The cryopreservation of spermatozoa was introduced in the 1960s as a route to fertility preservation. Despite the extensive progress that has been made in this field, the biological and biochemical mechanisms involved in cryopreservation have not been thoroughly elucidated to date. Various factors during the freezing process, including sudden temperature changes, ice formation and osmotic stress, have been proposed as reasons for poor sperm quality post-thaw. Little is known regarding the new aspects of sperm cryobiology, such as epigenetic and proteomic modulation of sperm and trans-generational effects of sperm freezing. This article reviews recent reports on molecular and cellular modifications of spermatozoa during cryopreservation in order to collate the existing understanding in this field. The aim is to discuss current freezing techniques and novel strategies that have been developed for sperm protection against cryo-damage, as well as evaluating the probable effects of sperm freezing on offspring health.

Oligodendrocytes are myelinating cells in the central nervous system that form the myelin sheath of axons to support rapid nerve conduction. Human endometrial stromal cells (EnSCs) are the abundant and easy available source for cell replacement therapy. In the present study, the EnSCs were coaxed to oligodendrocyte progenitor programming by induction of neuronal condition media, including bFGF, epidermal growth factor, and platelet-derived growth factor (PDGF)-AA signaling molecules as well as triiodothyronine. Differentiated cells were analyzed for expression of oligodendrocytic markers by quantitative reverse transcription PCR and immunocytochemistry. The results showed the expression of oligodendrocyte lineage markers such as nestin, PDGF receptor alpha (PDGFRα), Sox10, and Olig2 in the level of mRNAs. The expression of nestin and PDGFRα increased after 8 days posttreatment. Interestingly, the expression of nestin and PDGFRα genes at the levels of mRNA and proteins decreased 24 days after induction. The expression of A2B5, O4, and Olig2 proteins in EnSCs was confirmed using immunocytochemistry. The results confirmed that EnSCs could response to the signaling molecules which routinely applied for oligodendrocyte differentiation. Here for the first time, we demonstrated that EnSCs could be programmed into oligodendrocyte progenitor cells and may convince to consider these cells as suitable source for cell therapy of neurodegenerative diseases.

No abstract

MicroRNAs have a critical role in oligodendrocyte development including cell proliferation, differentiation, and myelin formation. MicroRNA 338 (miR-338) is necessary to promote oligodendrocyte differentiation by repressing negative regulators of oligodendrocyte differentiation. Oligodendrocytes (OLs) are responsible for myelin sheath synthesis around nerve fibers in the central nervous system (CNS) that form the myelin sheath of axons. Human endometrial-derived stromal cells (hEnSCs) are a new source of mesenchymal-like stem cells for cell replacement therapy. The hEnSCs, after treating with fibroblast growth factor 2/epidermal growth factor (20 ng/mL) and platelet-derived growth factor (PDGF)-AA (10 ng/mL) for 12 days, were divided in two groups: in the first group, the cells were treated by triiodothyronine (T3), and in the second group, the cells were infected by miR-338-green fluorescent protein-expressing lentiviruses. Six days after infection, the cells were collected and analyzed for the expression of stage-specific markers Nestin, microtubule-associated protein 2, neurofilament-L, oligodendrocyte lineage transcription factor, SRY-box containing gene 10, PDGF receptor alpha, 2',3'-cyclic nucleotide 3' phosphodiesterase, A2B5, O4, and myelin basic protein by immunocytochemistry and quantitative reverse transcription PCR. Result showed that in the infected cells, the expression of pre-oligodendrocyte markers was higher than that of T3-treated cells. The EnSCs can differentiate to oligodendrocyte cells by the overexpression of miR-338, and these cells can be used as a unique source for cell therapy of neurodegenerative disease.

No abstract

No abstract

No abstract

No abstract