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. 2020 Jun 30;10:10641. doi: 10.1038/s41598-020-67446-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Antisense oligonucleotide-mediated knockdown of SNORD26 and SNORD96A. HACs (n = 6) were transfected with either 100 nM SNORD26 or SNORD96A anti-sense oligonucleotides (ASO, black bars) or with scrambled version (white bars) of this ASO. (A) 24-h SNORD26, (B) 48-h SNORD26, (C) 24-h SNORD96A, (D) 48-h SNORD96A. SnoRNA, rRNAs, hypertrophic, chondrogenic and OA genes were determined by qRT-PCR. Alkaline phosphates activity was measured in cell lysates of parallel wells following (E) SNORD26 knockdown for 24 and 48 h; (F) SNORD96A knockdown for 24 and 48 h. PGE2 protein was measured in media following (G) SNORD26 knockdown for 24 and 48 h; (H) SNORD96A knockdown for 24 and 48 h. Statistical evaluation was undertaken using an independent samples t test relative to the corresponding control condition using GraphPad Prism. The p values are indicated; ^&p < 0.06; *p < 0.05; **p < 0.01. Data represents the mean value of six technical replicates and error bars represent standard error mean.