Journal
CELL BIOCHEMISTRY AND FUNCTION
Volume 32, Issue 2, Pages 209-216Publisher
WILEY
DOI: 10.1002/cbf.3005
Keywords
calcification; Enpp1; microarray; miRNA; vascular smooth muscle cell
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Funding
- Institute Strategic Programme Grant from the Biotechnology and Biological Sciences Research Council (BBSRC)
- Institute Career Path Fellowship from the Biotechnology and Biological Sciences Research Council (BBSRC)
- Biotechnology and Biological Sciences Research Council [BB/F023928/1, BBS/E/D/20221657] Funding Source: researchfish
- BBSRC [BBS/E/D/20221657, BB/F023928/1] Funding Source: UKRI
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Vascular calcification shares many similarities with skeletal mineralisation and involves the phenotypic trans-differentiation of vascular smooth muscle cells (VSMCs) to osteoblastic cells within a calcified environment. Various microRNAs (miRs) are known to regulate cell differentiation; however, their role in mediating VSMC calcification is not fully understood. miR-microarray analysis revealed the significant down-regulation of a range of miRs following nine days in culture, including miR-199b, miR-29a, miR-221, miR-222 and miR-31 (p<0.05). Subsequent studies investigated the specific role of the miR-221/222 family in VSMC calcification. Real-time quantitative polymerase chain reaction data confirmed the down-regulation of miR-221 (32.4%; p<0.01) and miR-222 (15.7%; p<0.05). VSMCs were transfected with mimics of miR-221 and miR-222, individually and in combination. Increased calcium deposition was observed in the combined treatment (two-fold; p<0.05) but not in individual treatments. Runx2 and Msx2 expression was increased during calcification, but no difference in expression was observed following transfection with miR mimics. Interestingly, miR-221 and miR-222 mimics induced significant changes in ectonucleotide phosphodiesterase 1 (Enpp1) and Pit-1 expression, suggesting that these miRs may modulate VSMC calcification through cellular inorganic phosphate and pyrophosphate levels. (c) 2013 The Authors. Cell Biochemistry and Function published by John Wiley & Sons, Ltd.
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