Редактирование: E2F2 (раздел)

==Publications==

{{medline-entry
|title=MicroRNA-31a-5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29896785
|abstract=The alteration of age-related molecules in the bone marrow microenvironment is one of the driving forces in osteoporosis. These molecules inhibit bone formation and promote bone resorption by regulating osteoblastic and osteoclastic activity, contributing to age-related bone loss. Here, we observed that the level of microRNA-31a-5p (miR-31a-5p) was significantly increased in bone marrow stromal cells (BMSCs) from aged rats, and these BMSCs demonstrated increased adipogenesis and aging phenotypes as well as decreased osteogenesis and stemness. We used the gain-of-function and knockdown approach to delineate the roles of miR-31a-5p in osteogenic differentiation by assessing the decrease of special AT-rich sequence-binding protein 2 (SATB2) levels and the aging of BMSCs by regulating the decline of [[E2F2]] and recruiting senescence-associated heterochromatin foci (SAHF). Notably, expression of miR-31a-5p, which promotes osteoclastogenesis and bone resorption, was markedly higher in BMSCs-derived exosomes from aged rats compared to those from young rats, and suppression of exosomal miR-31a-5p inhibited the differentiation and function of osteoclasts, as shown by elevated RhoA activity. Moreover, using antagomiR-31a-5p, we observed that, in the bone marrow microenvironment, inhibition of miR-31a-5p prevented bone loss and decreased the osteoclastic activity of aged rats. Collectively, our results reveal that miR-31a-5p acts as a key modulator in the age-related bone marrow microenvironment by influencing osteoblastic and osteoclastic differentiation and that it may be a potential therapeutic target for age-related osteoporosis.
|mesh-terms=* Animals
* Bone Marrow
* Bone Resorption
* Cell Differentiation
* Cells, Cultured
* Cellular Microenvironment
* Cellular Senescence
* Exosomes
* Female
* Mesenchymal Stem Cells
* MicroRNAs
* Osteoclasts
* Osteogenesis
* Rats
* Rats, Sprague-Dawley
|keywords=* aging
* bone marrow stromal cells
* exosomes
* microRNA-31a-5p
* osteoclasts
* senescence-associated heterochromatin foci
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6052401
}}
{{medline-entry
|title=In situ regeneration of retinal pigment epithelium by gene transfer of [[E2F2]]: a potential strategy for treatment of macular degenerations.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29188796
|abstract=The retinal pigment epithelium ([[RPE]]) interacts closely with photoreceptors to maintain visual function. In degenerative diseases such as Stargardt disease and age-related macular degeneration, the leading cause of blindness in the developed world, [[RPE]] cell loss is followed by photoreceptor cell death. [[RPE]] cells can proliferate under certain conditions, suggesting an intrinsic regenerative potential, but so far this has not been utilised therapeutically. Here, we used [[E2F2]] to induce [[RPE]] cell replication and thereby regeneration. In both young and old (2 and 18 month) wildtype mice, subretinal injection of non-integrating lentiviral vector expressing [[E2F2]] resulted in 47% of examined [[RPE]] cells becoming BrdU positive. [[E2F2]] induced an increase in [[RPE]] cell density of 17% compared with control vector-treated and 14% compared with untreated eyes. We also tested this approach in an inducible transgenic mouse model of [[RPE]] loss, generated through activation of diphtheria toxin-A gene. [[E2F2]] expression resulted in a 10-fold increase in BrdU uptake and a 34% increase in central [[RPE]] cell density. Although in mice this localised rescue is insufficiently large to be demonstrable by electroretinography, a measure of massed retinal function, these results provide proof-of-concept for a strategy to induce in situ regeneration of [[RPE]] for the treatment of [[RPE]] degeneration.
|mesh-terms=* Aging
* Animals
* Cell Proliferation
* Diphtheria Toxin
* Disease Models, Animal
* E2F2 Transcription Factor
* Gene Transfer Techniques
* Genetic Therapy
* Genetic Vectors
* Macular Degeneration
* Mice
* Mice, Transgenic
* Peptide Fragments
* Regeneration
* Retinal Pigment Epithelium

|full-text-url=https://sci-hub.do/10.1038/gt.2017.89
}}