Abstract
Emerging studies show that melatonin promotes cashmere development through hypodermic implantation. However, the impact and underlying mechanisms are currently unknown. In vitro study has previously demonstrated that melatonin induces cashmere growth by regulating the proliferation of goat secondary hair follicle stem cells (gsHFSCs), but there is limited information concerning the effects of melatonin on cell pluripotency. It is also known that Wnt signaling may actively participate in regulating cell proliferation and stem cell pluripotency. Therefore, in the current investigation, goat hair follicle stem cells were exposed to multiple concentrations of melatonin and different culture times to reveal the relationship between melatonin and the activation of Wnt signaling. A proportionally high Catenin beta-1 (CTNNB1) response was induced by 500 ng/L of melatonin, but it was then suppressed with the dosages over 1,000 ng/L. Greater amounts of CTNNB1 entered the cell nuclei by extending the exposure time to 72 h, which activated transcription factor 4/lymphoid enhancer-binding factor 1 and promoted the expression of the proliferation-related genes C-MYC, C-JUN, and CYCLIND1. Moreover, nuclear receptor ROR-alpha (RORα) and bone morphogenetic protein 4 (BMP4) were employed to analyze the underlying mechanism. RORα presented a sluggish concentration/time-dependent rise, but BMP4 was increased dramatically by melatonin exposure, which revealed that melatonin might participate in regulating the pluripotency of hair follicle stem cells. Interestingly, NOGGIN, which is a BMP antagonist and highly relevant to cell stemness, was also stimulated by melatonin. These findings demonstrated that melatonin exposure and/or NOGGIN overexpression in hair follicle stem cells might promote the expression of pluripotency markers Homeobox protein NANOG, Organic cation/carnitine transporter 4, and Hematopoietic progenitor cell antigen CD34. Our findings here provided a comprehensive view of Wnt signaling in melatonin stimulated cells and melatonin mediated stemness of gsHFSCs by regulating NOGGIN, which demonstrates a regulatory mechanism of melatonin enhancement on the growth of cashmere.
Highlights
Melatonin (N-acetyl-5-methoxytryptamine), a conserved pineal gland secretory product, which has been documented for more than 60 years is known to regulate many physiological events, such as circadian rhythmicity, seasonal adaptation, and reproductive changes (Johnston and Skene, 2015; Slominski et al, 2018)
Immunofluorescence and RTqPCR results suggested that melatonin mediated the activation of the Wnt pathway in goat secondary hair follicle stem cells (gsHFSCs) by modulating Catenin beta-1 (CTNNB1)
The expression of CTNNB1 reached a maximum value at 500 ng/L, abated with melatonin dosages over 1,000 ng/L (Figure 1B)
Summary
Melatonin (N-acetyl-5-methoxytryptamine), a conserved pineal gland secretory product, which has been documented for more than 60 years is known to regulate many physiological events, such as circadian rhythmicity, seasonal adaptation, and reproductive changes (Johnston and Skene, 2015; Slominski et al, 2018). The growth of cashmere is photoperiod-dependent, and shows seasonal changes in many goat breeds (Zhang et al, 2019b). Cashmere starts growing in late-summer, halts growth in mid-winter, and naturally sheds in spring. These cyclical changes shift through three periods of cell activity: anagen, catagen, and telogen (Zhang et al, 2014). Similar periodic processes of correlation have been noted between hair follicle growth and serum melatonin levels. Melatonin exhibits characteristic biological functions in regulating goat hair growth (Fu et al, 2014; Li et al, 2019; Yang et al, 2019b). There is limited information concerning the mechanism of melatonin action on hair growth
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