Hypertrichosis is one of the most common side effects of systemic
cyclosporine A therapy. It has been previously shown that
cyclosporine A induces anagen and inhibits catagen development in mice. In the present study, to explore the mechanisms of
cyclosporine A, we investigated the effects of
cyclosporine A on hair shaft elongation, hair follicle cell proliferation, apoptosis, and
mRNA expression of selected
growth factors using an organ culture model of mouse vibrissae. In this model,
cyclosporine A stimulated hair growth of normal mouse vibrissae follicles by inhibiting catagen-like development and promoting matrix cell proliferation. In addition,
cyclosporine A caused an increase in the expression of
vascular endothelial growth factor (
VEGF),
hepatocyte growth factor (HGF), and
nerve growth factor (
NGF), and inhibited
follistatin expression. Our findings provide an explanation for the clinically observed effects of
cyclosporine A on hair growth. The mouse vibrissae organ culture offers an attractive model for identifying factors involved in the modulation of hair growth.