Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8455217 | Matrix Biology | 2015 | 8 Pages |
Abstract
The complementary binding sequence of miR-26a and miR-26b was found in the 3â²-UTR of the prehypertrophic/hypertrophic-specific genes Cd200, Col10a1 as well as Col9a1 and Ctgf. Both miRNAs were expressed in cartilage and only miR-26a was downregulated in hypertrophic growth plate cartilage. MiR-26a could interact with the 3â²-UTR of Cd200 and Col10a1 in luciferase binding studies, but not with Col9a1 and Ctgf. However, protein expression of target genes and the ECM adaptor genes matrilin-3 and COMP was significantly altered in miR-26a mimic- or inhibitor-transfected chondrocytes, whereas the abundance of the cell surface receptor for insulin was not changed. In conclusion, miR-26a suppresses hypertrophic and ECM adaptor protein production. Dysregulation of miR-26a expression could contribute to ECM changes in cartilage diseases and this miRNA may therefore act as a therapeutic target.
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Authors
Julia Etich, Tatjana Holzer, Lena Pitzler, Björn Bluhm, Bent Brachvogel,