Register for email alerts and news feeds:
This journal | BMJ Group
rss
Journal of Clinical Pathology 2003;56:587-591; doi:10.1136/jcp.56.8.587
Copyright © 2003 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.
Journal of Clinical Pathology 2003;56:587-591
© 2003 BMJ Publishing Group Ltd. & Association of Clinical Pathologists

ORIGINAL ARTICLE

p27Kip1 protein expression in Hashimoto’s thyroiditis

G Troncone, A Iaccarino, A Caleo, D Bifano, G Pettinato, L Palombini

Dipartimento di Scienze Biomorfologiche e Funzionali, University "Federico II", 80131 Naples, Italy

Correspondence to:
Correspondence to:
Dr G Troncone, Dipartimento di Scienze Biomorfologiche e Funzionali, Università di Napoli Federico II, Via S. Pansini 5, 80131 Napoli, Italia;
gitronco{at}unina.it

Aims: Hashimoto’s thyroiditis (HT) is an autoimmune disease in which both proliferation and apoptosis are enhanced. p27Kip1 protein protects tissues from disease mechanisms that involve excessive cell proliferation and apoptosis. This study investigated whether there is loss of p27Kip1 expression in HT and whether p27Kip1 immunoreactivity has any relation to the proliferative indicator Ki-67. Because p27Kip1 is regulated through either degradation, mediated by the S phase kinase associated protein 2 (Skp2), or sequestration, via D3 cyclin, the expression of these proteins was also investigated.

Methods: Immunohistochemistry was used to assess p27Kip1, Ki-67, Skp2, and cyclin D3 expression in 19 cases of HT and in 10 normal thyroids. The results were evaluated by image analysis and reported as labelling indices (LIs) in both groups.

Results: The p27Kip1 LI was lower in HT than in normal thyroid (28% v 75%; p < 0.001), whereas Ki-67 (1.13% v 0.13%), Skp2 (0.74% v 0.15%), and cyclin D3 (1.56% v 0.00%) LIs were higher in HT than in normal thyroids (p < 0.001). There was no correlation between p27Kip1 and the expression of Ki-67, Skp2, and cyclin D3.

Conclusions: p27Kip1 downregulation is not exclusive to tumours but occurs also in HT, independently of the proliferative status and of changes in Skp2 and cyclin D3 expression. Further investigation is required to understand the mechanisms leading to p27 deregulation because these observations suggest that the regulation of p27Kip1 expression in epithelial thyroid cells may play a role in HT pathogenesis.

Keywords: thyroid; Hashimoto’s thyroiditis; p27Kip1; Ki-67; Skp2; cyclin D3

Abbreviations: HT, Hashimoto’s thyroiditis; IL, interleukin; LI, labelling index; Skp2, S phase kinase associated protein 2


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

This article has been cited by other articles:

  • Troncone, G, Iaccarino, A, Russo, M, Palmieri, E A, Volante, M, Papotti, M, Viglietto, G, Palombini, L (2007). Accumulation of p27(kip1) is associated with cyclin D3 overexpression in the oxyphilic (Hurthle cell) variant of follicular thyroid carcinoma. J. Clin. Pathol. 60: 377-381 [Abstract] [Full Text]  
  • Bond, M., Sala-Newby, G. B., Newby, A. C. (2004). Focal Adhesion Kinase (FAK)-dependent Regulation of S-phase Kinase-associated Protein-2 (Skp-2) Stability: A NOVEL MECHANISM REGULATING SMOOTH MUSCLE CELL PROLIFERATION. J. Biol. Chem. 279: 37304-37310 [Abstract] [Full Text]  

This Article

Services
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.

Pathology jobs

Pathology jobs