miR-125b inhibits osteoblastic differentiation by down-regulation of cell proliferation

Mizuno, Yosuke; Yagi, Ken; Tokuzawa, Yoshimi; Kanesaki-Yatsuka, Yukiko; Suda, Toshio; Katagiri, Takenobu; Fukuda, Tsuyoshi; Maruyama, Masayoshi; Okuda, Akihiko; Amemiya, Tomoyuki; Kondoh, Yasumitsu; Tashiro, Hideo; Okazaki, Yasushi

doi:10.1016/j.bbrc.2008.01.073

Cited by 274 publications

(215 citation statements)

References 24 publications

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“…In contrast, over-expression of miR-376a suppressed CDK2-dependent progenitor cell proliferation and resulted in arrested erythroid maturation. This is consistent with a previous report that the level of osteoblastic differentiation was lower when cell proliferation was inhibited [43]. Therefore, miR-376a modulates erythroid differentiation partly via interfering with cell cycle progression.…”

Section: Discussionsupporting

confidence: 93%

Regulation of erythroid differentiation by miR-376a and its targets

Wang

Yang

et al. 2011

Cell Res

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Lineage differentiation is a continuous process during which fated progenitor cells execute specific programs to produce mature counterparts. This lineage-restricted pathway can be controlled by particular regulators, which are usually exclusively expressed in certain cell types or at specific differentiation stages. Here we report that miR376a participates in the regulation of the early stages of human erythropoiesis by targeting cyclin-dependent kinase 2 (CDK2) and Argonaute 2 (Ago2). Among various human leukemia cell lines, miR-376a was only detected in K562 cells which originated from a progenitor common to the erythroid and megakaryotic lineages. Enforced expression of miR-376a or silencing of CDK2 and Ago2 by RNAi inhibits erythroid differentiation of K562 cells. Hematopoietic progenitor cells transduced with miR-376a showed a significant reduction of their erythroid clonogenic capacity. MiR-376a is relatively abundant in erythroid progenitor cells, where it reduces expression of CDK2 and maintains a low level of differentiation due to cell cycle arrest and decreased cell growth. Following erythroid induction, miR376a is significantly down-regulated and CDK2 is released from miR-376a inhibition, thereby facilitating the escape of progenitor cells from the quiescent state into erythroid differentiation. Moreover, our results establish a functional link between miR-376a and Ago2, a key factor in miRNA biogenesis and silencing pathways with novel roles in human hematopoiesis.

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Section: Discussionsupporting

confidence: 93%

Regulation of erythroid differentiation by miR-376a and its targets

Wang

Yang

et al. 2011

Cell Res

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“…miRNAs, as small molecular regulators of gene expression, play critical roles in regulation of many biological processes, including stem cell differentiation, (23) stem cell self-renewal, (24) skeletal muscle differentiation, granulopoiesis, and adipogenesis. (25) Recent studies showed that multiple miRNAs contribute to regulate osteoblast differentiation by controlling the levels of critical factors, including essential transcription factors and signaling molecules. For instance, miR-29, which is upregulated in the stage of mineralization, regulates osteoblast differentiation by inhibiting osteonectin.…”

Section: Discussionmentioning

confidence: 99%

miR-764-5p promotes osteoblast differentiation through inhibition of CHIP/STUB1 expression

Guo

Ren

Wang

et al. 2012

Journal of Bone and Mineral Research

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Differentiation of committed precursor cells into the osteoblast lineage is tightly regulated by several factors, including Runx2 and BMP2. We previously reported that C terminus of Hsc70-interacting protein/STIP1 homology and U-Box containing protein 1 (CHIP/STUB1) negatively regulated osteoblast differentiation through promoting Runx2 protein degradation. However, how CHIP is regulated during osteoblast differentiation remains unknown. In this study, we found that miR-764-5p is up-expressed during the osteoblast differentiation in calvarial and osteoblast progenitor cells, coupled with down-expression of CHIP protein. We observed that forced expression or inhibition of miR-764-5p decreased or increased the CHIP protein level through affecting its translation by targeting the 3 0 -UTR region. Perturbation of miR-764-5p resulted in altered differentiation fate of osteoblast progenitor cells and the role of miR-764-5p was reversed by overexpression of CHIP, whereas depletion of CHIP impaired the effect of miR-764-5p. Our data showed that miR-764-5p positively regulates osteoblast differentiation from osteoblast progenitor cells by repressing the translation of CHIP protein. ß

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“…A number of studies have indicated that miRNAs are essential to embryo development [7,8]. In particular, miR-125b, which is known to regulate cell proliferation [9,10] and differentiation [11][12][13], has been shown to be required for the development of lower organisms, such as Drosophila [14] and zebrafish [15]. The expression of miR-125b is also found in mouse preimplantation embryos although its exact role has not been eluciated [16].…”

Section: Hcomentioning

confidence: 99%