produced by Leishmania tropica in C57BL/6 mice. J Immunol. 2008;180(6):4090-4097.
[13]Satoh H, Billings P, Firestein GS,et al. Transforming growth factor beta expression during an inner ear immune response. Ann Otol Rhinol Laryngol. 2006;115(1):81-88.
[14]Kel JM, Girard-Madoux MJ, Reizis B,et al. TGF-beta is required to maintain the pool of immature Langerhans cells in the epidermis. J Immunol. 2010;185(6):3248-3255.
[15]Lee YW, Chung Y, Juhn SK,et al. Activation of the transforming growth factor beta pathway in bacterial otitis media. Ann Otol Rhinol Laryngol. 2011;120(3):204-213.
[16]Tateossian H, Hardisty-Hughes RE, Morse S,et al. Regulation of TGF-beta signalling by Fbxo11, the gene mutated in the Jeff otitis media mouse mutant. Pathogenetics. 2009;2(1):5.
[17]Zhao SQ, Li J, Liu H,et al. Role of interleukin-10 and transforming growth factor beta 1 in otitis media with effusion. Chin Med J (Engl). 2009;122(18):2149-2154.
[18]McCullar JS, Oesterle EC. Cellular targets of estrogen signaling in regeneration of inner ear sensory epithelia. Hear Res. 2009;252(1-2):61-70.
[19]Simeone DM, Zhang L, Graziano K,et al. Smad4 mediates activation of mitogen-activated protein kinases by TGF-beta in pancreatic acinar cells. Am J Physiol Cell Physiol. 2001; 281(1):C311-319.
[20]Wissel K, Wefstaedt P, Miller JM,et al. Differential brain-derived neurotrophic factor and transforming growth factor-beta expression in the rat cochlea following deafness. Neuroreport. 2006;17(12):1297-1301.
[21]Frenz DA, Liu W. Treatment with all-trans-retinoic acid decreases levels of endogenous TGF-beta(1) in the mesenchyme of the developing mouse inner ear. Teratology. 2000;61(4):297-304.
[22]Butts SC, Liu W, Li G,et al. Transforming growth factor-beta1 signaling participates in the physiological and pathological regulation of mouse inner ear development by all-trans retinoic acid. Birth Defects Res A Clin Mol Teratol. 2005; 73(4):218-228.
[23]Paradies NE, Sanford LP, Doetschman T, et al. Developmental expression of the TGF beta s in the mouse cochlea. Mech Dev. 1998;79(1-2):165-168.
[24]赵玉林,李晓萍,董明敏.转化生长因子在小鼠内耳发育中作用的研究[J].中国民政医学杂志, 2002,14(2):72-73.
[25]Kawamoto K, Yagi M, Stöver T,et al. Hearing and hair cells are protected by adenoviral gene therapy with TGF-beta1 and GDNF. Mol Ther. 2003;7(4):484-492.
[26]Malgrange B, Rigo JM, Coucke P,et al. Identification of factors that maintain mammalian outer hair cells in adult organ of Corti explants. Hear Res. 2002;170(1-2):48-58.
[27]Kim HJ, Kang KY, Baek JG, et al. Expression of TGFbeta family in the developing internal ear of rat embryos. J Korean Med Sci. 2006;21(1):136-142.