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Journal articles on the topic 'Chondrocyte redifferentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Twu, Chih-Wen, Marsha S. Reuther, Kristen K. Briggs, Robert L. Sah, Koichi Masuda, and Deborah Watson. "Effect of Oxygen Tension on Tissue-Engineered Human Nasal Septal Chondrocytes." Allergy & Rhinology 5, no. 3 (January 2014): ar.2014.5.0097. http://dx.doi.org/10.2500/ar.2014.5.0097.

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Tissue-engineered nasal septal cartilage may provide a source of autologous tissue for repair of craniofacial defects. Although advances have been made in manipulating the chondrocyte culture environment for production of neocartilage, consensus on the best oxygen tension for in vitro growth of tissue-engineered cartilage has not been reached. The objective of this study was to determine whether in vitro oxygen tension influences chondrocyte expansion and redifferentiation. Proliferation of chondrocytes from 12 patients expanded in monolayer under hypoxic (5% or 10%) or normoxic (21%) oxygen tension was compared over 14 days of culture. The highest performing oxygen level was used for further expansion of the monolayer cultures. At confluency, chondrocytes were redifferentiated by encapsulation in alginate beads and cultured for 14 days under hypoxic (5 or 10%) or normoxic (21%) oxygen tension. Biochemical and histological properties were evaluated. Chondrocyte proliferation in monolayer and redifferentiation in alginate beads were supported by all oxygen tensions tested. Chondrocytes in monolayer culture had increased proliferation at normoxic oxygen tension (p = 0.06), as well as greater accumulation of glycosaminoglycan (GAG) during chondrocyte redifferentiation (p < 0.05). Chondrocytes released from beads cultured under all three oxygen levels showed robust accumulation of GAG and type II collagen with a lower degree of type I collagen immunoreactivity. Finally, formation of chondrocyte clusters was associated with decreasing oxygen tension (p < 0.05). Expansion of human septal chondrocytes in monolayer culture was greatest at normoxic oxygen tension. Both normoxic and hypoxic culture of human septal chondrocytes embedded in alginate beads supported robust extracellular matrix deposition. However, GAG accumulation was significantly enhanced under normoxic culture conditions. Chondrocyte cluster formation was associated with hypoxic oxygen tension.

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2

Liau, Ling Ling, Muhammad Najib Fathi bin Hassan, Yee Loong Tang, Min Hwei Ng, and Jia Xian Law. "Feasibility of Human Platelet Lysate as an Alternative to Foetal Bovine Serum for In Vitro Expansion of Chondrocytes." International Journal of Molecular Sciences 22, no. 3 (January 28, 2021): 1269. http://dx.doi.org/10.3390/ijms22031269.

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Osteoarthritis (OA) is a degenerative joint disease that affects a lot of people worldwide. Current treatment for OA mainly focuses on halting or slowing down the disease progress and to improve the patient’s quality of life and functionality. Autologous chondrocyte implantation (ACI) is a new treatment modality with the potential to promote regeneration of worn cartilage. Traditionally, foetal bovine serum (FBS) is used to expand the chondrocytes. However, the use of FBS is not ideal for the expansion of cells mean for clinical applications as it possesses the risk of animal pathogen transmission and animal protein transfer to host. Human platelet lysate (HPL) appears to be a suitable alternative to FBS as it is rich in biological factors that enhance cell proliferation. Thus far, HPL has been found to be superior in promoting chondrocyte proliferation compared to FBS. However, both HPL and FBS cannot prevent chondrocyte dedifferentiation. Discrepant results have been reported for the maintenance of chondrocyte redifferentiation potential by HPL. These differences are likely due to the diversity in the HPL preparation methods. In the future, more studies on HPL need to be performed to develop a standardized technique which is capable of producing HPL that can maintain the chondrocyte redifferentiation potential reproducibly. This review discusses the in vitro expansion of chondrocytes with FBS and HPL, focusing on its capability to promote the proliferation and maintain the chondrogenic characteristics of chondrocytes.

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Hiemer, Bettina, Kathleen Achenbach, Juliane Pasold, Andreas Wree, and Rainer Bader. "Transient supplementation of growth factor TGF-β1 effectively initiates chondrogenic redifferentiation of human chondrocytes." Current Directions in Biomedical Engineering 3, no. 2 (September 7, 2017): 383–87. http://dx.doi.org/10.1515/cdbme-2017-0080.

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AbstractCartilage tissue is avascular with less regeneration potential and therefore, cartilage regeneration is still a major challenge for therapeutic approaches. Commonly used treatment strategies involve the transplantation of autologous chondrocytes into the defect. Before that, it is required to increase the cell number in vitro resulting in unwanted chondrocyte dedifferentiation. This could impair subsequent tissue regeneration. Both growth factors TGF-ß1 and IGF-1 are used as strong inducer of chondrogenic redifferentiation, however, a controlled application of TGF-ß1 is essential to avoid adverse effects. Therefore, in the present study, we investigated the time-dependent influence of TGF-ß1 administration on chondrocyte redifferentiation.Human chondrocytes were embedded in alginate and cultured in serum-free DMEM containing ascorbic acid, dexamethasone, ITSTM and IGF-1. TGF-β1 was supplemented for 3, 7 and 21 days. Afterwards, cell viability and synthesis of extracellular matrix (ECM) proteins was analyzed by histological staining.Live/dead staining of chondrocytes incubated with TGF-β1 for 21 days displayed an enhanced proliferation and formation of cell clusters resulting in excessive outgrowth of fibroblastic-like cells. However, exposure to TGF-β1 over only 7 days caused also cell clustering with moderate cell proliferation. Additionally, after 21 days of cultivation proteoglycan synthesis was identified by alcian blue staining after both TGF-β1 supplementation for 21 and also 7 days. Aggrecan was also detected in the periphery of the cell clusters after TGF-β1 incubation for only 7 days. Chondrocytes lacked proteoglycan expression after three-day TGF-β1 administration.We could show, that prolonged administration of TGF-β1 results in massive proliferation of chondrocytes which is accompanied by cell outgrowth. We found that TGF-ß1 exposure for seven days is sufficient for achievement of cell clustering without excessive cell proliferation, which is important for inducing subsequent chondrogenic differentiation. Results indicate that even an initial TGF-β1 administration could be sufficient for inducing chondrocyte proliferation and differentiation in vitro.

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Haseeb, Abdul, Ranjan Kc, Marco Angelozzi, Charles de Charleroy, Danielle Rux, Robert J. Tower, Lutian Yao, et al. "SOX9 keeps growth plates and articular cartilage healthy by inhibiting chondrocyte dedifferentiation/osteoblastic redifferentiation." Proceedings of the National Academy of Sciences 118, no. 8 (February 17, 2021): e2019152118. http://dx.doi.org/10.1073/pnas.2019152118.

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Cartilage is essential throughout vertebrate life. It starts developing in embryos when osteochondroprogenitor cells commit to chondrogenesis, activate a pancartilaginous program to form cartilaginous skeletal primordia, and also embrace a growth-plate program to drive skeletal growth or an articular program to build permanent joint cartilage. Various forms of cartilage malformation and degeneration diseases afflict humans, but underlying mechanisms are still incompletely understood and treatment options suboptimal. The transcription factor SOX9 is required for embryonic chondrogenesis, but its postnatal roles remain unclear, despite evidence that it is down-regulated in osteoarthritis and heterozygously inactivated in campomelic dysplasia, a severe skeletal dysplasia characterized postnatally by small stature and kyphoscoliosis. Using conditional knockout mice and high-throughput sequencing assays, we show here that SOX9 is required postnatally to prevent growth-plate closure and preosteoarthritic deterioration of articular cartilage. Its deficiency prompts growth-plate chondrocytes at all stages to swiftly reach a terminal/dedifferentiated stage marked by expression of chondrocyte-specific (Mgp) and progenitor-specific (Nt5e and Sox4) genes. Up-regulation of osteogenic genes (Runx2, Sp7, and Postn) and overt osteoblastogenesis quickly ensue. SOX9 deficiency does not perturb the articular program, except in load-bearing regions, where it also provokes chondrocyte-to-osteoblast conversion via a progenitor stage. Pathway analyses support roles for SOX9 in controlling TGFβ and BMP signaling activities during this cell lineage transition. Altogether, these findings deepen our current understanding of the cellular and molecular mechanisms that specifically ensure lifelong growth-plate and articular cartilage vigor by identifying osteogenic plasticity of growth-plate and articular chondrocytes and a SOX9-countered chondrocyte dedifferentiation/osteoblast redifferentiation process.

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Jeyakumar, Vivek, Eugenia Niculescu-Morzsa, Christoph Bauer, Zsombor Lacza, and Stefan Nehrer. "Redifferentiation of Articular Chondrocytes by Hyperacute Serum and Platelet Rich Plasma in Collagen Type I Hydrogels." International Journal of Molecular Sciences 20, no. 2 (January 14, 2019): 316. http://dx.doi.org/10.3390/ijms20020316.

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Matrix-assisted autologous chondrocyte transplantation (MACT) for focal articular cartilage defects often fails to produce adequate cartilage-specific extracellular matrix in vitro and upon transplantation results in fibrocartilage due to dedifferentiation during cell expansion. This study aimed to redifferentiate the chondrocytes through supplementation of blood-products, such as hyperacute serum (HAS) and platelet-rich plasma (PRP) in vitro. Dedifferentiated monolayer chondrocytes embedded onto collagen type I hydrogels were redifferentiated through supplementation of 10% HAS or 10% PRP for 14 days in vitro under normoxia (20% O2) and hypoxia (4% O2). Cell proliferation was increased by supplementing HAS for 14 days (p < 0.05) or by interchanging from HAS to PRP during Days 7–14 (p < 0.05). Sulfated glycosaminoglycan (sGAG) content was deposited under both HAS, and PRP for 14 days and an interchange during Days 7–14 depleted the sGAG content to a certain extent. PRP enhanced the gene expression of anabolic markers COL2A1 and SOX9 (p < 0.05), whereas HAS enhanced COL1A1 production. An interchange led to reduction of COL1A1 and COL2A1 expression marked by increased MMP13 expression (p < 0.05). Chondrocytes secreted less IL-6 and more PDGF-BB under PRP for 14 days (p < 0.0.5). Hypoxia enhanced TGF-β1 and BMP-2 release in both HAS and PRP. Our study demonstrates a new approach for chondrocyte redifferentiation.

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ZAUCKE, Frank, Robert DINSER, Patrik MAURER, and Mats PAULSSON. "Cartilage oligomeric matrix protein (COMP) and collagen IX are sensitive markers for the differentiation state of articular primary chondrocytes." Biochemical Journal 358, no. 1 (August 8, 2001): 17–24. http://dx.doi.org/10.1042/bj3580017.

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Primary chondrocytes dedifferentiate in serial monolayer with respect to their morphological and biosynthetic phenotype. They change from a round to a flattened fibroblast-like shape, and collagen I is secreted instead of the cartilage-specific collagen II. We analysed in detail the time course of dedifferentiation of mature bovine articular chondrocytes in monolayer for up to 32 weeks. Assessment of RNA expression by reverse transcription-PCR led to the identification of two novel phenotypical markers, the cartilage oligomeric matrix protein (COMP) and collagen IX, which are down-regulated faster than the widely accepted marker, collagen II. The different kinetics of COMP and collagen expression suggest differential regulation at the level of transcription. Immunostaining and metabolic labelling experiments confirmed the switch in the collagen expression pattern and the rapid down-regulation of de novo synthesis of COMP and collagen IX. Culture of chondrocytes in a three-dimensional matrix is known to stabilize the chondrocytic phenotype. We maintained cells for up to 28 weeks in an alginate bead system, which prevented dedifferentiation and led to a stabilization of collagen and COMP expression. Immunohistochemical analysis of the alginate beads revealed a similar distribution of matrix proteins to that found in vivo. Chondrocytes were transferred after a variable length of monolayer culture into the alginate matrix and the potential for redifferentiation was investigated. The re-expression of COMP and collagen IX was differentially regulated. The expression of COMP was re-induced within days after transfer into the three-dimensional matrix, while the expression of collagen IX was irreversibly down-regulated. In summary, these results demonstrate that the potential for redifferentiation decreases with increasing length of monolayer culture and show that the alginate bead system represents an attractive in vitro model to study the chondrocyte de- and re-differentiation processes, as well as extracellular matrix assembly.

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Finer, M. H., L. C. Gerstenfeld, D. Young, P. Doty, and H. Boedtker. "Collagen expression in embryonic chicken chondrocytes treated with phorbol myristate acetate." Molecular and Cellular Biology 5, no. 6 (June 1985): 1415–24. http://dx.doi.org/10.1128/mcb.5.6.1415.

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Growth of embryonic chicken sternal chondrocytes in the presence of phorbol-12-myristate-13-acetate (PMA), a potent tumor promoter, resulted in a dramatic morphological change from spherical floating cells to adherent fibroblastic cells. This morphological change was accompanied by a quantitative switch from synthesis of cartilage-specific type II procollagen to type I procollagen. Type II procollagen mRNA levels decreased 10-fold in PMA-treated cells. Activation of type I collagen genes led to the accumulation of type I procollagen mRNA levels comparable to those of type II mRNA in these cells. However, only type I procollagen mRNA was translated. In addition to gene activation, unprocessed pro alpha 1(I) transcripts present at low levels in control chondrocytes were processed to mature mRNA species. Redifferentiation of PMA-treated chondrocytes was possible if cells were removed from PMA after the morphological change and cessation of type II procollagen synthesis but before detectable amounts of type I procollagen were synthesized. Production of type I collagen thus marks a late phase of chondrocyte "dedifferentiation" from which reversion is no longer possible. Redifferentiated cell populations contained 24-fold more pro alpha 1(II) collagen mRNA than pro alpha 1(I) collagen mRNA, but the rates of procollagen synthesis were comparable. This suggests that the PMA-mediated dedifferentiation of chondrocytes as well as their redifferentiation is under both transcriptional and posttranscriptional regulation.

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Finer, M. H., L. C. Gerstenfeld, D. Young, P. Doty, and H. Boedtker. "Collagen expression in embryonic chicken chondrocytes treated with phorbol myristate acetate." Molecular and Cellular Biology 5, no. 6 (June 1985): 1415–24. http://dx.doi.org/10.1128/mcb.5.6.1415-1424.1985.

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Growth of embryonic chicken sternal chondrocytes in the presence of phorbol-12-myristate-13-acetate (PMA), a potent tumor promoter, resulted in a dramatic morphological change from spherical floating cells to adherent fibroblastic cells. This morphological change was accompanied by a quantitative switch from synthesis of cartilage-specific type II procollagen to type I procollagen. Type II procollagen mRNA levels decreased 10-fold in PMA-treated cells. Activation of type I collagen genes led to the accumulation of type I procollagen mRNA levels comparable to those of type II mRNA in these cells. However, only type I procollagen mRNA was translated. In addition to gene activation, unprocessed pro alpha 1(I) transcripts present at low levels in control chondrocytes were processed to mature mRNA species. Redifferentiation of PMA-treated chondrocytes was possible if cells were removed from PMA after the morphological change and cessation of type II procollagen synthesis but before detectable amounts of type I procollagen were synthesized. Production of type I collagen thus marks a late phase of chondrocyte "dedifferentiation" from which reversion is no longer possible. Redifferentiated cell populations contained 24-fold more pro alpha 1(II) collagen mRNA than pro alpha 1(I) collagen mRNA, but the rates of procollagen synthesis were comparable. This suggests that the PMA-mediated dedifferentiation of chondrocytes as well as their redifferentiation is under both transcriptional and posttranscriptional regulation.

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9

Bianchi, Vanessa J., Adrienne Lee, Jesse Anderson, Justin Parreno, John Theodoropoulos, David Backstein, and Rita Kandel. "Redifferentiated Chondrocytes in Fibrin Gel for the Repair of Articular Cartilage Lesions." American Journal of Sports Medicine 47, no. 10 (July 2, 2019): 2348–59. http://dx.doi.org/10.1177/0363546519857571.

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Background: Autologous chondrocyte implantation, which uses passaged chondrocytes, commonly leads to the formation of fibrocartilage. When chondrocytes are passaged to increase cell numbers, they lose their phenotype and ability to form hyaline cartilage. The use of transforming growth factor β (TGFβ) to redifferentiate passaged chondrocytes has been validated in vitro; however, it is unknown if redifferentiated chondrocytes will enhance defect repair when implanted in vivo. Furthermore, fibrin gel is used in orthopaedic surgery as a fixative and scaffold and could be an appropriate carrier to enhance retention of cells in the repair site. Purpose: To investigate if passaged redifferentiated chondrocytes in fibrin gel have the ability to form cartilage tissue and if these redifferentiated cells will enhance the formation of hyaline cartilage in vivo when implanted into critical-size osteochondral defects. Study Design: Controlled laboratory study. Methods: Rabbit and human chondrocytes were serially passaged twice in monolayer culture. Twice-passaged cells were used directly (dedifferentiated) or redifferentiated in high-density culture with TGFβ3. Dedifferentiated or redifferentiated cells were mixed with fibrin gel to form fibrin clots, which were cultured in vitro to assess the use of fibrin gel as a scaffold or implanted in vivo in a critical-size osteochondral defect in New Zealand White rabbit knee joints. Rabbits were sacrificed 6 weeks after implantation, and tissues were assessed histologically and by immunohistochemistry. Results: Redifferentiation of passaged chondrocytes by means of 3-dimensional culture in the presence of TGFβ3 improved the formation of cartilaginous tissues in vitro, and culture in fibrin gel did not affect the cell phenotype. Implantation of dedifferentiated cells in vivo resulted in fibrocartilaginous repair tissues. Redifferentiated chondrocyte implants resulted in granulation tissues containing the hyaline cartilage marker collagen type 2. Conclusion: Redifferentiated chondrocytes will maintain their chondrogenic differentiation in fibrin clots. Implanted redifferentiated chondrocytes show a different reparative response than dedifferentiated chondrocytes and do not appear to enhance repair at an early time point. Another study of longer duration is required to assess tissue maturation over time. Clinical Relevance: Redifferentiation of passaged chondrocytes with TGFβ3 before implantation does not improve defect repair in the first 6 weeks.

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Feyerabend, Frank, Frank Witte, Michael Kammal, and Regine Willumeit. "Unphysiologically High Magnesium Concentrations Support Chondrocyte Proliferation and Redifferentiation." Tissue Engineering 12, no. 12 (December 2006): 3545–56. http://dx.doi.org/10.1089/ten.2006.12.3545.

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11

Haudenschild, Dominik R., John M. McPherson, Ross Tubo, and Fran�ois Binette. "Differential expression of multiple genes during articular chondrocyte redifferentiation." Anatomical Record 263, no. 1 (2001): 91–98. http://dx.doi.org/10.1002/ar.1079.

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12

Babur, Betul Kul, Parisa Ghanavi, Peter Levett, William B. Lott, Travis Klein, Justin J. Cooper-White, Ross Crawford, and Michael R. Doran. "The Interplay between Chondrocyte Redifferentiation Pellet Size and Oxygen Concentration." PLoS ONE 8, no. 3 (March 15, 2013): e58865. http://dx.doi.org/10.1371/journal.pone.0058865.

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Meretoja, Ville V., Rebecca L. Dahlin, Sarah Wright, F. Kurtis Kasper, and Antonios G. Mikos. "Articular Chondrocyte Redifferentiation in 3D Co-cultures with Mesenchymal Stem Cells." Tissue Engineering Part C: Methods 20, no. 6 (June 2014): 514–23. http://dx.doi.org/10.1089/ten.tec.2013.0532.

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Schuurman, Wouter, Debby Gawlitta, Travis J. Klein, Werner ten Hoope, Mattie H. P. van Rijen, Wouter J. A. Dhert, P. René van Weeren, and Jos Malda. "Zonal Chondrocyte Subpopulations Reacquire Zone-Specific Characteristics during in Vitro Redifferentiation." American Journal of Sports Medicine 37, no. 1_suppl (November 2009): 97–104. http://dx.doi.org/10.1177/0363546509350978.

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Furukawa, Katsuko S., Hideyuki Suenaga, Kenshi Toita, Akiko Numata, Junzo Tanaka, Takashi Ushida, Yasuyuki Sakai, and Tetsuya Tateishi. "Rapid and Large-Scale Formation of Chondrocyte Aggregates by Rotational Culture." Cell Transplantation 12, no. 5 (July 2003): 475–79. http://dx.doi.org/10.3727/000000003108747037.

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Chondrocytes in articular cartilage synthesize collagen type II and large sulfated proteoglycans, whereas the same cells cultured in monolayer (2D) dedifferentiate into fibroblastic cells and express collagen type I and small proteoglycans. On the other hand, a pellet culture system was developed as a method for preventing the phenotypic modulation of chondrocytes and promoting the redifferentiation of dedifferentiated ones. Because the pellet culture system forms only one cell aggregate each tube by a centrifugator, the pellet could not be applied to produce a tissue-engineered cartilage. Therefore, we tried to form chondrocyte aggregates by a rotational culture, expecting to form a large number of aggregates at once. In order to increase cell–cell interactions and decrease chondrocyte–material interaction, dishes with low retention of protein adsorption and cell adhesiveness were used. In addition, rotational shaking of the dish including cells was attempted to increase the cell–cell interaction. The shaking speed was set at 80 rpm, so the cells would be distributed in the center of the dish to augment the frequency of cell–cell contact. Under these conditions, bovine articular chondrocytes started aggregating in a few hours. At 24–36 h of rotational culture, aggregates with smooth surfaces were observed. Parameters such as increase of culture time and addition of TGF-β controlled diameters of the aggregates. There were many fusiform cells at the periphery of the aggregates, where the cells tended to form a multilayered zone in cross sections. In addition, lacune-like structure, which was almost the same as pellet culture, was observed. It was found that the internal structure of the aggregates was similar to that of pellets reported previously. Therefore, the aggregates formed by a rotational culture could become an essential component to make tissue-engineered artificial cartilage.

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von Bomhard, Achim, Joseph Faust, Alexander F. Elsaesser, Silke Schwarz, Katharina Pippich, and Nicole Rotter. "Impact of expansion and redifferentiation under hypothermia on chondrogenic capacity of cultured human septal chondrocytes." Journal of Tissue Engineering 8 (January 1, 2017): 204173141773265. http://dx.doi.org/10.1177/2041731417732655.

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A critical limitation in the cultivation of cartilage for tissue engineering is the dedifferentiation in chondrocytes, mainly during in vitro amplification. Despite many previous studies investigating the influence of various conditions, no data exist concerning the effects of hypothermia. Our aim has been to influence chondrocyte dedifferentiation in vitro by hypothermic conditions. Chondrocytes were isolated from cartilage biopsies and seeded in monolayer and in three-dimensional pellet-cultures. Each cell culture was either performed at 32.2°C or 37°C during amplification. Additionally, the influence of the redifferentiation of chondrocytes in three-dimensional cell culture was examined at 32.2°C and 37°C after amplification at 32.2°C or 37°C. An 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was used to measure cell proliferation in monolayer, whereas the polymerase chain reaction and immunohistochemical and histological staining were used in three-dimensional pellet-cultures. Real-time polymerase chain reaction was employed to measure the relative expression of the target genes collagen II, collagen I, aggrecan and versican. Ratios were estimated between collagen II/collagen I and aggrecan/versican to evaluate differentiation. A higher value of these ratios indicated an advantageous status of differentiation. In monolayer, hypothermia at 32.2°C slowed down the proliferation rate of chondrocytes significantly, being up to two times lower at 32.2°C compared with culture at 37°C. Simultaneously, hypothermia in monolayer decelerated dedifferentiation. The ratio of aggrecan/versican was significantly higher at 32.2°C compared with that at 37°C. In three-dimensional pellet-culture, the chondrocytes redifferentiated at 32.2°C and at 37°C, and this process is more distinct at 37°C than at 32.2°C. Similar results were obtained for the ratios of collagen II/collagen I and aggrecan/versican and were supported by immunochemical and histological staining. Thus, hypothermic conditions for chondrocytes are mainly advantageous in monolayer culture. In three-dimensional pellet-culture, redifferentiation predominates at 37°C compared with at 32.2°C. In particular, the results from the monolayer cultures show potential in the avoidance of dedifferentiation.

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Homicz, Mark R., Stanley H. Chia, Barbara L. Schumacher, Koichi Masuda, Eugene J. Thonar, Robert L. Sah, and Deborah Watson. "Human Septal Chondrocyte Redifferentiation in Alginate, Polyglycolic Acid Scaffold, and Monolayer Culture." Laryngoscope 113, no. 1 (January 2003): 25–32. http://dx.doi.org/10.1097/00005537-200301000-00005.

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Levett, Peter A., Ferry P. W. Melchels, Karsten Schrobback, Dietmar W. Hutmacher, Jos Malda, and Travis J. Klein. "Chondrocyte redifferentiation and construct mechanical property development in single-component photocrosslinkable hydrogels." Journal of Biomedical Materials Research Part A 102, no. 8 (September 2, 2013): 2544–53. http://dx.doi.org/10.1002/jbm.a.34924.

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Kim, Min-Sook, Hyung-Kyu Kim, and Deok-Woo Kim. "Cartilage tissue engineering for craniofacial reconstruction." Archives of Plastic Surgery 47, no. 5 (September 15, 2020): 392–403. http://dx.doi.org/10.5999/aps.2020.01095.

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Severe cartilage defects and congenital anomalies affect millions of people and involve considerable medical expenses. Tissue engineering offers many advantages over conventional treatments, as therapy can be tailored to specific defects using abundant bioengineered resources. This article introduces the basic concepts of cartilage tissue engineering and reviews recent progress in the field, with a focus on craniofacial reconstruction and facial aesthetics. The basic concepts of tissue engineering consist of cells, scaffolds, and stimuli. Generally, the cartilage tissue engineering process includes the following steps: harvesting autologous chondrogenic cells, cell expansion, redifferentiation, <i>in vitro</i> incubation with a scaffold, and transfer to patients. Despite the promising prospects of cartilage tissue engineering, problems and challenges still exist due to certain limitations. The limited proliferation of chondrocytes and their tendency to dedifferentiate necessitate further developments in stem cell technology and chondrocyte molecular biology. Progress should be made in designing fully biocompatible scaffolds with a minimal immune response to regenerate tissue effectively.

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Lauer, Jasmin C., Mischa Selig, Melanie L. Hart, Bodo Kurz, and Bernd Rolauffs. "Articular Chondrocyte Phenotype Regulation through the Cytoskeleton and the Signaling Processes That Originate from or Converge on the Cytoskeleton: Towards a Novel Understanding of the Intersection between Actin Dynamics and Chondrogenic Function." International Journal of Molecular Sciences 22, no. 6 (March 23, 2021): 3279. http://dx.doi.org/10.3390/ijms22063279.

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Numerous studies have assembled a complex picture, in which extracellular stimuli and intracellular signaling pathways modulate the chondrocyte phenotype. Because many diseases are mechanobiology-related, this review asked to what extent phenotype regulators control chondrocyte function through the cytoskeleton and cytoskeleton-regulating signaling processes. Such information would generate leverage for advanced articular cartilage repair. Serial passaging, pro-inflammatory cytokine signaling (TNF-α, IL-1α, IL-1β, IL-6, and IL-8), growth factors (TGF-α), and osteoarthritis not only induce dedifferentiation but also converge on RhoA/ROCK/Rac1/mDia1/mDia2/Cdc42 to promote actin polymerization/crosslinking for stress fiber (SF) formation. SF formation takes center stage in phenotype control, as both SF formation and SOX9 phosphorylation for COL2 expression are ROCK activity-dependent. Explaining how it is molecularly possible that dedifferentiation induces low COL2 expression but high SF formation, this review theorized that, in chondrocyte SOX9, phosphorylation by ROCK might effectively be sidelined in favor of other SF-promoting ROCK substrates, based on a differential ROCK affinity. In turn, actin depolymerization for redifferentiation would “free-up” ROCK to increase COL2 expression. Moreover, the actin cytoskeleton regulates COL1 expression, modulates COL2/aggrecan fragment generation, and mediates a fibrogenic/catabolic expression profile, highlighting that actin dynamics-regulating processes decisively control the chondrocyte phenotype. This suggests modulating the balance between actin polymerization/depolymerization for therapeutically controlling the chondrocyte phenotype.

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Lee, Dug Keun, Kyoung Baek Choi, In Suk Oh, Sun U. Song, Sally Hwang, Chae-Lyul Lim, Jong-Pil Hyun, et al. "Continuous Transforming Growth Factor β1Secretion by Cell-Mediated Gene Therapy Maintains Chondrocyte Redifferentiation." Tissue Engineering 11, no. 1-2 (January 2005): 310–18. http://dx.doi.org/10.1089/ten.2005.11.310.

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Schuh, Elena, Sandra Hofmann, Kathryn Stok, Holger Notbohm, Ralph Müller, and Nicole Rotter. "Chondrocyte redifferentiation in 3D: The effect of adhesion site density and substrate elasticity." Journal of Biomedical Materials Research Part A 100A, no. 1 (October 4, 2011): 38–47. http://dx.doi.org/10.1002/jbm.a.33226.

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Chen, Wei-Hong, Hen-Yu Liu, Ching-Yu Tsai, Chia-che Wu, Hong-Jian Wei, Alice Liu, Ming-Tang Lai, Chiung-Fang Huang, and Win-Ping Deng. "The Potential Use of Platelet-Rich Plasma to Reconstruct the Microtia Chondrocyte in Human Auricular Cartilage Regeneration." Journal of Nanomaterials 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/250615.

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Microtia is characterized as an incomplete auricular development and surgical reconstruction for microtia is still limited even with emerging developments. This study aimed to apply bionanomaterials (PRP/collagen scaffold) for human auricular neocartilage reconstruction by using microtia chondrocytes. The results showed that PRP (TGF-β1 750 pg/mL and 1 ng/mL) increased cell viability of microtia chondrocytes during in vitro 9-day cultures. Additionally, chondrogenic-specific mRNA of Aggrecan and type II collagen (Col II) was significantly and continuously expressed with PRP treatment during the 21-day in vitro expansion. Tissue engineering of auricular neocartilage was performed by seeding microtia chondrocytes in bionanomaterials (PRP/collagen scaffold) 3-dimensional (3D) cultures. Immunohistochemistry (IHC) of Col II showed intensive signals between cells and matrix after 4-week cultures. Conclusion. Our results demonstrated that PRP promotes proliferation and redifferentiation of microtia chondrocytes and provides regenerative potentials in auricular neocartilage reconstruction.

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Ito, A., T. Aoyama, J. Tajino, M. Nagai, S. Yamaguchi, H. Iijima, X. Zhang, H. Akiyama, and H. Kuroki. "Effects of culturing temperature on extracellular matrix formation and redifferentiation of expanded human chondrocyte." Osteoarthritis and Cartilage 22 (April 2014): S170. http://dx.doi.org/10.1016/j.joca.2014.02.318.

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Miot, Sylvie, Tim Woodfield, Alma U. Daniels, Rosemarie Suetterlin, Iman Peterschmitt, Michael Heberer, Clemens A. van Blitterswijk, Jens Riesle, and Ivan Martin. "Effects of scaffold composition and architecture on human nasal chondrocyte redifferentiation and cartilaginous matrix deposition." Biomaterials 26, no. 15 (May 2005): 2479–89. http://dx.doi.org/10.1016/j.biomaterials.2004.06.048.

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26

Parreno, Justin, Vanessa J. Bianchi, Corey Sermer, Suresh C. Regmi, David Backstein, Tannin A. Schmidt, and Rita A. Kandel. "Adherent agarose mold cultures: An in vitro platform for multi-factorial assessment of passaged chondrocyte redifferentiation." Journal of Orthopaedic Research® 36, no. 9 (April 24, 2018): 2392–405. http://dx.doi.org/10.1002/jor.23896.

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27

Pei, Ming, and Fan He. "Extracellular matrix deposited by synovium-derived stem cells delays replicative senescent chondrocyte dedifferentiation and enhances redifferentiation." Journal of Cellular Physiology 227, no. 5 (January 23, 2012): 2163–74. http://dx.doi.org/10.1002/jcp.22950.

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28

Rakic, Rodolphe, Bastien Bourdon, Magalie Hervieu, Thomas Branly, Florence Legendre, Nathalie Saulnier, Fabrice Audigié, Stéphane Maddens, Magali Demoor, and Philippe Galera. "RNA Interference and BMP-2 Stimulation Allows Equine Chondrocytes Redifferentiation in 3D-Hypoxia Cell Culture Model: Application for Matrix-Induced Autologous Chondrocyte Implantation." International Journal of Molecular Sciences 18, no. 9 (August 24, 2017): 1842. http://dx.doi.org/10.3390/ijms18091842.

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29

Pahoff, Stephen, Christoph Meinert, Onur Bas, Long Nguyen, Travis J. Klein, and Dietmar W. Hutmacher. "Effect of gelatin source and photoinitiator type on chondrocyte redifferentiation in gelatin methacryloyl-based tissue-engineered cartilage constructs." Journal of Materials Chemistry B 7, no. 10 (2019): 1761–72. http://dx.doi.org/10.1039/c8tb02607f.

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30

Varela-Eirín, Marta, Paula Carpintero-Fernández, Agustín Sánchez-Temprano, Adrián Varela-Vázquez, Carlos Luis Paíno, Antonio Casado-Díaz, Alfonso Calañas Continente, et al. "Senolytic activity of small molecular polyphenols from olive restores chondrocyte redifferentiation and promotes a pro-regenerative environment in osteoarthritis." Aging 12, no. 16 (August 3, 2020): 15882–905. http://dx.doi.org/10.18632/aging.103801.

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31

Kim, Yun Hee, and Jin Woo Lee. "Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen." Journal of Cellular Physiology 218, no. 3 (March 2009): 623–30. http://dx.doi.org/10.1002/jcp.21637.

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32

Yao, Yongchang, Feng Zhang, Patricia Xiaotian Pang, Kai Su, Ruijie Zhou, Yingjun Wang, and Dong-An Wang. "In vitro study of chondrocyte redifferentiation with lentiviral vector-mediated transgenic TGF-β3 and shRNA suppressing type I collagen in three-dimensional culture." Journal of Tissue Engineering and Regenerative Medicine 5, no. 8 (May 5, 2011): e219-e227. http://dx.doi.org/10.1002/term.425.

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33

Duval, Elise, Sylvain Leclercq, Jean-Marc Elissalde, Magali Demoor, Philippe Galéra, and Karim Boumédiene. "Hypoxia-inducible factor 1α inhibits the fibroblast-like markers type I and type III collagen during hypoxia-induced chondrocyte redifferentiation: Hypoxia not only induces type II collagen and aggrecan, but it also inhibits type I and type III collagen in the hypoxia-inducible factor 1α-dependent redifferentiation of chondrocytes." Arthritis & Rheumatism 60, no. 10 (October 2009): 3038–48. http://dx.doi.org/10.1002/art.24851.

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34

Ecke, Lutter, Scholka, Hansch, Becker, and Anderer. "Tissue Specific Differentiation of Human Chondrocytes Depends on Cell Microenvironment and Serum Selection." Cells 8, no. 8 (August 19, 2019): 934. http://dx.doi.org/10.3390/cells8080934.

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Abstract:

Therapeutic options to cure osteoarthritis (OA) are not yet available, although cell-based therapies for the treatment of traumatic defects of cartilage have already been developed using, e.g., articular chondrocytes. In order to adapt cell-based therapies to treat OA, appropriate cell culture conditions are necessary. Chondrocytes require a 3-dimensional (3D) environment for redifferentiation after 2-dimensional (2D) expansion. Fetal bovine serum (FBS) is commonly used as a medium supplement, although the usage of a xenogeneic serum could mask the intrinsic behavior of human cells in vitro. The aim of this study was to compare human articular chondrocytes cultivated as monolayers (2D) and the development of microtissues (3D) in the presence of FBS with those cultivated with human serum (HS). Evaluation of the expression of various markers via immunocytochemistry on monolayer cells revealed a higher dedifferentiation degree of chondrocytes cultivated with HS. Scaffold-free microtissues were generated using the agar overlay technique, and their differentiation level was evaluated via histochemistry and immunohistochemistry. Microtissues cultivated in the medium with FBS showed a higher redifferentiation level. This was evidenced by bigger microtissues and a more cartilage-like composition of the matrix with not any/less positivity for cartilage-specific markers in HS versus moderate-to-high positivity in FBS-cultured microtissues. The present study showed that the differentiation degree of chondrocytes depends both on the microenvironment of the cells and the serum type with FBS achieving the best results. However, HS should be preferred for the engineering of cartilage-like microtissues, as it rather enables a "human-based" situation in vitro. Hence, cultivation conditions might be further optimized to gain an even more adequate and donor-independent redifferentiation of chondrocytes in microtissues, e.g., designing a suitable chemically-defined serum supplement.

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Tallheden, Tommi, Camilla Karlsson, Andreas Brunner, Josefine van der Lee, Rupert Hagg, Roberto Tommasini, and Anders Lindahl. "Gene expression during redifferentiation of human articular chondrocytes." Osteoarthritis and Cartilage 12, no. 7 (July 2004): 525–35. http://dx.doi.org/10.1016/j.joca.2004.03.004.

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36

Malda, J., C. A. van Blitterswijk, M. Grojec, D. E. Martens, J. Tramper, and J. Riesle. "Expansion of Bovine Chondrocytes on Microcarriers Enhances Redifferentiation." Tissue Engineering 9, no. 5 (October 2003): 939–48. http://dx.doi.org/10.1089/107632703322495583.

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Lee, Tae-Jin, Suk Ho Bhang, Wan-Guen La, Hee Seok Yang, Jun Yeup Seong, Haeshin Lee, Gun-Il Im, Soo-Hong Lee, and Byung-Soo Kim. "Spinner-flask culture induces redifferentiation of de-differentiated chondrocytes." Biotechnology Letters 33, no. 4 (December 2, 2010): 829–36. http://dx.doi.org/10.1007/s10529-010-0488-1.

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38

G., Schulze-Tanzil, P. de Souza, H. Villegas Castrejon, John T., Merker H.-J., Scheid A., and Shakibaei M. "Redifferentiation of dedifferentiated human chondrocytes in high-density cultures." Cell and Tissue Research 308, no. 3 (June 1, 2002): 371–79. http://dx.doi.org/10.1007/s00441-002-0562-7.

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39

Sanchez, M., E. Gionti, G. Pontarelli, A. Arcella, and F. De Lorenzo. "Expression of type X collagen is transiently stimulated in redifferentiating chondrocytes pretreated with retinoic acid." Biochemical Journal 276, no. 1 (May 15, 1991): 183–87. http://dx.doi.org/10.1042/bj2760183.

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Abstract:

Growth of quail chondrocytes in the presence of retinoic acid (RA) results in the suppression of the differentiated phenotype. RA-treated chondrocytes recover their differentiated phenotype if they are cultured for an additional 15 days in the absence of RA. A few days after removal from RA, treated chondrocytes acquire the polygonal morphology characteristic of chondrocytes growing as attached cells; they also gradually resume collagen II expression and synthesize cultures. The levels of collagen X mRNA decrease during the second week of culture in the absence of RA. Finally, at the end of 15 days, the absolute levels of collagen II and collagen X mRNAs are very similar in control and recovering chondrocytes.

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40

Malda, J., E. Kreijveld, J. S. Temenoff, C. A. van Blitterswijk, and J. Riesle. "Expansion of human nasal chondrocytes on macroporous microcarriers enhances redifferentiation." Biomaterials 24, no. 28 (December 2003): 5153–61. http://dx.doi.org/10.1016/s0142-9612(03)00428-9.

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41

Caron, M. J., P. J. Emans, L. Voss, D. A. Surtel, M. M. Coolsen, L. W. van Rhijn, and T. J. Welting. "Redifferentiation of human articular chondrocytes in 2D versus 3D culture." Osteoarthritis and Cartilage 20 (April 2012): S146. http://dx.doi.org/10.1016/j.joca.2012.02.210.

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42

Yang, Jing Jing, Yong Mei Chen, Jian Fang Liu, Takayuki Kurokawa, and Jian Ping Gong. "Spontaneous Redifferentiation of Dedifferentiated Human Articular Chondrocytes on Hydrogel Surfaces." Tissue Engineering Part A 16, no. 8 (August 2010): 2529–40. http://dx.doi.org/10.1089/ten.tea.2009.0647.

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43

Heyland, Jan, Katharina Wiegandt, Christiane Goepfert, Stefanie Nagel-Heyer, Eduard Ilinich, Udo Schumacher, and Ralf Pörtner. "Redifferentiation of chondrocytes and cartilage formation under intermittent hydrostatic pressure." Biotechnology Letters 28, no. 20 (August 11, 2006): 1641–48. http://dx.doi.org/10.1007/s10529-006-9144-1.

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44

Dufour, Alexandre, Frédéric Mallein-Gerin, and Emeline Perrier-Groult. "Direct Perfusion Improves Redifferentiation of Human Chondrocytes in Fibrin Hydrogel with the Deposition of Cartilage Pericellular Matrix." Applied Sciences 11, no. 19 (September 24, 2021): 8923. http://dx.doi.org/10.3390/app11198923.

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Abstract:

Articular cartilage has limited potential for self-repair, and cell-based strategies combining scaffolds and chondrocytes are currently used to treat cartilage injuries. However, achieving a satisfying level of cell redifferentiation following expansion remains challenging. Hydrogels and perfusion bioreactors are known to exert beneficial cues on chondrocytes; however, the effect of a combined approach on the quality of cartilage matrix deposited by cells is not fully understood. Here, we combined soluble factors (BMP-2, Insulin, and Triiodothyronine, that is, BIT), fibrin hydrogel, direct perfusion and human articular chondrocytes (HACs) to engineer large cartilage tissues. Following cell expansion, cells were embedded in fibrin gels and cultivated under either static or perfusion conditions. The nature of the matrix synthesized was assessed by Western blotting and immunohistochemistry. The stability of cartilage grafts and integration with native tissue were also investigated by subcutaneous implantation of human osteochondral cylinders in nude mice. Perfusion preconditioning improved matrix quality and spatial distribution. Specifically, perfusion preconditioning resulted in a matrix rich in type II collagen but not in type I collagen, indicating the reconstruction of hyaline cartilage. Remarkably, the production of type VI collagen, the main component of the pericellular matrix, was also increased, indicating that chondrocytes were connecting to the hyaline matrix they produced.

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45

Wiegandt, K., J. Heyland, C. Goepfert, S. Nagel-Heyer, U. Schumacher, and R. Pörtner. "Effect of intermittent loading on redifferentiation of chondrocytes and cartilage formation." Journal of Biomechanics 39 (January 2006): S576—S577. http://dx.doi.org/10.1016/s0021-9290(06)85384-4.

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46

Zeng, Lei, Xiaofeng Chen, Qing Zhang, Feng Yu, Yuli Li, and Yongchang Yao. "Redifferentiation of dedifferentiated chondrocytes in a novel three‐dimensional microcavitary hydrogel." Journal of Biomedical Materials Research Part A 103, no. 5 (August 20, 2014): 1693–702. http://dx.doi.org/10.1002/jbm.a.35309.

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47

Lin, Lin, Qi Shen, Tao Xue, Xiaoning Duan, Xin Fu, and Changlong Yu. "Sonic Hedgehog Improves Redifferentiation of Dedifferentiated Chondrocytes for Articular Cartilage Repair." PLoS ONE 9, no. 2 (February 12, 2014): e88550. http://dx.doi.org/10.1371/journal.pone.0088550.

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48

Schrobback, K., T. Klein, M. Schütz, D. Hutmacher, D. Leavesley, Z. Upton, and J. Malda. "P203 Phenotypic characterization and redifferentiation of human articular chondrocytes expanded on microcarriers." Osteoarthritis and Cartilage 15 (2007): B139. http://dx.doi.org/10.1016/s1063-4584(07)61558-1.

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49

Caron, M. M. J., P. J. Emans, M. M. E. Coolsen, L. Voss, D. A. M. Surtel, A. Cremers, L. W. van Rhijn, and T. J. M. Welting. "Redifferentiation of dedifferentiated human articular chondrocytes: comparison of 2D and 3D cultures." Osteoarthritis and Cartilage 20, no. 10 (October 2012): 1170–78. http://dx.doi.org/10.1016/j.joca.2012.06.016.

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50

Yang, K. G. Auw, D. B. F. Saris, R. E. Geuze, Y. J. M. Van Der Helm, M. H. P. Van Rijen, A. J. Verbout, W. J. A. Dhert, and L. B. Creemers. "Impact of Expansion and Redifferentiation Conditions on Chondrogenic Capacity of Cultured Chondrocytes." Tissue Engineering 12, no. 9 (September 2006): 2435–47. http://dx.doi.org/10.1089/ten.2006.12.2435.

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