Sox21 deletion in mice causes postnatal growth deficiency without physiological disruption of hypothalamic-pituitary endocrine axes

Leonard Y M Cheung, Hideyuki Okano, Sally A. Camper

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The hypothalamic-pituitary axes are the coordinating centers for multiple endocrine gland functions and physiological processes. Defects in the hypothalamus or pituitary gland can cause reduced growth and severe short stature, affecting approximately 1 in 4000 children, and a large percentage of cases of pituitary hormone deficiencies do not have an identified genetic cause. SOX21 is a protein that regulates hair, neural, and trophoblast stem cell differentiation. Mice lacking Sox21 have reduced growth, but the etiology of this growth defect has not been described. We studied the expression of Sox21 in hypothalamic-pituitary development and examined multiple endocrine axes in these mice. We find no evidence of reduced intrauterine growth, food intake, or physical activity, but there is evidence for increased energy expenditure in mutants. In addition, despite changes in pituitary hormone expression, hypothalamic-pituitary axes appear to be functional. Therefore, SOX21 variants may be a cause of non-endocrine short stature in humans.

Original languageEnglish
Pages (from-to)213-223
Number of pages11
JournalMolecular and Cellular Endocrinology
Volume439
DOIs
Publication statusPublished - 2017 Jan 5

Fingerprint

Pituitary Hormones
Growth
Physiological Phenomena
Endocrine Glands
Defects
Neural Stem Cells
Trophoblasts
Pituitary Gland
Stem cells
Hair
Energy Metabolism
Hypothalamus
Cell Differentiation
Eating
Exercise
Proteins

Keywords

  • Hypothalamus
  • Metabolism
  • Pituitary
  • SOX21
  • SoxB1

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Cite this

Sox21 deletion in mice causes postnatal growth deficiency without physiological disruption of hypothalamic-pituitary endocrine axes. / Cheung, Leonard Y M; Okano, Hideyuki; Camper, Sally A.

In: Molecular and Cellular Endocrinology, Vol. 439, 05.01.2017, p. 213-223.

Research output: Contribution to journalArticle

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