SOX9
- Known as:
- SOX9
- Catalog number:
- NBP1-36508
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9
Related genes to: SOX9
- Gene:
- SOX9 NIH gene
- Name:
- SRY-box 9
- Previous symbol:
- CMD1, CMPD1
- Synonyms:
- SRA1
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-25
- Date modifiied:
- 2018-06-25
Related products to: SOX9
Related articles to: SOX9
- Kartogenin (KGN) is a potent inducer of chondrogenic differentiation, but its biomedical application is limited by poor aqueous solubility and the lack of efficient delivery systems. In this study, hybrid nanosystems composed of KGN-loaded liposomes (LK) coated with amphiphilic hyaluronic acid (HA) derivatives were developed to combine favorable carrier properties with HA-mediated biological targeting. Native HA was hydrophobically modified with dodecyl (C12) or octadecyl (C18) chains at low or high degrees of substitution (DS), yielding three amphiphilic derivatives: HAC12L, HAC18L, and HAC18H. Polymer-coated liposomes were characterized by dynamic light scattering and ζ-potential measurements, while lipid bilayer organization was evaluated by differential scanning calorimetry (DSC) and cryogenic transmission electron microscopy (cryo-TEM). Increasing hydrophobic modification enhanced polymer-liposome association and altered liposome surface organization. HAC18H provided the strongest KGN retention but also introduced greater membrane heterogeneity. All HA derivatives exhibited good cytocompatibility toward human umbilical cord Wharton's jelly mesenchymal stem cells (hUC-MSCs) within the concentration range of 1-40 µg/mL, and polymer coating reduced the cytotoxicity of KGN-loaded liposomes compared with uncoated systems. In a 14-day stimulation model, the hybrid formulations induced structure- and dose-dependent upregulation of chondrogenic markers (SOX9, ACAN, COL2A1) with minimal induction of COL1A1, consistent with activation of early chondrogenic differentiation pathways. Among the tested systems, LK-HAC18L exhibited the most balanced chondrogenic profile, as assessed by combined gene expression, lineage specificity, and CD44 receptor engagement. Overall, these findings indicate that controlled hydrophobic modification of HA modestly modulates KGN release behavior while influencing its biological activity, providing a promising platform for cartilage regeneration applications. - Source: PubMed
Publication date: 2026/07/09
Wytrwal MagdalenaOclon EwaRzepa SylwiaPardyak LauraFilipek KatarzynaKucharski MiroslawGórniewicz-Lorens MagdalenaSzczubiałka Krzysztof - Osteoarthritis (OA) involves chronic inflammation and oxidative stress, both of which impair cartilage regeneration. To counteract these pathological processes, bone marrow mesenchymal stromal cell (BMSC)-derived exosomes have emerged as a promising therapy. These exosomes promote chondrogenesis and facilitate chemokine-guided cell homing. However, hostile microenvironments compromise their efficacy. This study developed a cell-free, ROS-responsive boronate-vinyl (BV) hydrogel platform encapsulating BMSC-derived exosomes overexpressing CircSERPINE2 (BV@cSERPINE2-Exo), which were isolated via ultracentrifugation from lentivirus-transduced BMSCs. This platform enables sustained microenvironmental modulation and functional cartilage regeneration. The hydrogel forms through dynamic boronate ester crosslinking between phenylboronic acid-modified poly γ-glutamic acid and polyvinyl alcohol (PVA). It exhibits rapid gelation, shear-thinning injectability, and potent ROS-scavenging capacity. ROS-triggered cleavage of the boronate ester bonds ensures controlled exosome release. In vitro, BV@cSERPINE2-Exo shifted LPS-stimulated macrophages from an M1 to M2 phenotype by decreasing iNOS and IL-1β levels and increasing Arg-1 and IL-10. Concurrently, the system protected chondrocytes from TNF-α-induced degeneration by downregulating MMP13 and restoring COL2A1, SOX9, and proteoglycan synthesis. In a rat patellar cartilage defect model, intra-articular injection of BV@cSERPINE2-Exo promoted deposition of cartilage-specific extracellular matrix and achieved near-complete hyaline cartilage-like repair within 8 weeks. This repair was superior to that in the BV hydrogel or unmodified exosome control groups. These results establish a smart, injectable biomaterial strategy that integrates precise ROS-responsive circRNA delivery with immunomodulation, offering a promising early intervention strategy for cartilage defect repair and the prevention of osteoarthritis progression. - Source: PubMed
Publication date: 2026/07/01
Zhu MingDai ShiminCui JingquanZhao ZhiboWei XingchenLi PingLi Wei - To investigate the genetic etiology of fetal postural anomalies using whole-exome sequencing (WES) and elucidate the genotype-phenotype correlation between prenatal sonographic findings and molecular signatures. - Source: PubMed
Publication date: 2026/07/09
Qin YayunWang TingYi MeiqiLi HuiZeng LingLiu LijunSong Jieping - Cells derived from the endocardium, epicardium, cardiac neural crest, and second heart field play a critical role in the formation of the valvuloseptal structures of the heart. Previous studies have shown that the expression of the transcription factor SOX9 in these cell populations is essential in the regulation of this process. SOX9 interacts with other SOX family members including SOX5 and SOX6 to cooperatively regulate other developmental events. Although SOX6 has documented roles in the postnatal heart, its role in cardiac development has not yet been examined. For the current study we decided to investigate the importance of SOX6 in valvuloseptal morphogenesis. Expression studies revealed that SOX6 is expressed in many of the cell lineages that contribute to the formation of the heart. Given the pattern of SOX6 expression in the endocardium and endocardial-derived cells as well as in the coronary endothelium, we focused on the role of SOX6 in these cell populations by generating endothelial/endocardial-specific Sox6 knockout mice. These conditional knockout mice presented with ventricular septal defects, enlarged atrioventricular valves, and coronary abnormalities. Cardiovascular defects observed in the endothelial/endocardial-specific Sox6 knockout mouse demonstrate that SOX6 plays an important role in valvuloseptal development. - Source: PubMed
Publication date: 2026/07/09
Tarolli Hannah GHarvey Andrew BDevji InaraDeepe Raymond NDrummond Jenna RWolters Renélyn AWessels Andy - Human-induced pluripotent stem cells (hiPSCs) represent a promising cell source for cartilage regeneration because of their self-renewal capacity and chondrogenic potential. However, the propensity of hiPSC-derived chondrocytes to undergo hypertrophic maturation remains a major obstacle to generating stable articular cartilage. Here, we identified core binding factor β (CBFβ) as a critical regulator of early chondrogenic identity and a suppressor of hypertrophic transition during hiPSC-derived cartilage organoid formation. CBFβ expression was markedly diminished in degenerative articular cartilage from both human osteoarthritis (OA) specimens and mouse OA models, and cartilage-specific ablation of Cbfβ accelerated cartilage structural deterioration and matrix loss. Notably, CBFβ was secreted by non-mineralizing cells, including chondrocytes and vascular smooth muscle cells, suggesting an autocrine/paracrine regulatory role. Pharmacological inhibition with Brefeldin A reduced extracellular CBFβ levels, whereas blockade of exosome release by GW4869 had minimal effect, indicating a secretion-associated mechanism independent of exosomes. Recombinant human CBFβ (rhCBFβ) treatment enhanced the chondrocyte phenotype by upregulating early chondrogenic markers (SOX9, COL2A1) while suppressing hypertrophic and catabolic markers ( RUNX2, MMP13). In hiPSC-derived cartilage organoids, rhCBFβ enhanced matrix deposition and increased COL2A1 and SOX9 expression. Transcriptomic profiling and qRT-PCR validation further demonstrated that rhCBFβ activated cartilage matrix-associated and anti-hypertrophic transcriptional programs, including upregulation of PTHRP, HIF1α, HDAC4, MGP, CILP, and ALK5, together with suppression of RUNX2.Collectively, these findings establish CBFβ as a key regulator of articular cartilage homeostasis and highlights its therapeutic potential for cartilage regeneration in OA. The ability of rhCBFβ to preserve early chondrogenic identity while preventing hypertrophic maturation offers a promising strategy for cartilage tissue engineering. Further preclinical studies are warranted to evaluate its efficacy and accelerate clinical translation for OA therapy. - Source: PubMed
Publication date: 2026/07/08
Che XiangguoJin XianLee Dong-KyoHeo Eun-JungPark MinOh JinyoungKim Hee-JuneKim Hyun-JuKim Hyung-RyongChoi Je-Yong