Targeted Skin Overexpression of the Mineralocorticoid Receptor in Mice Causes Epidermal Atrophy, Premature Skin Barrier Formation, Eye Abnormalities, and Alopecia

    August 2007 in “ American Journal of Pathology ”
    Yannis Sainte–Marie, A. Toulon, Ralf Paus, Ève Maubec, Aïcha Cherfa, M Grossin, V. Descamps, Maud Clemessy, Jean Marie Gasc, Michel Peuchmaur, Adam B. Glick, Nicolette Farman, Frédéric Jaisser
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    TLDR Overexpressing the mineralocorticoid receptor in mouse skin causes skin thinning, early skin barrier development, eye issues, and hair loss.
    The document from 2007 presents a study on the effects of overexpressing the human mineralocorticoid receptor (hMR) in the skin of mice. The study found that this genetic modification led to early postnatal death, which could be prevented by antagonizing MR signaling or by administering doxycycline. The double-transgenic mice showed premature skin barrier formation, reduced hair follicle density, epidermal atrophy, increased keratinocyte apoptosis, and premature eye opening. When MR overexpression was initiated after birth, the mice developed progressive alopecia and hair follicle cysts. The study, which involved 33 mice (18 controls and 15 double-transgenic), suggests that MR signaling plays a crucial role in skin and hair follicle physiology, and its dysregulation can lead to significant abnormalities. The exact number of mice used in the study was not mentioned in all parts of the provided text.
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