title: Transforming growth factor-beta receptor type I and type II expression during murine hair follicle development and cycling.
abstract: Although the TGF-beta family of growth factors probably regulates skin and hair follicle development, its exact role is still quite ill-defined. Here, we characterize the correlative expression pattern of the interdependent high affinity receptor proteins for TGF-beta1 and TGF-beta3, TGF-beta receptor type I (TGF-betaRI) and TGF-beta receptor type II (TGF-betaRII), during hair follicle development and cycling in C57BL/6 mice. During neonatal follicle development, TGF-betaRII immunoreactivity is confined to epithelial cells. Focal epidermal TGF-betaRII expression is seen even before actual hair placode formation. In contrast to the TGF-betaRII immunoreactivity in the outer root sheath, precortical hair matrix and inner root sheath cells were TGF-betaRII negative during hair bulb morphogenesis. TGF-betaRI (Alk-5) immunoreactivity largely overlapped the TGF-betaRII expression pattern, but was more widespread. During hair follicle cycling in adolescent mice, TGF-betaRII immunoreactivity was restricted to follicles, and was strikingly hair cycle dependent (maximal immunoreactivity: anagen VI and early catagen). Again, TGF-betaRI (Alk-5) immunoreactivity co-localized with TGF-betaRII immunoreactivity, but was more extensive. Reverse transcriptase polymerase chain reaction analysis of TGF-betaRII mRNA confirmed peak transcript levels in back skin with most hair follicles in the anagen VI-catagen transformation. mRNA levels of TGF-betaRI (Alk-5) did not vary significantly during the hair cycle, whereas those of TGF-betaRI (threonine-serine kinase 7 L) declined during early anagen, and were maximal during the anagen-catagen transition. This provides a basis for defining the choreography of TGF-beta-related signalling during hair follicle morphogenesis and cycling, introduces intraepidermal TGF-betaRII immunoreactivity as a marker for imminent follicle development, and supports the concept that both TGF-betaRII and TGF-betaRI stimulation is involved in, but not restricted to, the control of catagen induction.
authors.affiliation: Department of Dermatology, Charité, Humboldt-Universität Berlin, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Paus
authors.forename: K
authors.initials: K
authors.lastname: Foitzik
authors.forename: P
authors.initials: P
authors.lastname: Welker
authors.forename: S
authors.initials: S
authors.lastname: Bulfone-Paus
authors.forename: S
authors.initials: S
authors.lastname: Eichmüller
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development / Q000378:metabolism; D004622:Embryo, Mammalian / Q000502:physiology; D005314:Embryonic and Fetal Development; D005260:Female; D015870:Gene Expression; D018859:Hair Follicle / Q000196:embryology* / Q000254:growth & development / Q000378:metabolism*; D007536:Isomerism; D051379:Mice; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D012867:Skin / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D014018:Tissue Distribution
chemical_list: D018125:Receptors, Transforming Growth Factor beta