Transport Properties of Cartilaginous Tissues

Jackson, Alicia R.; Gu, Wei Yong

doi:10.2174/157339709787315320

Cited by 84 publications

(74 citation statements)

References 125 publications

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“…Diffusion coefficients ( Â 10 À 10 m 2 /s) of glucosamine are 2.5 in NP, 2.08 in IA, 1.7 in OA and 1.4 in CEP whereas that of vancomycin are, respectively, 0.3, 0.25, 0.15 and 0.1. Molal partition coefficients at the CEP and OA boundaries are, respectively, 0.81 and 0.89 for glucose and 0.14 and 0.16 for vancomycin (Jackson and Gu, 2009;Maroudas, 1976;Maroudas et al, 1975;Meulemans et al, 1989).…”

Section: Solute Molecular Sizementioning

confidence: 99%

Computational pharmacokinetics of solute penetration into human intervertebral discs—Effects of endplate permeability, solute molecular weight and disc size

Motaghinasab

Shirazi-Adl

Urban

et al. 2012

Journal of Biomechanics

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Section: Solute Molecular Sizementioning

confidence: 99%

Computational pharmacokinetics of solute penetration into human intervertebral discs—Effects of endplate permeability, solute molecular weight and disc size

Motaghinasab

Shirazi-Adl

Urban

et al. 2012

Journal of Biomechanics

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“…Blood vessels are located at the tissue margins and nutritional supply occurs by diffusion. 13 In this aspect, chondrocytes differ from other somatic cells. The effects of oxidative stress on cartilaginous tissue and chondrocytes are still unknown.…”

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confidence: 99%

Oxidative stress induces senescence in chondrocytes

Brandl¹,

Hartmann²,

Bechmann³

et al. 2011

Journal Orthopaedic Research

116

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Cellular senescence is a program activated during diverse situations of cell stress. Chondrocytes differ from other somatic cells as articular cartilage is an avascular tissue. The effects of oxidative stress on chondrocytes are still unknown. Our studies were to investigate into the proliferation potential, cytological features and the telomere linked stress response system of human osteoarthritic chondrocytes, subjected to acute or prolonged oxidant challenge with hydrogen peroxide. Telomere length was measured using the telomere restriction fragment assay, gene expression was determined by RT-PCR. Sub-lethal doses of oxidative stress induced cell-cycle arrest, senescentmorphological features and senescence-associated b-galactosidase positivity. Prolonged oxidative treatment had no effects on cell proliferation or morphology. Sub-lethal and prolonged low doses of oxidative stress considerably accelerated telomere attrition. The effects of sublethal oxidative stress regarding proliferation and telomere biology were more distinct in senescent cells. Acute oxidant insult caused upregulation of p21 expression to levels comparable to senescent cells. TRF2 protects telomere ends and showed elevated expression levels. SIRT1 and XRCC5 enable cells to cope with unfavorable growing conditions. Both were up-regulated after oxidant insult, but expression levels decreased in aging cells. Taken Keywords: cellular senescence; oxidative stress; telomeres; DNA damage; human chondrocytes Cellular aging or senescence refers to metabolically active somatic cells having entered a state of permanent growth arrest. Replicative senescence has been associated with telomere shortening. Telomeres consist of noncoding repetitive DNA sequences and associated proteins located at the end of linear chromosomes. Human telomeres form a 2,000-30,000 base pair (bp) array of duplex DNA strand of TTAGGG repeats, ending in a 100-200 bp nucleotide 3 0 single strand overhang invading the duplex array to form a lariat-like loop structure (t-loop). Telomeric repeats ensure the complete replication of encoding DNA. Chromosome ends, uncapped by telomeres, are susceptive to degradation and fusion and can activate DNA damage checkpoints. 1 A six-protein complex-known as telosome or shelterin complex-functions to form and maintain the t-loop structure. TRF1 and TRF2 are part of the core telomeric proteins. Various signaling pathways coordinating telomere function and cell cycle regulation start off the telosome complex. TRF1 modulates the length of telomeres. TRF2 is important for stabilizing the t-loop structure. 2,3 XRCC5 and SIRT1 are associated with the telomerenucleo-protein complex and link telomere biology and DNA damage checkpoints with genes involved in other cellular stress responses. XRCC5 is involved in repairing DNA double-strand breaks. 4,5 SIRT1 is a negative regulator of p53 and prevents growth arrest, senescence, and apoptosis. 6 Telomere uncapping, DNA damage foci at telomeres 7 and oxidative insults cause p21 elevation. The p21...

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“…Its value is related to the diffusivity of small ions inside the tissue, which depend on tissue composition and structure [22,23]. Using an electrical conductivity method, the effect of matrix composition on solute permeability has been studied in hydrogels and cartilaginous tissues [24,25]. In this study, we adopted this method to study the impact of 4 °C storage on cartilage ECM solute permeability.…”

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confidence: 99%

Impact of Hypothermia upon Chondrocyte Viability and Cartilage Matrix Permeability after 1 Month of Refrigerated Storage

Brockbank

Rahn

Wright

et al. 2011

Transfus Med Hemother

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Background: The purpose of this research was to assess the extracellular matrix and chondrocytes of articular cartilage during refrigerated storage and to determine whether changes could be detected in the time frame that cartilage is stored for clinical use. Methods: Porcine cartilage was stored as either bisected femoral heads with bone attached or plugs without the underlying bone in culture medium with fetal bovine serum for 1 month at 4 °C. Metabolic activity was tested using a resazurin reduction method on intact tissue and viable cell recovery after enzymatic tissue digestion at each time point. Cartilage plug permeability was evaluated by measuring electrical conductivity. Results: Storage in culture medium provided good cartilage viability and metabolic function for 7 days; however, significant changes were observed in femoral heads (p < 0.05). All mean chondrocyte assessment values were <30% of fresh controls at 28 days. Cartilage plugs tended to perform better after 7 days of storage than the femoral heads and retained significantly higher metabolic activity (mean = 94.5% vs. 70.5%; p < 0.05). Cartilage plugs demonstrated consistent changes in electrical conductivity after 28 days of storage (p < 0.05). Conclusion: Refrigerated storage of cartilage results in both loss of chondrocyte viability and matrix permeability.

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Transport Properties of Cartilaginous Tissues

Cited by 84 publications

References 125 publications

Computational pharmacokinetics of solute penetration into human intervertebral discs—Effects of endplate permeability, solute molecular weight and disc size

Computational pharmacokinetics of solute penetration into human intervertebral discs—Effects of endplate permeability, solute molecular weight and disc size

Oxidative stress induces senescence in chondrocytes

Impact of Hypothermia upon Chondrocyte Viability and Cartilage Matrix Permeability after 1 Month of Refrigerated Storage

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