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在咽弓发育过程中，miR-27通过抑制粘着斑激酶来调节软骨形成。

miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development.

作者信息

Kara Nergis, Wei Chunyao, Commanday Alexander C, Patton James G

机构信息

Department of Biological Sciences, Vanderbilt University, Nashville, TN, United States.

Department of Biological Sciences, Vanderbilt University, Nashville, TN, United States.

出版信息

Dev Biol. 2017 Sep 1;429(1):321-334. doi: 10.1016/j.ydbio.2017.06.013. Epub 2017 Jun 16.

DOI:10.1016/j.ydbio.2017.06.013
PMID:28625871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5582384/
Abstract

Cranial neural crest cells are a multipotent cell population that generate all the elements of the pharyngeal cartilage with differentiation into chondrocytes tightly regulated by temporal intracellular and extracellular cues. Here, we demonstrate a novel role for miR-27, a highly enriched microRNA in the pharyngeal arches, as a positive regulator of chondrogenesis. Knock down of miR-27 led to nearly complete loss of pharyngeal cartilage by attenuating proliferation and blocking differentiation of pre-chondrogenic cells. Focal adhesion kinase (FAK) is a key regulator in integrin-mediated extracellular matrix (ECM) adhesion and has been proposed to function as a negative regulator of chondrogenesis. We show that FAK is downregulated in the pharyngeal arches during chondrogenesis and is a direct target of miR-27. Suppressing the accumulation of FAK in miR-27 morphants partially rescued the severe pharyngeal cartilage defects observed upon knock down of miR-27. These data support a crucial role for miR-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.

摘要

颅神经嵴细胞是一种多能细胞群体，可生成咽软骨的所有成分，其向软骨细胞的分化受到细胞内和细胞外时间线索的严格调控。在此，我们证明了miR-27（一种在咽弓中高度富集的微小RNA）作为软骨生成的正向调节因子的新作用。敲低miR-27会导致咽软骨几乎完全丧失，这是通过减弱增殖并阻断软骨前体细胞的分化实现的。粘着斑激酶（FAK）是整合素介导的细胞外基质（ECM）粘附的关键调节因子，并且已被提出作为软骨生成的负向调节因子发挥作用。我们表明，在软骨生成过程中，FAK在咽弓中表达下调，并且是miR-27的直接靶标。抑制miR-27 morphants中FAK的积累部分挽救了敲低miR-27后观察到的严重咽软骨缺陷。这些数据支持miR-27通过调节FAK在促进咽弓软骨分化中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/66ef784cc444/nihms902440f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/2d249fe93d77/nihms902440f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/bb82e889aaac/nihms902440f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/11b83af1d338/nihms902440f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/f4fb2bf71e35/nihms902440f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/57bffb65541f/nihms902440f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/5b123da352b0/nihms902440f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/66ef784cc444/nihms902440f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/2d249fe93d77/nihms902440f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/bb82e889aaac/nihms902440f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/11b83af1d338/nihms902440f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/f4fb2bf71e35/nihms902440f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/57bffb65541f/nihms902440f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/5b123da352b0/nihms902440f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/228c/5582384/66ef784cc444/nihms902440f7.jpg

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