pISSN 2093-3665
eISSN 2093-3673
pISSN 2093-3665
eISSN 2093-3673
The growth factors, endpoints, sources, and cell types, melatonin as a therapeutic factor, in spermatogonial stem cells
| Source | Cell | GF | Endpoint | Reference (yr) |
|---|---|---|---|---|
| Mice | Testes | - | Melatonin improve the degenerative and apoptotic changes in the basement membrane and epithelial cells of the spermatogenic tubules in testes of mice. | Hemadi et al. (2013) [30] |
| Rat | Testes | - | Melatonin decrease in the average number of caspase-3 positive cells in the seminiferous tubules is a sign of the increase of germ cells. | Abd El Aziz and Metwally (2013) [31] |
| Mice | SSCs | FBS | 1. Melatonin block the secretion of proteins caspase-3, caspase-12, and CHOP. 2. Melatonin decrease the secretion of PUMA and P53 proteins. |
Cui et al. (2017) [32] |
| Goat | Testes (SSCs c, Sertoli cells, peritubular myoid cells and Leydig cells) | FBS, SCF, fibroblast growth factor, insulin-like growth factor, GDNF | 1. Melatonin promoted proliferation and inhibit differentiation of goat SSCs. 2. Melatonin up-regulates the expression of steroidogenesis-related genes via the nuclear receptor RORα. |
Deng et al. (2017) [33] |
| Mice | SSCs | FBS | Melatonin increases MnSOD and SIRT1 expression, which decrease cell ROS and p53, respectively. | Li et al. (2018) [34] |
| Mice | SSCs, Leydig cells | FBS, EGF, bFGF, LIF, GDNF | 1. Melatonin inhibited the induction of apoptosis on Leydig cells. 2. Leydig cells secretes CSF-1 and induces the self-renewal process of SSCs. |
Du et al. (2018) [35] |
| Mice | Testes | - | Melatonin destroys the ROS due to the production of Sod, Gpx, and Cat. So, it brings the production of P-ATM and P53 to the normal level and stops cell arrest and apoptosis in SSCs. | Zhang et al. (2019) [36] |
| Mice | Testes | None | Melatonin alleviates LPS‐induced ERS and inflammation in spermatogonial stem cells. | Yang et al. (2021) [37] |
| Mice (C57BL/6 J) | Testes | - | Melatonin protect SSCs from Cr(VI)-induced damage by scavenging ROS, by suppressing ATM-p53 phosphorylation and the MAPK pathway, as well as by restoring H3K9me3 levels in cell cycle promoter and apoptosis-related regions. | Li et al. (2022) [38] |
GF, growth factor; SSC, spermatogonial stem cell; FBS, fetal bovine serum; CHOP, C/EBP homologous protein; PUMA, p53 upregulated modulator of apoptosis; SCF, stem cell factor; RORα, related orphan receptor-α; MnSOD, manganese superoxide dismutase; SIRT1, sirtuin type 1; EGF, epidermal growth factor; bFGF, basic fibroblast growth factor; LIF, leukemia inhibitory factor; GDNF, glial cell line-derived neurotrophic factor; ROS, reactive oxygen species; LPS, lipopolysaccharide; ERS, endoplasmic reticulum stress; Cr(VI), chromium; H3K9me3, histone 3 lysine 9 trimethylation; -, not applicable.
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