| Literature DB >> 33095425 |
Rui Hua1, Qing-Jun Chu1, Yao Zhou1, Xuan Zhou1, Da-Xiong Huang1, Yong-Tong Zhu2.
Abstract
At present, infertile patients with maturation arrest (MA) are difficult to obtain mature sperm. Spermatogenesis and its molecular mechanism are still not clear. Patients with MA and normal spermatogenesis (NS) were collected. iTRAQ-based proteomic approach was performed to reveal the different proteins between them. To validate the confidence of proteome data, the individual samples were analyzed by Western blotting (WB), quantitative polymerase chain reaction (qPCR), and immunofluorescence. The miR-449a and CEP55 were determined by Luciferase assay. Mouse GC-1 cells were transfected with CEP55 siRNAs, miR-449a mimic, or inhibitor, and cell proliferation was determined. Compared with NS, 27 proteins were differentially expressed in MA, and CEP55 protein was the most significant difference. WB and qPCR showed that CEP55 levels were significantly elevated in NS than MA. In transfected cells, overexpression of miR-449a and knockdown of CEP55 both downregulated CEP55 expression and decreased cell proliferation. miR-449a suppresses mouse spermatogonia proliferation via inhibition of CEP55.Entities:
Keywords: CEP55; Proliferation; Spermatogonia; miR-449a
Year: 2020 PMID: 33095425 DOI: 10.1007/s43032-020-00354-9
Source DB: PubMed Journal: Reprod Sci ISSN: 1933-7191 Impact factor: 3.060