Bo-Jie Lin1, Guan-Yu Lin2, Jiang-Ying Zhu3, Guo-Qian Yin2, Dan Huang2, Yu-Yong Yan2. 1. Department of Plastic and Aesthetic Surgery, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, 530021, Guangxi Province, PR China. Electronic address: linbojie@aliyun.com. 2. Department of Plastic and Aesthetic Surgery, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, 530021, Guangxi Province, PR China. 3. Academy of Humanities and Social Sciences, Guangxi Medical University, No.22 Shuangyong Road, Nanning, 530021, Guangxi Province, PR China; Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, 530021, Guangxi Province, PR China.
Abstract
BACKGROUND: The failure of hair follicle regeneration is the major cause of alopecia, which is a highly prevalent disease worldwide. Dermal papilla (DP) cells play important role in the regulation of hair follicle regeneration. However, the molecular mechanism of how dermal papilla cells direct follicle regeneration is still to be elucidated. METHODS: In vitro DP 3D culturing and in vivo nude mice DP sphere implanted models were used to examine the molecular regulation of DP cells and follicle regeneration. qRT-PCR and Western blotting were used to detect gene and protein expression, respectively. Immunofluorescence was used to detect the expression level of Wnt10b, Ki-67 and β-catenin. Luciferase assay was used to examine the relationship among PCAT1, miR-329 and Wnt10b. ALP activity was measured by ELISA. H&E staining was used to measure follicle growth in skin tissues. RESULTS: Up-regulation of PCAT1 and Wnt10b, however, down-regulation of miR-329 were found in the in vitro 3D dermal papilla. Bioinformatics analysis and luciferase assays demonstrated that PCAT1 promoted Wnt10b expression by sponging miR-329. Knockdown of PCAT1 suppressed the proliferation and activity, as well as ALP and other DP markers of DP cells by targeting miR-329. Knockdown of PCAT1 regulated miR-329/Wnt10b axis to attenuate β-catenin expression and nucleus translocation to inhibit Wnt/β-catenin signaling. Furthermore, knockdown of PCAT1 suppressed DP sphere induced follicle regeneration and hair growth in nude mice. CONCLUSION: PCAT1 maintains characteristics of DP cells by targeting miR-329 to activating Wnt/β-catenin signaling pathway, thereby promoting hair follicle regeneration.
BACKGROUND: The failure of hair follicle regeneration is the major cause of alopecia, which is a highly prevalent disease worldwide. Dermal papilla (DP) cells play important role in the regulation of hair follicle regeneration. However, the molecular mechanism of how dermal papilla cells direct follicle regeneration is still to be elucidated. METHODS: In vitro DP 3D culturing and in vivo nude miceDP sphere implanted models were used to examine the molecular regulation of DP cells and follicle regeneration. qRT-PCR and Western blotting were used to detect gene and protein expression, respectively. Immunofluorescence was used to detect the expression level of Wnt10b, Ki-67 and β-catenin. Luciferase assay was used to examine the relationship among PCAT1, miR-329 and Wnt10b. ALP activity was measured by ELISA. H&E staining was used to measure follicle growth in skin tissues. RESULTS: Up-regulation of PCAT1 and Wnt10b, however, down-regulation of miR-329 were found in the in vitro 3D dermal papilla. Bioinformatics analysis and luciferase assays demonstrated that PCAT1 promoted Wnt10b expression by sponging miR-329. Knockdown of PCAT1 suppressed the proliferation and activity, as well as ALP and other DP markers of DP cells by targeting miR-329. Knockdown of PCAT1 regulated miR-329/Wnt10b axis to attenuate β-catenin expression and nucleus translocation to inhibit Wnt/β-catenin signaling. Furthermore, knockdown of PCAT1 suppressed DP sphere induced follicle regeneration and hair growth in nude mice. CONCLUSION: PCAT1 maintains characteristics of DP cells by targeting miR-329 to activating Wnt/β-catenin signaling pathway, thereby promoting hair follicle regeneration.