Article

Identification of Id1 in acquired middle ear cholesteatoma

Department of Otolaryngology, Xi'an Jiao University, Xi'an, People's Republic of China.
Archives of Otolaryngology - Head and Neck Surgery (Impact Factor: 1.75). 04/2008; 134(3):306-10. DOI: 10.1001/archotol.134.3.306
Source: PubMed

ABSTRACT To determine (1) the relationship between chronic inflammatory changes in the ossicular chain area (OCA) and the formation of cholesteatoma and (2) the correlates between aberrant gene expression and abnormal proliferation of cholesteatoma.
Two hundred sixty-four ears with chronic otitis media that had undergone ear surgery were included in this study for statistical analysis of the relationship between abnormalities in the OCA and cholesteatoma. Fourteen middle ear cholesteatoma specimens were collected for immunohistochemical analysis of candidate molecules involved in the abnormal proliferation of keratinocytes. A cell model was used for verification of candidate molecule involvement.
The formation of cholesteatoma was accompanied by chronic inflammatory changes in the OCA, including granulated tissue, adhesion, and stagnating effusion. The inhibitor of the DNA-binding (Id1) gene, which is involved in controlling cell cycle progression, was abundantly expressed in cholesteatoma epithelium. In vitro studies indicate that Id1 regulated the expression of nuclear factor kappaB, cyclin D1, proliferating cell nuclear antigen, and cell cycle progression of keratinocytes,
Chronic inflammation in the OCA is closely related to the formation of cholesteatoma. The Id1/nuclear factor kappaB/cyclin D1/proliferating cell nuclear antigen signaling pathway is involved in the abnormal proliferation of keratinocytes in acquired cholesteatoma.

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    • "For example, NF-κB was reported to be found in cholesteatoma epithelium, but it appeared to be inactivated [2]. However, a recent report suggested that activated NF-κB plays a role in cellular hyperplasia of cholesteatoma [3]. Generally, in normal resting cells, NF-κB is localized within the cytoplasm as a heterodimeric complex composed of p50 and p65 subunits bound to members of the class of inhibitory proteins called inhibitor kappa B (IκB). "
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