Articular cartilage contains four distinct zones, extending from the surface to the subchondral bone. Freshly isolated chondrocytes from the superficial zone of articular cartilage retain a collagenase-P-resistant cell-associated matrix. In the studies described here, the protein Del1 was identified as a component of the cell-associated matrix of superficial zone chondrocytes from adult bovine articular cartilage. Very little Del1 was associated with freshly isolated deep zone chondrocytes. Western blot analysis of articular cartilage cell and tissue extracts using polyclonal antibodies specific for Del1 showed Del1 was present in an insoluble cell-associated fraction. Extracts of the superficial zone of articular cartilage were found to be enriched in Del1 compared to the deeper layers of the tissue. Immunohistochemical staining of full-thickness articular cartilage with anti-Del1 antibodies also showed an enrichment of Del1 in the superficial zone. These observations are the first to describe the protein Del1 in a nonendothelial, nonfetal tissue.
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http://dx.doi.org/10.1006/bbrc.2001.5377 | DOI Listing |
J Tissue Eng
January 2025
Department of Sports Medicine and Joint Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Bone marrow stimulation treatment by bone marrow stromal cells (BMSCs) released from the bone medullary cavity and differentiated into cartilage via microfracture surgery is a frequently employed technique for treating articular cartilage injuries, yet the treatment presents a main drawback of poor cartilage regeneration in the elderly. Prior research indicated that aging could decrease the stemness capacity of BMSCs, thus we made a hypothesis that increasing old BMSCs (OBMSCs) stemness might improve the results of microfracture in the elderly. First, we investigated the correlation between microfracture outcomes and BMSCs stemness using clinical data and animal experiments.
View Article and Find Full Text PDFAm J Sports Med
January 2025
Department of Orthopaedics, Warren Alpert Medical School of Brown University/Rhode Island Hospital, Providence, Rhode Island, USA.
Background: Meniscal injuries that fail to heal instigate catabolic changes in the knee's microenvironment, posing a high risk for developing posttraumatic osteoarthritis (PTOA). Previous research has suggested that human cartilage-derived progenitor cells (hCPCs) can stimulate meniscal repair in a manner that depends on stromal cell-derived factor 1 (SDF-1) pathway activity.
Hypothesis: Overexpressing the SDF-1 receptor CXCR4 in hCPCs will increase cell trafficking and further improve the repair efficacy of meniscal injuries.
J Biomed Mater Res B Appl Biomater
January 2025
Department of Mechanical Engineering, Cleveland State University, Cleveland, Ohio, USA.
Osteoarthritis (OA) is a prevalent joint disorder that is characterized by the degeneration of articular cartilage in synovial joints. Most of the current treatment options for this disorder tend to focus on symptom management rather than addressing the underlying progression of the disease. Cartilage tissue engineering has emerged as a promising approach to address the limitations of current OA treatments, aiming to regenerate cartilage and restore the natural function of affected joints.
View Article and Find Full Text PDFCurr Pain Headache Rep
January 2025
Department of Anesthesiology, Perioperative, and Pain Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA, USA.
Purpose Of Review: Knee osteoarthritis (OA) is a gradual deterioration of articular cartilage characterized by pain and physical dysfunction. Although analgesic pharmacological agents are the first-line treatment for knee OA, they are not effective for all patients. In this study, we evaluate the efficacy of an intra-articular injection treatment using platelet-rich plasma (PRP) in reducing pain and improving functional ability.
View Article and Find Full Text PDFFASEB J
January 2025
School of Pharmacy, Anhui Medical University, Hefei, China.
The activation of acid-sensing ion channel 1a (ASIC1a) in response to extracellular acidification leads to an increase in extracellular calcium influx, thereby exacerbating the degeneration of articular chondrocytes in rheumatoid arthritis (RA). It has been suggested that the inhibition of extracellular calcium influx could potentially impede chondrocyte ferroptosis. The cystine transporter, solute carrier family 7 member 11 (SLC7A11), is recognized as a key regulator of ferroptosis.
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