Single cell sorting identifies progenitor cell population from full thickness bovine articular cartilage

Yu, Yancun; Zhang, Hongjun; Buckwalter, Joseph A.; Martin, James A.

doi:10.1016/j.joca.2014.07.002

Cited by 44 publications

(47 citation statements)

References 31 publications

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“…CCL5 has been reported to be involved also in MSCs recruitment [54], and thus it is considered attractive for regenerative therapies. As already reported [85], high levels of CXCL12/SDF-1α in chondro-progenitor secretome may indicate their ability to mobilize other endogenous progenitor cells within injured articular joints and recruit immune cells in order to help in mediating tissue repair.…”

Section: Discussionsupporting

confidence: 56%

Progenitor Cells Activated by Platelet Lysate in Human Articular Cartilage as a Tool for Future Cartilage Engineering and Reparative Strategies

Carluccio

Martinelli

Palamà

et al. 2020

Cells

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Regenerative strategies for human articular cartilage are still challenging despite the presence of resident progenitor cell population. Today, many efforts in the field of regenerative medicine focus on the use of platelet derivatives due to their ability to reactivate endogenous mechanisms supporting tissue repair. While their use in orthopedics continues, mechanisms of action and efficacy need further characterization. We describe that the platelet lysate (PL) is able to activate chondro-progenitor cells in a terminally differentiated cartilage tissue. Primary cultures of human articular chondrocytes (ACs) and cartilage explants were set up from donor hip joint biopsies and were treated in vitro with PL. PL recruited a chondro-progenitors (CPCs)-enriched population from ex vivo cartilage culture, that showed high proliferation rate, clonogenicity and nestin expression. CPCs were positive for in vitro tri-lineage differentiation and formed hyaline cartilage-like tissue in vivo without hypertrophic fate. Moreover, the secretory profile of CPCs was analyzed, together with their migratory capabilities. Some CPC-features were also induced in PL-treated ACs compared to fetal bovine serum (FBS)-control ACs. PL treatment of human articular cartilage activates a stem cell niche responsive to injury. These facts can improve the PL therapeutic efficacy in cartilage applications.

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Section: Discussionsupporting

confidence: 56%

Progenitor Cells Activated by Platelet Lysate in Human Articular Cartilage as a Tool for Future Cartilage Engineering and Reparative Strategies

Carluccio

Martinelli

Palamà

et al. 2020

Cells

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“…The digestion media was then centrifuged (300 G for 10 mins) and resuspended, cells were seeded into multiple 35 mm dishes. To determine if phagocytic cells were enriched in the superficial zone, chondrocytes from the upper 1/3 cartilage were separated from the bottom 2/3 prior to cell isolation using a customized fixture [9]. All cells were allowed to adapt to culture conditions for at least two days before measuring phagocytic activities.…”

Section: Methodsmentioning

confidence: 99%

“…The overall pattern of CPC gene expression revealed by microarray analysis is more akin to synovial fibroblasts and mesenchymal stem cells than chondrocytes [8]. Unlike pluripotent MSCs, CPCs are limited in their ability to form different tissues; however, as their name implies, CPCs reliably generate hyaline cartilage under chondrogenic conditions [9]. …”

Section: Introductionmentioning

confidence: 99%

Enhanced phagocytic capacity endows chondrogenic progenitor cells with a novel scavenger function within injured cartilage

Zhou

Zhang

Buckwalter

et al. 2016

Osteoarthritis and Cartilage

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Objective Articular cartilage harbors chondrogenic progenitor cells (CPCs), a population that responds chemotactically to cell death. Because this behavior is reminiscent of macrophages, we hypothesized that CPCs have macrophage-like capabilities for scavenging cell and tissue debris through phagocytosis. Design CPCs, chondrocytes, synoviocytes, and macrophages were cultured with fluorophore-labeled chondrocyte debris for 3, 6, 12, or 24 hours. Debris internalization was quantified by confocal microscopy and flow cytometry. Confocal microscopy was also used to test CPCs and chondrocytes for uptake of fluorophore-labeled fibronectin fragments (Fn-fs), a form of extracellular matrix debris. Lysosome activity and mass in CPCs and chondrocytes were measured using fluorescent probes. The relative expression of phagocytosis-related genes and proteins was evaluated by polymerase chain reaction (PCR) and immunoblotting, respectively. Pulse-chase experiments were performed to determine if the debris internalized by CPCs and chondrocytes was cleared, and if clearance was affected by a cathepsin B inhibitor. Results More macrophages, synoviocytes, and CPCs internalized cell debris than chondrocytes at all time points. While uptake remained flat in chondrocytes at ~10%, in the other cell types it peaked at more than 60% after 12 – 24 hours. Relative to chondrocytes, CPCs showed significantly higher rates of Fn-fs engulfment, greater lysosome activity and mass, and over-expressed phagocytosis-related genes and proteins. Pulse-chase experiments revealed time- and cathepsin B- dependent clearance of cell debris in CPCs, but not in chondrocytes. Conclusions CPCs phagocytized cell and matrix debris much more efficiently than chondrocytes, supporting the hypothesis that they play a macrophage-like role in injured cartilage.

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“…We subjected fresh intact human and animal articular cartilage specimens, maintained in environments simulating in vivo conditions, to a range of acute impacts, repetitive loadings, and direct mechanical injuries. Investigations using these explants have revealed that injurious mechanical loads stimulate biologic responses that cause progressive cell death and activate chondrocyte progenitor cells (CPCs) (Table S1) …”

Section: Class I: Explant and Whole Joint Modelsmentioning

confidence: 99%

Complementary models reveal cellular responses to contact stresses that contribute to post‐traumatic osteoarthritis

Martin

Anderson

Goetz

et al. 2016

Journal Orthopaedic Research

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Two categories of joint overloading cause post-traumatic osteoarthritis (PTOA): single acute traumatic loads/impactions and repetitive overloading due to incongruity/instability. We developed and refined three classes of complementary models to define relationships between joint overloading and progressive cartilage loss across the spectrum of acute injuries and chronic joint abnormalities: explant and whole joint models that allow probing of cellular responses to mechanical injury and contact stresses, animal models that enable study of PTOA pathways in living joints and pre-clinical testing of treatments, and patient-specific computational models that define the overloading that causes OA in humans. We coordinated methodologies across models so that results from each informed the others, maximizing the benefit of this complementary approach. We are incorporating results from these investigations into biomathematical models to provide predictions of PTOA risk and guide treatment. Each approach has limitations, but each provides opportunities to elucidate PTOA pathogenesis. Taken together, they help define levels of joint overloading that cause cartilage destruction, show that both forms of overloading can act through the same biologic pathways, and create a framework for initiating clinical interventions that decrease PTOA risk.

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Single cell sorting identifies progenitor cell population from full thickness bovine articular cartilage

Cited by 44 publications

References 31 publications

Progenitor Cells Activated by Platelet Lysate in Human Articular Cartilage as a Tool for Future Cartilage Engineering and Reparative Strategies

Progenitor Cells Activated by Platelet Lysate in Human Articular Cartilage as a Tool for Future Cartilage Engineering and Reparative Strategies

Enhanced phagocytic capacity endows chondrogenic progenitor cells with a novel scavenger function within injured cartilage

Complementary models reveal cellular responses to contact stresses that contribute to post‐traumatic osteoarthritis

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