It seems that CHPs are making an impact for researchers study intervertebral disc degeneration! Another interesting paper published in JCI Insight focused on intervertebral disc (and cartilage) degeneration. Researchers looked at the role of the actin-branching Arp2/3 complex has in maintaining the health of the IVD and cartilage through the regulation of cell-ECM interactions. In this study, they showed that the mutant mice (Arp2/3 deficient mice) had an abundance of aberrant, disorganized collagen fibers when compared to the healthy control mice. This was confirmed with CHP staining, as seen in Figure 5 (above). They concluded the study saying that "the Arp2/3 complex is critical for cell-matrix interactions, matrix homeostasis, and TonEBP-dependent osmoadaptation in the intervertebral disc and cartilage.....with important implications in intervertebral disc degeneration and osteoarthritis, as well as growth plate cartilage defects which contribute to several pathologies in the pediatric population."

ABSTRACT: Extracellular matrix and osmolarity influence the development and homeostasis of skeletal tissues through Rho GTPase-mediated alteration of the actin cytoskeleton. This study investigated whether the actin-branching Arp2/3 complex, a downstream effector of the Rho GTPases Cdc42 and Rac1, plays a critical role in maintaining the health of matrix-rich and osmotically loaded intervertebral discs and cartilage. Mice with constitutive intervertebral disc and cartilage-specific deletion of the critical Arp2/3 subunit Arpc2 (Col2-Cre; Arpc2f/f) developed chondrodysplasia and spinal defects. Since these mice did not survive to adulthood, we generated mice with inducible Arpc2 deletion in disc and cartilage (Acan-CreERT2; Arpc2f/f). Inactivation of Arp2/3 at skeletal maturity resulted in growth plate closure, loss of proteoglycan content in articular cartilage, and degenerative changes in the intervertebral disc at 1 year of age. Chondrocytes with Arpc2 deletion showed compromised cell spreading on both collagen and fibronectin. Pharmacological inhibition of Cdc42 and Arp2/3 prevented the osmoadaptive transcription factor TonEBP/NFAT5 from recruiting co-factors in response to a hyperosmolarity challenge. Together, these findings suggest that Arp2/3 plays a critical role in cartilaginous tissues through the regulation of cell-extracellular matrix interactions and modulation of TonEBP-mediated


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