Effect of inhibiting prolactin secretion on secondary hair follicle development in cashmere goats

TL;DR

This study explores how blocking prolactin affects the development of secondary hair follicles in cashmere goats, revealing key genes involved in the process.

Contribution

The study identifies the Kit and Fos genes as mediators of prolactin's effect on secondary hair follicle activation in cashmere goats.

Findings

Inhibiting prolactin secretion reduced active secondary hair follicles and hair bulb width in cashmere goats.

Prolactin promotes dermal papilla cell proliferation and migration at 150 ng/mL concentration.

The Kit gene mediates prolactin's regulation of follicle activation through Fos stimulation.

Abstract

This study aims to investigate the molecular mechanisms by which inhibiting prolactin (PRL) secretion affects secondary hair follicle (SHF) development in cashmere goats.

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.

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 in vitro experiment indicated that 150 ng/mL PRL promoted (p<0.05) the proliferation and migration of DPCs.

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.

Figures