Lack of annexin 1 results in an increase in corticotroph number in male but not female mice.

Journal Article (Journal Article)

Annexin 1 (ANXA1) is a member of the annexin family of phospholipid- and calcium-binding proteins with a well demonstrated role in early delayed (30 min to 3 h) inhibitory feedback of glucocorticoids in the pituitary. We have examined corticotrophs in wild-type and ANXA1 knockout mice to determine the effects of lack of ANXA1 in male and female animals. Anterior pituitary tissue from ANXA1 wild-type, heterozygote and null mice was fixed and examined (i) by confocal immunocytochemistry to determine the number of corticotrophs and (ii) by electron microscopy to examine the size, secretory granule population and secretory machinery of corticotrophs. No differences in these parameters were detected in female mice. In male ANXA1 null mice, there were approximately four-fold more corticotrophs than in wild-type animals. However, the corticotrophs in ANXA1 null mice were smaller and had reduced numbers of secretory granules (the reduction in granules paralleled the reduction in cell size). No differences in the numerical density of folliculo-stellate, gonadotroph, lactotroph or somatotroph cells were detected in male ANXA1 null mice. Plasma corticosterone, adrenocorticotrophic hormone (ACTH) and pituitary pro-opiomelanocortin mRNA were unchanged but pituitary ACTH content was increased in male ANXA1 null mice. Interleukin (IL)-6 pituitary content was significantly elevated in male and reduced in female ANXA1 null mice compared to wild-type. In conclusion, these data indicate that ANXA1 deficiency is associated with gender-specific changes in corticotroph number and structure, via direct actions of ANXA1 and/or indirect changes in factors such as IL-6.

Full Text

Duke Authors

Cited Authors

  • Morris, JF; Omer, S; Davies, E; Wang, E; John, C; Afzal, T; Wain, S; Buckingham, JC; Flower, RJ; Christian, HC

Published Date

  • November 2006

Published In

Volume / Issue

  • 18 / 11

Start / End Page

  • 835 - 846

PubMed ID

  • 17026533

Pubmed Central ID

  • PMC1855440

International Standard Serial Number (ISSN)

  • 0953-8194

Digital Object Identifier (DOI)

  • 10.1111/j.1365-2826.2006.01481.x


  • eng

Conference Location

  • United States