The Roles of Collagen XVIII and Its Endostatin Domain in Wound Healing, Hair Follicle Cycling, and Bone Development

January 2009

Lotta Seppinen

collagen XVIII endostatin hair follicle cycling Wnt/beta-catenin signaling angiogenesis

Studysummary This study suggests that collagen XVIII and its variant endostatin may play a role in regulating Wnt-signaling in hair follicles, affecting wound healing and skeletal development in mice.

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The study explored the roles of collagen XVIII and its endostatin domain in wound healing, hair follicle cycling, and bone development. Collagen XVIII, a basement membrane proteoglycan, had variants that influenced Wnt/beta-catenin signaling. The C-terminal domain, endostatin, inhibited tumor growth and angiogenesis. Lack of collagen XVIII accelerated wound healing, while endostatin overexpression delayed it and caused abnormal wound capillaries. In bone development, collagen XVIII deficiency led to delayed ossification, but changes were mild and transient. In hair follicle cycling, endostatin overexpression delayed growth due to impaired angiogenesis, while lack of collagen XVIII accelerated the hair cycle onset. The study suggested that collagen XVIII, particularly its longest variant, might regulate Wnt-signaling in hair follicles.

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