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Overexpression of miR-669m inhibits erythroblast differentiation

MicroRNAs (miRNAs), one of small non-coding RNAs, regulate many cell functions through their post-transcriptionally downregulation of target genes. Accumulated studies have revealed that miRNAs are involved in hematopoiesis. In the present study, we investigated effects of miR-669m overexpression on...

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Detalles Bibliográficos
Autores principales: Kotaki, Ryutaro, Kawashima, Masaharu, Yamaguchi, Asuka, Suzuki, Naoto, Koyama-Nasu, Ryo, Ogiya, Daisuke, Okuyama, Kazuki, Yamamoto, Yuichiro, Takamatsu, Masako, Kurosaki, Natsumi, Ando, Kiyoshi, Murata, Akihiko, Ohtsuka, Masato, Nakagawa, So, Katagiri, Koko, Kotani, Ai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7419302/
https://www.ncbi.nlm.nih.gov/pubmed/32782283
http://dx.doi.org/10.1038/s41598-020-70442-y
Descripción
Sumario:MicroRNAs (miRNAs), one of small non-coding RNAs, regulate many cell functions through their post-transcriptionally downregulation of target genes. Accumulated studies have revealed that miRNAs are involved in hematopoiesis. In the present study, we investigated effects of miR-669m overexpression on hematopoiesis in mouse in vivo, and found that erythroid differentiation was inhibited by the overexpression. Our bioinformatic analyses showed that candidate targets of miR-669m which are involved in the erythropoiesis inhibition are A-kinase anchoring protein 7 (Akap7) and X-linked Kx blood group (Xk) genes. These two genes were predicted as targets of miR-669m by two different in silico methods and were upregulated in late erythroblasts in a public RNA-seq data, which was confirmed with qPCR. Further, miR-669m suppressed luciferase reporters for 3′ untranslated regions of Akap7 and Xk genes, which supports these genes are direct targets of miR-669m. Physiologically, miR-669m was not expressed in the erythroblast. In conclusion, using miR-669m, we found Akap7 and Xk, which may be involved in erythroid differentiation, implying that manipulating these genes could be a therapeutic way for diseases associated with erythropoiesis dysfunction.