Expression of tenascin-C and the integrinα9 subunit in regeneration of rat nasal mucosa after chemical injury:: involvement in migration and proliferation of epithelial cells

被引:29
作者
Yoshimura, E
Majima, A
Sakakura, Y
Sakakura, T
Yoshida, T
机构
[1] Mie Univ, Sch Med, Dept Pathol, Tsu, Mie 5148507, Japan
[2] Mie Univ, Sch Med, Dept Otorhinolaryngol, Mie 5148507, Japan
关键词
D O I
10.1007/s004180050356
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Nasal mucosa covered by pseudostratified cillated epithelia can be injured by microbial infection and physical and chemical agents. To elucidate mechanisms of regeneration, erosion of rat nasal mucosa was produced by intranasal instillation of trichloroacetic acid, and tissue specimens were then sequentially obtained after 1-14 days. Since tenascin-C (TN-C) and its receptor, alpha 9 beta 1 integrin, are assumed to play important roles in regeneration of stratified squamous epithelia, their expression was evaluated by immunohistochemistry and in situ hybridization. Three to five days after the injury, TN-C mRNA was found in epithelial cells of migrating fronts and in epithelial sheets recovering ulcerated surfaces between the fronts and normal regions. TN-C deposition was increased under such sheets. Enhanced alpha 9 staining was also evident in the involved epithelium. 5-Bromo-2'-deoxyuridine incorporation assays revealed significant increase in proliferating cells in cell sheets over TN-C deposits at 3-7 days. Therefore, we conclude that regenerating epithelial cells produce and secrete TN-C, associated with an increase in a9 expression, and that interactions between these molecules could regulate migration and proliferation of the epithelial cells in an autocrine manner.
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页码:259 / 264
页数:6
相关论文
共 30 条
[1]   THE DISTRIBUTION OF IMMUNOREACTIVE TENASCIN IN THE EPITHELIAL-MESENCHYMAL JUNCTIONAL AREAS OF BENIGN AND MALIGNANT SQUAMOUS EPITHELIA [J].
ANBAZHAGAN, R ;
SAKAKURA, T ;
GUSTERSON, BA .
VIRCHOWS ARCHIV B-CELL PATHOLOGY INCLUDING MOLECULAR PATHOLOGY, 1990, 59 (01) :59-63
[2]   IMMUNOLOCALIZATION OF TENASCIN AND CELLULAR FIBRONECTINS IN DIVERSE GLOMERULOPATHIES [J].
ASSAD, L ;
SCHWARTZ, MM ;
VIRTANEN, I ;
GOULD, VE .
VIRCHOWS ARCHIV B-CELL PATHOLOGY INCLUDING MOLECULAR PATHOLOGY, 1993, 63 (05) :307-316
[3]   TENASCIN - AN EXTRACELLULAR-MATRIX PROTEIN INVOLVED IN TISSUE INTERACTIONS DURING FETAL DEVELOPMENT AND ONCOGENESIS [J].
CHIQUETEHRISMANN, R ;
MACKIE, EJ ;
PEARSON, CA ;
SAKAKURA, T .
CELL, 1986, 47 (01) :131-139
[4]   TENASCIN INTERFERES WITH FIBRONECTIN ACTION [J].
CHIQUETEHRISMANN, R ;
KALLA, P ;
PEARSON, CA ;
BECK, K ;
CHIQUET, M .
CELL, 1988, 53 (03) :383-390
[5]   Mitogenesis, cell migration, and loss of focal adhesions induced by tenascin-C interacting with its cell surface receptor, annexin II [J].
Chung, CY ;
MurphyUllrich, JE ;
Erickson, HP .
MOLECULAR BIOLOGY OF THE CELL, 1996, 7 (06) :883-892
[6]  
EKBLOM P, 1989, INT J DEV BIOL, V33, P771
[7]   Keratinocytes in human wounds express alpha v beta 6 integrin [J].
Haapasalmi, K ;
Zhang, K ;
Tonnesen, M ;
Olerud, J ;
Sheppard, D ;
Salo, T ;
Kramer, R ;
Clark, RAF ;
Uitto, VJ ;
Larjava, H .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1996, 106 (01) :42-48
[8]  
Hanamura N, 1997, INT J CANCER, V73, P10, DOI 10.1002/(SICI)1097-0215(19970926)73:1<10::AID-IJC2>3.0.CO
[9]  
2-4
[10]  
ILUNGA K, 1997, INT J DEV BIOL, V41, P569