Miz1 Is Required for Hair Follicle Structure and Hair Morphogenesis

This study found that injecting a mixture of epidermal stem cells and dermal papilla cells can induce hair follicle regeneration and well-ordered epidermis formation in mice.

This study found that in mice, inactivating beta-catenin in the dermal papilla reduces hair follicle progenitor proliferation and disrupts the hair cycle.

Skin cells can help create early hair-like structures in lab cultures.

This study suggests that the down-regulation of 14-3-3 proteins in wild-type keratinocytes, absent in Smad4 mutant keratinocytes, might contribute to the failure of hair follicles to initiate catagen in Smad4 knockout mice.

This study found that in neonatal mice, the absence of the NG2 proteoglycan leads to reduced epidermal thickness and delayed subcutis thickening due to impaired proliferation and adipocyte deficiencies.

This study found that knocking out the transactivation domain of Miz1 in mouse keratinocytes disrupted hair follicle orientation, caused irregular pigmentation, and increased keratinocyte proliferation, indicating Miz1's role in hair follicle development and morphogenesis.

This study found that 17-beta-estradiol inhibits hair growth in mice by blocking hair follicles in the telogen phase, whereas an estrogen receptor antagonist promotes hair growth by initiating anagen.

Human hair follicles can be used to create skin-like tissue for wound healing and drug testing.

This study found that dermal papilla cells may play a critical role in hair follicle development and cycling by promoting epidermal proliferation and potentially mediating systemic factors that influence follicle behavior.