Figure 2.

Bioactivity of BMP7-derived peptides p[63−82] and p[113−132] on OA-HACs

Complete peptide library screening quantitative real-time PCR dataset for peptides p[63−82] and p[113−132] is presented. (A) SOX9, COL2A1, and NKX3-2 mRNA expression in the 18 OA-HAC pool exposed to 1,000, 100, 10, or 1 nM of peptide p[63−82] and p[113−132] is shown and presented relative to control (black bars) and alongside full-length BMP7 (white bars). (B) Similar to (A) but for chondrocyte hypertrophy-associated genes RUNX2, COL10A1, and ALPL. (C) Similar to (A) but for cartilage extracellular matrix remodeling-associated genes MMP13 and ADAMTS5 and inflammation-related genes COX-2 and IL-6. (D) Glycosaminoglycan (GAG) content (normalized to total protein content) on an independent cohort of three individual OA-HAC donors treated with 100 nM peptides p[63−82] and p[113−132] for 24 h. Corresponding gene expression data are shown in Figure S3. (E) Alkaline phosphatase (ALP) activity (normalized to total protein content) in similar samples from (D). (F) Prostaglandin E₂ (PGE₂) levels in culture supernatant in similar samples from (D). (G) In the same OA-HAC pool of 18 OA-HAC donors from the peptide library screening, sequence dependency of peptides p[63−82] and p[113−132] was determined by exposing the OA-HAC pool to scrambled versions of peptides p[63−82] and p[113−132] (100 nM, 24 h). Expression of COL2A1, RUNX2, COL10A1, and COX-2 mRNAs is shown. Error bars represent mean ± SEM, and statistical significance for peptide conditions or BMP7 versus control condition as determined by unpaired two-tailed Student’s t test is represented as ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001.