کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5531911 | 1401819 | 2017 | 14 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development](/preview/png/5531911.png)
- miR-27 is highly enriched in the pharyngeal arches during zebrafish development.
- miR-27 deficiency leads to complete loss of pharyngeal cartilage.
- Proliferation and differentiation of pre-chondrogenic cells are regulated by miR-27.
- FAK is a direct target of miR-27, with complementary expression patterns.
- Suppressing FAK levels partially rescues the cartilage defects in miR-27 morphants.
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.
Journal: Developmental Biology - Volume 429, Issue 1, 1 September 2017, Pages 321-334