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Mir125b2 缺陷型小鼠中 MIR125B 转录物和骨表型的表达。

The expression of MIR125B transcripts and bone phenotypes in Mir125b2-deficient mice.

机构信息

Department of Orthodontics, Division of Oral Health and Development, Hiroshima University Hospital, Hiroshima, Japan.

Neuroprotection Research Laboratories, Department of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United States of America.

出版信息

PLoS One. 2024 Jul 8;19(7):e0304074. doi: 10.1371/journal.pone.0304074. eCollection 2024.

DOI:10.1371/journal.pone.0304074
PMID:38976685
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11230526/
Abstract

MIR125B, particularly its 5p strand, is apparently involved in multiple cellular processes, including osteoblastogenesis and osteoclastogenesis. Given that MIR125B is transcribed from the loci Mir125b1 and Mir125b2, three mature transcripts (MIR125B-5p, MIR125B1-3p, and MIR125B2-3p) are generated (MIR125B-5p is common to both); however, their expression profiles and roles in the bones remain poorly understood. Both primary and mature MIR125B transcripts were differentially expressed in various organs, tissues, and cells, and their expression patterns did not necessarily correlate in wild-type (WT) mice. We generated Mir125b2 knockout (KO) mice to examine the contribution of Mir125b2 to MIR125B expression profiles and bone phenotypes. Mir125b2 KO mice were born and grew normally without any changes in bone parameters. Interestingly, in WT and Mir125b2 KO, MIR125B-5p was abundant in the calvaria and bone marrow stromal cells. These results indicate that the genetic ablation of Mir125b2 does not impinge on the bones of mice, attracting greater attention to MIR125B-5p derived from Mir125b1. Future studies should investigate the conditional deletion of Mir125b1 and both Mir125b1 and Mir125b2 in mice.

摘要

MIR125B,特别是其 5p 链,显然参与了多种细胞过程,包括成骨细胞发生和破骨细胞发生。鉴于 MIR125B 是从 Mir125b1 和 Mir125b2 基因座转录而来的,因此产生了三种成熟的转录物(MIR125B-5p、MIR125B1-3p 和 MIR125B2-3p)(MIR125B-5p 对两者都通用);然而,它们在骨骼中的表达谱和作用仍知之甚少。初级和成熟的 MIR125B 转录物在不同的器官、组织和细胞中都有差异表达,其表达模式在野生型(WT)小鼠中不一定相关。我们生成了 Mir125b2 敲除(KO)小鼠,以研究 Mir125b2 对 MIR125B 表达谱和骨骼表型的贡献。Mir125b2 KO 小鼠出生并正常生长,骨骼参数没有任何变化。有趣的是,在 WT 和 Mir125b2 KO 中,MIR125B-5p 在颅骨和骨髓基质细胞中丰富。这些结果表明,Mir125b2 的遗传缺失不会影响小鼠的骨骼,这引起了对源自 Mir125b1 的 MIR125B-5p 的更大关注。未来的研究应该在小鼠中研究 Mir125b1 和 Mir125b1 和 Mir125b2 的条件性缺失。

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