毛囊真皮鞘细胞中过表达Noggin对皮肤及毛囊生长的作用.

BACKGROUND: Noggin is an inhibitory molecule of bone morphogenetic protein (BMP) signaling, which can bind to BMP2/4 to form a complex, thereby blocking BMP signaling and affecting normal development. Some studies have suggested that dermal sheath cells are a kind of dermal stem cells that can self-renew for a long time, and participate in the formation of dermal papilla and dermal sheath during hair follicle regeneration. During the development of hair follicles, Noggin is involved in the induction of hair follicle regeneration, and its loss leads to a decrease in hair follicle number and slows hair follicle growth. However, little is known about the Noggin in the study of hair follicle dermal sheaths. OBJECTIVE: To study the biological function of Noggin protein in the dermal sheath of hair follicles. METHODS: The dermal sheath specific α-SMA-Cre ERT2 tool mice were used to specifically overexpress Noggin protein in the dermal sheath. At 8 and 9 days after birth, αSMA-CreER; pMES-Noggin mice in the experimental group and αSMA-CreER mice in the control group were injected with 4-hydroxytamoxifen. At 21, 23, and 28 days after birth, mouse skin tissues were obtained. Hematoxylin-eosin staining was used to observe hair follicle growth and subcutaneous fat layer thickness, and immunohistochemical staining was used to analyze cell phenotype. RESULTS AND CONCLUSION: Based on the findings of hematoxylin-eosin staining, we found that the growth of hair follicle was not affected, but the growth and development of subcutaneous adipose tissue of hair follicles were seriously impacted, presenting with the subcutaneous fat layer becoming thinned. The immunohistochemical results indicated that the decrease of BMP signaling may result in the thinning of the hair follicle fat layer. This discovery expands the understanding of dermal sheath cells and Noggin protein, and provides an important basis for more accurate understanding of hair follicle regeneration and tissue growth mechanisms. [ABSTRACT FROM AUTHOR]