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1.
Development ; 149(11)2022 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-35451016

RESUMO

It has been established in the mouse model that during embryogenesis joint cartilage is generated from a specialized progenitor cell type, distinct from that responsible for the formation of growth plate cartilage. We recently found that mesodermal progeny of human pluripotent stem cells gave rise to two types of chondrogenic mesenchymal cells in culture: SOX9+ and GDF5+ cells. The fast-growing SOX9+ cells formed in vitro cartilage that expressed chondrocyte hypertrophy markers and readily underwent mineralization after ectopic transplantation. In contrast, the slowly growing GDF5+ cells derived from SOX9+ cells formed cartilage that tended to express low to undetectable levels of chondrocyte hypertrophy markers, but expressed PRG4, a marker of embryonic articular chondrocytes. The GDF5+-derived cartilage remained largely unmineralized in vivo. Interestingly, chondrocytes derived from the GDF5+ cells seemed to elicit these activities via non-cell-autonomous mechanisms. Genome-wide transcriptomic analyses suggested that GDF5+ cells might contain a teno/ligamento-genic potential, whereas SOX9+ cells resembled neural crest-like progeny-derived chondroprogenitors. Thus, human pluripotent stem cell-derived GDF5+ cells specified to generate permanent-like cartilage seem to emerge coincidentally with the commitment of the SOX9+ progeny to the tendon/ligament lineage.


Assuntos
Cartilagem Articular , Condrócitos , Células-Tronco Pluripotentes , Animais , Cartilagem Articular/citologia , Cartilagem Articular/metabolismo , Diferenciação Celular , Condrócitos/citologia , Condrócitos/metabolismo , Condrócitos/patologia , Condrogênese , Fator 5 de Diferenciação de Crescimento/metabolismo , Humanos , Hipertrofia , Camundongos , Células-Tronco Pluripotentes/citologia , Células-Tronco Pluripotentes/metabolismo
2.
J Arthroplasty ; 36(8): 3004-3009, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-33812708

RESUMO

BACKGROUND: The relationship between industry payments and academic influence, as measured by the Hirsch index (h-index) and number of publications, among adult reconstruction surgeons is not well characterized. The aims of the present study are to determine the relationship between an adult reconstruction surgeons' academic influence and their relevant industry payments and National Institutes of Health (NIH) funding. METHODS: Adult reconstruction surgeons were identified through the websites for the orthopedic surgery residency programs in the United States during the 2019-2020 academic year. Academic influence was approximated by each physician's h-index and total number of publications. Industry payment data were obtained through the Open Payments Database, and NIH funding was determined through the NIH website. Mann-Whitney U testing and Spearman correlations were performed to examine relevant associations. RESULTS: Surgeons who received industry research payments had a higher mean h-index (16.1 vs 10.2, P < .001) and mean number of publications (79.1 vs 35.9, P < .001) than physicians who received no industry research payments. Surgeons receiving NIH funding had a higher mean h-index (48.1 vs 10.4, P < .001) and mean number of publications (294.5 vs 36.8, P < .001) than surgeons who did not receive NIH funding. There was no association between the average h-index (P = .668) and number of publications (P = .387) among adult reconstruction surgeons receiving industry nonresearch funding. CONCLUSION: h-index and total publications do not seem to be associated with industry nonresearch payments in the field of total joint arthroplasty. Altogether, these data suggest that industry bias may not play a strong role in total joint arthroplasty.


Assuntos
Indústrias , Cirurgiões , Adulto , Artroplastia , Humanos , Estados Unidos
3.
Cell Mol Life Sci ; 77(13): 2543-2563, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31915836

RESUMO

The cartilage of joints, such as meniscus and articular cartilage, is normally long lasting (i.e., permanent). However, once damaged, especially in large animals and humans, joint cartilage is not spontaneously repaired. Compensating the lack of repair activity by supplying cartilage-(re)forming cells, such as chondrocytes or mesenchymal stromal cells, or by transplanting a piece of normal cartilage, has been the basis of therapy for biological restoration of damaged joint cartilage. Unfortunately, current biological therapies face problems on a number of fronts. The joint cartilage is generated de novo from a specialized cell type, termed a 'joint progenitor' or 'interzone cell' during embryogenesis. Therefore, embryonic chondroprogenitors that mimic the property of joint progenitors might be the best type of cell for regenerating joint cartilage in the adult. Pluripotent stem cells (PSCs) are expected to differentiate in culture into any somatic cell type through processes that mimic embryogenesis, making human (h)PSCs a promising source of embryonic chondroprogenitors. The major research goals toward the clinical application of PSCs in joint cartilage regeneration are to (1) efficiently generate lineage-specific chondroprogenitors from hPSCs, (2) expand the chondroprogenitors to the number needed for therapy without loss of their chondrogenic activity, and (3) direct the in vivo or in vitro differentiation of the chondroprogenitors to articular or meniscal (i.e., permanent) chondrocytes rather than growth plate (i.e., transient) chondrocytes. This review is aimed at providing the current state of research toward meeting these goals. We also include our recent achievement of successful generation of "permanent-like" cartilage from long-term expandable, hPSC-derived ectomesenchymal chondroprogenitors.


Assuntos
Cartilagem/fisiologia , Condrócitos/fisiologia , Condrogênese , Células-Tronco Pluripotentes/citologia , Engenharia Tecidual , Linhagem da Célula , Humanos , Células-Tronco Mesenquimais/citologia , Mesoderma/citologia , Crista Neural/citologia
4.
Stem Cell Reports ; 11(2): 440-453, 2018 08 14.
Artigo em Inglês | MEDLINE | ID: mdl-30057264

RESUMO

Cartilage pellets generated from ectomesenchymal progeny of human pluripotent stem cells (hPSCs) in vitro eventually show signs of commitment of chondrocytes to hypertrophic differentiation. When transplanted subcutaneously, most of the surviving pellets were fully mineralized by 8 weeks. In contrast, treatment with the adenylyl cyclase activator, forskolin, in vitro resulted in slightly enlarged cartilage pellets containing an increased proportion of proliferating immature chondrocytes that expressed very low levels of hypertrophic/terminally matured chondrocyte-specific genes. Forskolin treatment also enhanced hyaline cartilage formation by reducing type I collagen gene expression and increasing sulfated glycosaminoglycan accumulation in the developed cartilage. Chondrogenic mesoderm from hPSCs and dedifferentiated nasal chondrocytes responded similarly to forskolin. Furthermore, forskolin treatment in vitro increased the frequency at which the cartilage pellets maintained unmineralized chondrocytes after subcutaneous transplantation. Thus, the post-transplantational fate of chondrocytes originating from hPSC-derived chondroprogenitors can be controlled during their genesis in vitro.


Assuntos
Cartilagem/citologia , Diferenciação Celular , Condrócitos/citologia , Condrogênese , Células-Tronco Pluripotentes/citologia , Biomarcadores , Proteína Morfogenética Óssea 4/metabolismo , Cartilagem/metabolismo , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/genética , Proliferação de Células/efeitos dos fármacos , Condrócitos/metabolismo , Condrogênese/efeitos dos fármacos , Condrogênese/genética , Colforsina/farmacologia , Colágeno/genética , Colágeno/metabolismo , Colágeno Tipo XI/genética , Colágeno Tipo XI/metabolismo , Biologia Computacional/métodos , AMP Cíclico/metabolismo , Expressão Gênica , Perfilação da Expressão Gênica , Ontologia Genética , Glicosaminoglicanos/biossíntese , Humanos , Células-Tronco Pluripotentes/metabolismo , Transplante de Células-Tronco
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