Concurrent Alterations in Selected mRNAs and miR-30 Family Members in Canine Osteoarthritic Joint Tissues

Background: Osteoarthritis (OA) is a chronic whole-joint disease involving extracellular matrix remodeling, inflammatory signaling, immune–stromal interactions, and sensory-associated processes. MicroRNAs (miRNAs) may contribute to post-transcriptional regulation within these interconnected molecular domains, but concurrent mRNA and miRNA expression patterns remain insufficiently characterized in naturally occurring canine OA. Methods: A total of 12 formalin-fixed, paraffin-embedded (FFPE) canine tissue specimens were classified as osteoarthritic joint tissues (OA; n = 7) and control joint tissues without radiographic or histopathological evidence of OA (C-JT; n = 5). RT-qPCR was used to quantify 17 selected mRNAs involved in extracellular matrix remodeling, chronic inflammatory signaling, immune–stromal interactions, and neuroinflammatory and sensory-associated processes, together with five miR-30 family members. Statistical comparisons were performed on ΔCq values using two-sided unpaired Welch’s t-tests followed by Benjamini–Hochberg false discovery rate correction. Results: Compared with C-JT, OA tissues showed significantly higher expression of ADAMTS5, MMP2, MMP13, COL2A1, SPARC, HP, VEGFA, IGFBP6, and ASIC3 after false discovery rate correction. MMP9, IL1B, IL1R1, IL1RAP, JAK2, TYK2, NGFB, and NTRK1 did not differ significantly between the two joint-tissue groups. MiR-30b was significantly downregulated in OA, whereas miR-30c, miR-30d, and miR-30e were significantly upregulated; miR-30a did not differ significantly. Exploratory database-supported miRNA–gene connectivity was used for candidate prioritization but was not interpreted as evidence of direct regulation in canine joint tissue. Conclusions: Canine osteoarthritic capsulosynovial tissues exhibit concurrent alterations in selected mRNAs and miR-30 family members across matrix-remodeling, immune–stromal, and sensory-associated molecular domains. These findings identify OA-associated expression patterns but do not establish pathway activation, direct miRNA–mRNA regulation, or disease progression. They provide a focused molecular basis for future mechanistic studies of post-transcriptional regulation in naturally occurring canine OA.