Effect of inhibiting prolactin secretion on secondary hair follicle development in cashmere goats
Effect of inhibiting prolactin secretion on secondary hair follicle development in cashmere goats
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Objective: This study aims to investigate the molecular mechanisms by which inhibiting prolactin (PRL) secretion affects secondary hair follicle (SHF) development in cashmere goats.Methods: A total of 20 cashmere goats were randomly assigned to either a bromocriptine (PRL inhibitor, BCT, 0.06 mg/kg BW) treatment (BCT+) or a control (BCT-) group. Blood and skin samples were collected monthly during telogen, and cashmere samples were collected after grow. Furthermore, the dermal papilla cells (DPCs) were isolated from SHF and cultured with PRL.Results: The results showed that the percentage of active SHF in telogen decreased (p<0.05) in the BCT+ group. The inhibition of PRL secretion reduced (p<0.05) the serum PRL concentration, and the expression of the PRL, SPRLR, Kit, and Fos genes. Transcriptome analysis of skin tissues identified differentially expressed genes. The results of the <i>in vitro</i> experiment indicated that 150 ng/mL PRL promoted (p<0.05) the proliferation and migration of DPCs.Conclusion: The Kit gene mediates PRL’s regulation of SHF activation by stimulating the activation of Fos. These findings demonstrate that inhibiting PRL secretion in telogen can reduce the number of activated SHFs and width of hair bulbs.
Abstract
Objective: This study aims to investigate the molecular mechanisms by which inhibiting prolactin (PRL) secretion affects secondary hair follicle (SHF) development in cashmere goats. Methods: A total of 20 cashmere goats were randomly assigned to either a bromocriptine (PRL inhibitor, BCT, 0.06 mg/kg BW) treatment (BCT+) or a control (BCT-) group. Blood and skin samples were collected monthly during telogen, and cashmere samples were collected after grow. Furthermore, the dermal papilla cells (DPCs) were isolated from SHF and cultured with PRL. Results: The results showed that the percentage of active SHF in telogen decreased (p<0.05) in the BCT+ group. The inhibition of PRL secretion reduced (p<0.05) the serum PRL concentration, and the expression of the PRL, SPRLR, Kit, and Fos genes. Transcrip tome analysis of skin tissues identified differentially expressed genes. The results of the in vitro experiment indicated that 150 ng/mL PRL promoted (p<0.05) the proliferation and migration of DPCs. Conclusion: The Kit gene mediates PRL’s regulation of SHF activation by stimulating the activation of Fos. These findings demonstrate that inhibiting PRL secretion in telogen can reduce the number of activated SHFs and width of hair bulbs.