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

Citation
Cheung, L. Y. M., et al. “Sox21 Deletion In Mice Causes Postnatal Growth Deficiency Without Physiological Disruption Of Hypothalamic-Pituitary Endocrine Axes.”. Molecular And Cellular Endocrinology, pp. 213-223.
Center University of Michigan
Author Leonard Y M Cheung, Hideyuki Okano, Sally A Camper
Keywords hypothalamus, Metabolism, Pituitary, SOX21, SoxB1
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.

Year of Publication
2017
Journal
Molecular and cellular endocrinology
Volume
439
Number of Pages
213-223
Date Published
12/2017
ISSN Number
1872-8057
DOI
10.1016/j.mce.2016.09.005
Alternate Journal
Mol. Cell. Endocrinol.
PMID
27616671
PMCID
PMC5123967
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