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Journal articles on the topic 'Endoplasmic reticulum. Bones Cartilage'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Kambe, K., A. Yamamoto, T. Yoshimori, K. Hirayoshi, R. Ogawa, and Y. Tashiro. "Preferential localization of heat shock protein 47 in dilated endoplasmic reticulum of chicken chondrocytes." Journal of Histochemistry & Cytochemistry 42, no. 7 (1994): 833–41. http://dx.doi.org/10.1177/42.7.8014466.

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We investigated the distribution of heat shock protein 47 (hsp47) in cultured chicken embryonic chondrocytes and epiphyseal chondrocytes of tibial bones from 1-day-old to 6-week-old chickens. Northern blot and immunoblot analyses revealed that hsp47 exists in epiphyseal cartilage and cultured chondrocytes. Confocal laser immunofluorescence microscopy showed that hsp47 was localized mainly in the many granular structures found in the cytoplasm that contain Type II collagen. Epiphyseal cartilage and cultured chondrocytes were embedded in LR White resin and hsp47 was detected by protein A-immunog

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2

Rajpar, M. Helen, Ben McDermott, Louise Kung, et al. "Targeted Induction of Endoplasmic Reticulum Stress Induces Cartilage Pathology." PLoS Genetics 5, no. 10 (2009): e1000691. http://dx.doi.org/10.1371/journal.pgen.1000691.

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3

Yammani, R. R., J. Haywood, and R. F. Loeser. "Endoplasmic reticulum (ER) stress inhibits IGF-1 function in articular cartilage." Osteoarthritis and Cartilage 24 (April 2016): S180—S181. http://dx.doi.org/10.1016/j.joca.2016.01.355.

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4

Zhu, M., S. Zhou, Z. Huang, J. Wen, and H. Li. "Ca2+-Dependent Endoplasmic Reticulum Stress Regulates Mechanical Stress–Mediated Cartilage Thinning." Journal of Dental Research 95, no. 8 (2016): 889–96. http://dx.doi.org/10.1177/0022034516640206.

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5

Wang, Jiangxue, Yu Gao, Ying Hou, et al. "Evaluation on Cartilage Morphology after Intra-Articular Injection of Titanium Dioxide Nanoparticles in Rats." Journal of Nanomaterials 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/452767.

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Nanoscale wear particles would generate from orthopedic implants with nanoscale surface topography because of residual stress. In this study, the effect ofTiO2nanoparticles on articular cartilage was investigated by intra-articular injection in rats. Using contrast-enhanced high-resolution microcomputed tomography (micro-CT) technology, the decreased thickness of articular cartilage in distal femur was determined at 1, 7, 14, and 30 days after nanoparticle exposure. A strong linear correlation (r=0.928,P<0.0001) was observed with the results obtained by needle probe testing. After exposure

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6

Li, Huang, Xiang-Yu Zhang, Tuo-Jiang Wu, et al. "Endoplasmic Reticulum Stress Regulates Rat Mandibular Cartilage Thinning under Compressive Mechanical Stress." Journal of Biological Chemistry 288, no. 25 (2013): 18172–83. http://dx.doi.org/10.1074/jbc.m112.407296.

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7

Qu, Jining, Daigang Lu, Hua Guo, Wusheng Miao, Ge Wu, and Meifen Zhou. "PFKFB3 modulates glycolytic metabolism and alleviates endoplasmic reticulum stress in human osteoarthritis cartilage." Clinical and Experimental Pharmacology and Physiology 43, no. 3 (2016): 312–18. http://dx.doi.org/10.1111/1440-1681.12537.

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8

Horky, D., and F. Tichy. "Submicroscopic structure of canine articular cartilage." Veterinární Medicína 49, No. 6 (2012): 207–16. http://dx.doi.org/10.17221/5697-vetmed.

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Canine articular cartilage was studied in male dogs at age 1, 4, 5 and 8 years. Samples collected from four hip joints and two humeral joints in each age category were processed by standard methods to be examined by scanning and transmission electron microscopy. The cartilage of both joints was similar in structure. In the superficial cartilage layer of one-year-old animals, individual spindle-shaped chondrocytes in the extracellular matrix were, together with associated collagen fibrils, located parallel to the surface. When viewed by scanning electron microscopy, they were distinctly promine

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9

Yuan, Xiaoliang, Haiqing Liu, Linfu Li, et al. "The Roles of Endoplasmic Reticulum Stress in the Pathophysiological Development of Cartilage and Chondrocytes." Current Pharmaceutical Design 23, no. 11 (2017): 1693–704. http://dx.doi.org/10.2174/1381612822666161025152423.

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10

Xu, Ting, Zhiyuan Gu, Huiling Wu, Hua Yao, and Guohua Wang. "Expression of endoplasmic reticulum stress protein in rabbit condyle cartilage following anterior disk displacement." Journal of Oral Pathology & Medicine 47, no. 6 (2018): 606–12. http://dx.doi.org/10.1111/jop.12715.

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11

Neacsu, Cristian Dan, Ya-Ping Ko, Andreas Tagariello, et al. "Matrilin-1 Is Essential for Zebrafish Development by Facilitating Collagen II Secretion." Journal of Biological Chemistry 289, no. 3 (2013): 1505–18. http://dx.doi.org/10.1074/jbc.m113.529933.

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Matrilin-1 is the prototypical member of the matrilin protein family and is highly expressed in cartilage. However, gene targeting of matrilin-1 in mouse did not lead to pronounced phenotypes. Here we used the zebrafish as an alternative model to study matrilin function in vivo. Matrilin-1 displays a multiphasic expression during zebrafish development. In an early phase, with peak expression at about 15 h post-fertilization, matrilin-1 is present throughout the zebrafish embryo with exception of the notochord. Later, when the skeleton develops, matrilin-1 is expressed mainly in cartilage. Morp

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12

Schmitz, Markus, Alexander Becker, Alexander Schmitz, et al. "Disruption of Extracellular Matrix Structure May Cause Pseudoachondroplasia Phenotypes in the Absence of Impaired Cartilage Oligomeric Matrix Protein Secretion." Journal of Biological Chemistry 281, no. 43 (2006): 32587–95. http://dx.doi.org/10.1074/jbc.m601976200.

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Pseudoachondroplasia and multiple epiphyseal dysplasia are two dominantly inherited chondrodysplasias associated with mutations in cartilage oligomeric matrix protein (COMP). The rarely available patient biopsies show lamellar inclusions in the endoplasmic reticulum. We studied the pathogenesis of these chondrodysplasias by expressing several disease-causing COMP mutations in bovine primary chondrocytes and found that COMP-associated chondrodysplasias are not exclusively storage diseases. Although COMP carrying the mutations D469Δ and D475N was retained within the endoplasmic reticulum, secret

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13

Yammani, R. R., and L. Tan. "Aging induces endoplasmic reticulum (ER) stress and apoptosis in non-human primate knee articular cartilage." Osteoarthritis and Cartilage 27 (April 2019): S96—S97. http://dx.doi.org/10.1016/j.joca.2019.02.139.

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14

Uehara, Y., J. Hirose, S. Yamabe, et al. "Endoplasmic reticulum stress-induced apoptosis contributes to articular cartilage degeneration via C/EBP homologous protein." Osteoarthritis and Cartilage 22, no. 7 (2014): 1007–17. http://dx.doi.org/10.1016/j.joca.2014.04.025.

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15

Takada, Koji, Jun Hirose, Kei Senba, et al. "Enhanced apoptotic and reduced protective response in chondrocytes following endoplasmic reticulum stress in osteoarthritic cartilage." International Journal of Experimental Pathology 92, no. 4 (2011): 232–42. http://dx.doi.org/10.1111/j.1365-2613.2010.00758.x.

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16

Rellmann, Yvonne, Isabel Gronau, Uwe Hansen, and Rita Dreier. "4-Phenylbutyric Acid Reduces Endoplasmic Reticulum Stress in Chondrocytes That Is Caused by Loss of the Protein Disulfide Isomerase ERp57." Oxidative Medicine and Cellular Longevity 2019 (October 29, 2019): 1–12. http://dx.doi.org/10.1155/2019/6404035.

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Objective. The integrity of cartilage depends on the correct synthesis of extracellular matrix (ECM) components. In case of insufficient folding of proteins in the endoplasmic reticulum (ER) of chondrocytes, ECM proteins aggregate, ER stress evolves, and the unfolded protein response (UPR) is initiated. By this mechanism, chondrocytes relieve the stress condition or initiate cell death by apoptosis. Especially persistent ER stress has emerged as a pathogenic mechanism in cartilage diseases, such as chondrodysplasias and osteoarthritis. As pharmacological intervention is not available yet, it i

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17

Hughes, Alexandria, Alexandra Oxford, Ken Tawara, Cheryl Jorcyk, and Julia Oxford. "Endoplasmic Reticulum Stress and Unfolded Protein Response in Cartilage Pathophysiology; Contributing Factors to Apoptosis and Osteoarthritis." International Journal of Molecular Sciences 18, no. 3 (2017): 665. http://dx.doi.org/10.3390/ijms18030665.

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18

Takada, K., J. Hirose, and H. Mizuta. "205 ENHANCED APOPTOTIC AND REDUCED PROTECTIVE RESPONSE IN CHONDROCYTES FOLLOWING ENDOPLASMIC RETICULUM STRESS IN OSTEOARTHRHIC CARTILAGE." Osteoarthritis and Cartilage 19 (September 2011): S101—S102. http://dx.doi.org/10.1016/s1063-4584(11)60232-x.

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19

Wroblewski, J., M. Engström, A. Skottner, K. Madsen, and U. Friberg. "Subcellular location of IGF-I in chondrocytes from rat rib growth plate." Acta Endocrinologica 115, no. 1 (1987): 37–43. http://dx.doi.org/10.1530/acta.0.1150037.

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Abstract. Ultrathin cryosections of segments of growth plates from rat rib and isolated, gelatin-embedded chondrocytes from the same source were used to demonstrate the ultrastructural location of IGF-I in the different layers of the growth plate. Sections were incubated with a polyclonal rabbit antiserum to free IGF-I and colloidal gold coated with goat anti-rabbit IgGs. The gold label was present in all chondrocytes, localized almost exclusively to the cytoplasm. Particularly the cells in the proliferating zone displayed considerable amounts of gold label. In these cells, gold label was pred

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20

Bezamat, Mariana, Kathleen Deeley, Shahryar Khaliq, et al. "Are mTOR and Endoplasmic Reticulum Stress Pathway Genes Associated with Oral and Bone Diseases?" Caries Research 53, no. 3 (2018): 235–41. http://dx.doi.org/10.1159/000492675.

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The purpose of this cohort study was to identify associations between combined oral and bone disease phenotypes and genes present in cell regulatory pathways. The studied pathways play important roles in cellular growth, proliferation, differentiation, and homeostasis. DNA samples extracted from whole saliva of 3,912 individuals were genotyped and these data analyzed according to dental caries experience, periapical lesions, periodontitis, osteoporosis, or temporomandibular joint discomfort. Samples were obtained from the Dental Registry and DNA Repository project at the University of Pittsbur

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21

Patra, D., J. Bryan, X. Xing, and L. J. Sandell. "196 DISRUPTION OF LIPID HOMEOSTASIS IN CARTILAGE-SPECIFIC SITE-1 PROTEASE KNOCKOUT MICE RESULTS IN ENDOPLASMIC RETICULUM STRESS AND POOR CARTILAGE PRODUCTION." Osteoarthritis and Cartilage 16 (September 2008): S95. http://dx.doi.org/10.1016/s1063-4584(08)60242-3.

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22

Patra, Debabrata, Xiaoyun Xing, Sherri Davies, et al. "Site-1 protease is essential for endochondral bone formation in mice." Journal of Cell Biology 179, no. 4 (2007): 687–700. http://dx.doi.org/10.1083/jcb.200708092.

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Site-1 protease (S1P) has an essential function in the conversion of latent, membrane-bound transcription factors to their free, active form. In mammals, abundant expression of S1P in chondrocytes suggests an involvement in chondrocyte function. To determine the requirement of S1P in cartilage and bone development, we have created cartilage-specific S1P knockout mice (S1Pcko). S1Pcko mice exhibit chondrodysplasia and a complete lack of endochondral ossification even though Runx2 expression, Indian hedgehog signaling, and osteoblastogenesis is intact. However, there is a substantial increase in

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23

Hecht, J., J. L. Alcorn, A. C. Veerisetty, M. Hossain, F. Chiu, and K. L. Posey. "Novel model for age-related osteoarthritis - endoplasmic reticulum stress in articular cartilage induces joint degeneration in mice." Osteoarthritis and Cartilage 28 (April 2020): S194. http://dx.doi.org/10.1016/j.joca.2020.02.315.

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24

Ishikawa, Yoshihiro, and Hans Peter Bächinger. "An Additional Function of the Rough Endoplasmic Reticulum Protein Complex Prolyl 3-Hydroxylase 1·Cartilage-associated Protein·Cyclophilin B." Journal of Biological Chemistry 288, no. 44 (2013): 31437–46. http://dx.doi.org/10.1074/jbc.m113.498063.

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25

Izumi, Soutarou, Atsushi Saito, Soshi Kanemoto, et al. "The Endoplasmic Reticulum Stress Transducer BBF2H7 Suppresses Apoptosis by Activating the ATF5-MCL1 Pathway in Growth Plate Cartilage." Journal of Biological Chemistry 287, no. 43 (2012): 36190–200. http://dx.doi.org/10.1074/jbc.m112.373746.

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26

Tan, Li, Thomas C. Register, and Raghunatha R. Yammani. "Age-Related Decline in Expression of Molecular Chaperones Induces Endoplasmic Reticulum Stress and Chondrocyte Apoptosis in Articular Cartilage." Aging and disease 11, no. 5 (2020): 1091. http://dx.doi.org/10.14336/ad.2019.1130.

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27

Liu, Kangping, Rubin Fan, and Zhenlei Zhou. "Endoplasmic reticulum stress, chondrocyte apoptosis and oxidative stress in cartilage of broilers affected by spontaneous femoral head necrosis." Poultry Science 100, no. 8 (2021): 101258. http://dx.doi.org/10.1016/j.psj.2021.101258.

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28

Aigner, Thomas, Tilman Rau, Manuel Niederhagen, et al. "Achondrogenesis Type IA (Houston-Harris): A Still-Unresolved Molecular Phenotype." Pediatric and Developmental Pathology 10, no. 4 (2007): 328–34. http://dx.doi.org/10.2350/06-07-0134.1.

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Achondrogenesis type IA (Houston-Harris) is an extremely rare lethal chondrodysplasia with a characteristic severe disarrangement of endochondral ossification. The growth plate cartilage completely lacks columnar-zone formation and shows chondrocyte expansion due to intracellular vacuoles. This article on a new case of achondrogenesis type IA confirms these findings and demonstrates, on the ultrastructural level, the retention of fine fibrillar material within the rough endoplasmic reticulum (rER). Molecular analysis in the presented case of achondrogenesis type IA did not reveal mutations in

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29

Kourí, Juan B., Lourdes Rojas, Elizabeth Pérez, and Karin A. Abbud-Lozoya. "Modifications of Golgi Complex in Chondrocytes from Osteoarthrotic (OA) Rat Cartilage." Journal of Histochemistry & Cytochemistry 50, no. 10 (2002): 1333–39. http://dx.doi.org/10.1177/002215540205001006.

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The status of the Golgi complex in normal vs osteoarthrotic (OA) cartilage has not yet been studied. A monoclonal antibody, MAb 58-K-9, allowed scoring of Golgi labeling intensity. In addition, ultrastructural assessment enabled us to focus on the distribution and relation between the endoplasmic reticulum (ER) and Golgi membranes. The study was performed in both normal and partially menisectomized OA-induced rat cartilage 20 and 45 days after surgery. Comparing Golgi immunolabeling intensities (mean ± SEM) revealed a highly significant difference between normal (9.98 ± 1.25), 20-day (2.49 ± 0

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30

Tan, L., C. Carlson, and R. Yammani. "Dietary fatty acid palmitate induces endoplasmic reticulum stress, chondrocyte death and cartilage lesions in the knee joint of mice." Osteoarthritis and Cartilage 28 (April 2020): S68. http://dx.doi.org/10.1016/j.joca.2020.02.103.

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31

Briggs, Michael D., Ella P. Dennis, Helen F. Dietmar, and Katarzyna A. Pirog. "New developments in chondrocyte ER-stress and related diseases." F1000Research 9 (April 24, 2020): 290. http://dx.doi.org/10.12688/f1000research.22275.1.

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Cartilage comprises a single cell type, the chondrocyte, embedded in a highly complex extracellular matrix. Disruption to the cartilage growth plate leads to reduced bone growth and results in a clinically diverse group of conditions known as genetic skeletal diseases (GSDs). Similarly, long-term degradation of articular cartilage can lead to osteoarthritis (OA), a disease characterised by joint pain and stiffness. As professionally secreting cells, chondrocytes are particularly susceptible to endoplasmic reticulum (ER) stress and this has been identified as a core disease mechanism in a group

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32

Staponas, Alfredas, Vida Gražienë, and Laima Leonavičienë. "Can low concentrations of Papain help repair articular cartilage defects?" Open Life Sciences 2, no. 1 (2007): 87–98. http://dx.doi.org/10.2478/s11535-007-0005-2.

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AbstractIn the present study, we investigate the capability of low concentrations of Papain to stimulate cartilage mesenchymal cells proliferation and transformation to chondrocytes and evaluate the healing capability of partial thickness defects in medial condyle cartilage of 30 rabbits’ knee joints. Papain 0.1 mg/ml and Ringer saline l ml each were injected intra-articularly to rabbits of experimental and control groups (15 animals each). Healthy cartilage from lateral condyle and cartilage from medial condyle where the surgical defect was created were studied histologically and by TEM. The

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33

Goya, Nj, M. Gupta, and K. Joshi. "Ultrastructure of Chondrocytes in Osteoarthritic Femoral Articular Cartilage." Kathmandu University Medical Journal 11, no. 3 (2015): 221–25. http://dx.doi.org/10.3126/kumj.v11i3.12508.

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Background Osteoarthritis (OA) is a common problem in elderly, but it is not an inevitable feature of ageing. About 80-90% of individuals of both sexes have radiographic evidence of OA by the time they reach an age of 65. But not all of them have the symptoms like pain and decreased joint motion. Objective The objective of the present study was conducted to find out whether the osteoarthritic changes in human articular cartilage are similar to the ageing process or not. Methods Femoral articular cartilage specimens obtained from 13 osteoarthritic patients (52-80years) undergoing total knee rep

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34

Seegmiller, Robert E., Brandon D. Bomsta, Laura C. Bridgewater, et al. "The Heterozygous Disproportionate Micromelia (Dmm) Mouse: Morphological Changes in Fetal Cartilage Precede Postnatal Dwarfism and Compared With Lethal Homozygotes Can Explain the Mild Phenotype." Journal of Histochemistry & Cytochemistry 56, no. 11 (2008): 1003–11. http://dx.doi.org/10.1369/jhc.2008.951673.

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The disproportionate micromelia ( Dmm) mouse has a mutation in the C-propeptide coding region of the Co/2a1 gene that causes lethal dwarfism when homozygous ( Dmm/Dmm) but causes only mild dwarfism observable ∼1-week postpartum when heterozygous ( Dmm/+). The purpose of this study was 2-fold: first, to analyze and quantify morphological changes that precede the expression of mild dwarfism in Dmm/+ animals, and second, to compare morphological alterations between Dmm/+ and Dmm/Dmm fetal cartilage that may correlate with the marked skeletal differences between mild and lethal dwarfism. Light and

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35

Tan, Li, Lindsey R. Harper, Alexandra Armstrong, Cathy S. Carlson, and Raghunatha R. Yammani. "Dietary saturated fatty acid palmitate promotes cartilage lesions and activates the unfolded protein response pathway in mouse knee joints." PLOS ONE 16, no. 2 (2021): e0247237. http://dx.doi.org/10.1371/journal.pone.0247237.

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Increased intake of dietary saturated fatty acids has been linked to obesity and the development of Osteoarthritis (OA). However, the mechanism by which these fats promote cartilage degradation and the development of OA is not clearly understood. Here, we report the effects of consumption of common dietary saturated and unsaturated fatty acids, palmitate and oleate, respectively, on body weight, metabolic factors, and knee articular cartilage in a mouse model of diet-induced obesity. Mice fed on a diet rich in saturated or unsaturated fatty acid gained an equal amount of weight; however, mice

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36

Alberch, P., G. A. Lewbart, and Emily A. Gale. "The fate of larval chondrocytes during the metamorphosis of the epibranchial in the salamander, Eurycea bislineata." Development 88, no. 1 (1985): 71–83. http://dx.doi.org/10.1242/dev.88.1.71.

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The metamorphosis of the epibranchial cartilage, a skeletal component of the hyobranchial apparatus, in the salamander Eurycea bislineata entails a combination of the reabsorption of a larval cartilaginous element with the simultaneous genesis of an adult cartilage in the same place. In this study we focus on the fate of the larval chondrocytes. Two hypotheses are considered: one, larval cells simply die off during metamorphosis, or, alternatively, they dedifferentiate and participate in the formation of the adult element. Thyroxine treatment and experimental tissue manipulation coupled with m

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37

Vonk, Lucienne A., Behrouz Zandieh Doulabi, Chun-Ling Huang, Marco N. Helder, Vincent Everts, and Ruud A. Bank. "Endoplasmic reticulum stress inhibits collagen synthesis independent of collagen-modifying enzymes in different chondrocyte populations and dermal fibroblasts." Biochemistry and Cell Biology 88, no. 3 (2010): 539–52. http://dx.doi.org/10.1139/o09-174.

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Chondrocytes respond to glucose deprivation with a decreased collagen synthesis due to disruption of a proper functioning of the endoplasmic reticulum (ER): ER stress. Since the mechanisms involved in the decreased synthesis are unknown, we have investigated whether chaperones and collagen-modifying enzymes are affected by glucose deprivation. Chondrocytes obtained from nucleus pulposus, annulus fibrosus, articular cartilage, and meniscus and dermal fibroblasts were cultured under control conditions or exposed to the ER stress-inducing treatments of tunicamycin addition or glucose withdrawal.

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38

Rong, Ke, Qing‐quan Xia, Xu‐hua Wu, et al. "Articular Cartilage Stem Cells Influence the Postoperative Repair of Hip Replacement by Regulating Endoplasmic Reticulum Stress in Chondrocytes via PERK Pathway." Orthopaedic Surgery 12, no. 2 (2020): 609–16. http://dx.doi.org/10.1111/os.12644.

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39

Wu, Meng-Huang, Ching-Yu Lee, Tsung-Jen Huang, et al. "MLN4924, a Protein Neddylation Inhibitor, Suppresses the Growth of Human Chondrosarcoma through Inhibiting Cell Proliferation and Inducing Endoplasmic Reticulum Stress-Related Apoptosis." International Journal of Molecular Sciences 20, no. 1 (2018): 72. http://dx.doi.org/10.3390/ijms20010072.

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Chondrosarcoma, a heterogeneous malignant bone tumor, commonly produces cartilage matrix, which generally has no response to conventional therapies. Studies have reported that MLN4924, a NEDD8-activating enzyme inhibitor, achieves antitumor effects against numerous malignancies. In this study, the suppressive effects of MLN4924 on human chondrosarcoma cell lines were investigated using in vitro and in vivo assays, which involved measuring cell viability, cytotoxicity, apoptosis, proliferation, cell cycles, molecule-associated cell cycles, apoptosis, endoplasmic reticulum (ER) stress, and tumor

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40

Reddy, R. Mallikarjuna, Srikanth A, Sofia Kouser, et al. "Pharmacological Evaluation of the Impact of Fluoride-Contaminated Drinking Water on Brain Cognitive Function and Bone Health in Nalgonda and Warangal Rural Districts of Telangana in India." International Journal of Pharmaceutical Sciences and Nanotechnology 13, no. 4 (2020): 5036–46. http://dx.doi.org/10.37285/ijpsn.2020.13.4.10.

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A systematic groundwater analysis was carried out in six villages of Narsampet in Warangal district and two villages of Narketpally in Nalgonda district of Telangana in India. These water samples were collected from respective areas and evaluated under four different categories viz. physico-chemical parameters (such as pH, Electric Conductivity (EC), Total Dissolved Solids (TDS), Turbidity, Alkalinity, Hardness, Chloride, Nitrates, Sulphates, Fluoride, Iron content) as per standard methods, behavioral changes i.e. measurement of learning and memory ability of rats (Rectangular maze, Morris wat

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41

Ratcliffe, A., P. R. Fryer, and T. E. Hardingham. "Proteoglycan biosynthesis in chondrocytes: protein A-gold localization of proteoglycan protein core and chondroitin sulfate within Golgi subcompartments." Journal of Cell Biology 101, no. 6 (1985): 2355–65. http://dx.doi.org/10.1083/jcb.101.6.2355.

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The intracellular pathway of cartilage proteoglycan biosynthesis was investigated in isolated chondrocytes using a protein A-gold electron microscopy immunolocalization procedure. Proteoglycans contain a protein core to which chondroitin sulfate and keratan sulfate chains and oligosaccharides are added in posttranslational processing. Specific antibodies have been used in this study to determine separately the distribution of the protein core and chondroitin sulfate components. In normal chondrocytes, proteoglycan protein core was readily localized only in smooth-membraned vesicles which co-la

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42

Gu, YunTao, Jian Chen, ZhuLong Meng, et al. "Diazoxide prevents H 2 O 2 -induced chondrocyte apoptosis and cartilage degeneration in a rat model of osteoarthritis by reducing endoplasmic reticulum stress." Biomedicine & Pharmacotherapy 95 (November 2017): 1886–94. http://dx.doi.org/10.1016/j.biopha.2017.09.082.

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43

Remirez, Diadelis, Ricardo González, Nelson Merino, Sandra Rodriguez, and Odelsa Ancheta. "Inhibitory effects of Spirulina in zymosan-induced arthritis in mice." Mediators of Inflammation 11, no. 2 (2002): 75–79. http://dx.doi.org/10.1080/09629350220131917.

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The anti-inflammatory effect of microalgae Spirulina was studied in zymosan-induced arthritis in mice. Four days after the intra-articular injection of zymosan (15 mg/ml), Spirulina (100 and 400 mg/kg per-orally) was administered to animals for 8 days. The mice were than killed and β-glucuronidase was measured in the synovial fluid. Each knee joint was totally removed for histopathological studies. Spirulina significantly reduced the levels of β-glucuronidase that had been increased by zymosan. Histopathological and ultrastructural studies showed inhibition of the inflammatory reaction, wherea

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44

Rellmann, Yvonne, and Rita Dreier. "Different Forms of ER Stress in Chondrocytes Result in Short Stature Disorders and Degenerative Cartilage Diseases: New Insights by Cartilage-Specific ERp57 Knockout Mice." Oxidative Medicine and Cellular Longevity 2018 (December 17, 2018): 1–14. http://dx.doi.org/10.1155/2018/8421394.

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Cartilage is essential for skeletal development by endochondral ossification. The only cell type within the tissue, the chondrocyte, is responsible for the production of macromolecules for the extracellular matrix (ECM). Before proteins and proteoglycans are secreted, they undergo posttranslational modification and folding in the endoplasmic reticulum (ER). However, the ER folding capacity in the chondrocytes has to be balanced with physiological parameters like energy and oxygen levels. Specific cellular conditions, e.g., a high protein demand, or pathologic situations disrupt ER homeostasis

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Jin, Xinxin, Xiaomin Kang, Liting Zhao, et al. "Cartilage Ablation of Sirt1 Causes Inhibition of Growth Plate Chondrogenesis by Hyperactivation of mTORC1 Signaling." Endocrinology 160, no. 12 (2019): 3001–17. http://dx.doi.org/10.1210/en.2019-00427.

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Abstract A growing body of evidence implies a pivotal role of sirtuin-1 (Sirt1) in chondrocyte function and homeostasis; however, its underlying mechanisms mediating chondrogenesis, which is an essential process for physiological skeletal growth, are still poorly understood. In the current study, we generated TamCartSirt1−/− [Sirt1 conditional knockout (cKO)] mice to explore the role of Sirt1 during postnatal endochondral ossification. Compared with control mice, cKO mice exhibited growth retardation associated with inhibited chondrocyte proliferation and hypertrophy, as well as activated apop

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Patra, D., X. Xing, J. Bryan, C. Franz, E. Hunziker, and L. J. Sandell. "10 DISRUPTION OF ENDOPLASMIC RETICULUM STRESS SIGNALING IN CARTILAGE-SPECIFIC SITE-1 PROTEASE KNOCKOUT MICE RESULTS IN ABNORMAL MATRIX AND LACK OF ENDOCHONDRAL OSSIFICATION." Osteoarthritis and Cartilage 15 (December 2007): C20. http://dx.doi.org/10.1016/s1063-4584(07)61646-x.

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Hashimoto, Yusuke, Takami Tomiyama, Yoshiki Yamano, and Hiroshi Mori. "Mutation (D472Y) in the Type 3 Repeat Domain of Cartilage Oligomeric Matrix Protein Affects Its Early Vesicle Trafficking in Endoplasmic Reticulum and Induces Apoptosis." American Journal of Pathology 163, no. 1 (2003): 101–10. http://dx.doi.org/10.1016/s0002-9440(10)63634-6.

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Liu, Jinqiang, Hongxu Yang, Hongyun Zhang, et al. "Biomechanically reduced expression of Derlin-3 is linked to the apoptosis of chondrocytes in the mandibular condylar cartilage via the endoplasmic reticulum stress pathway." Archives of Oral Biology 118 (October 2020): 104843. http://dx.doi.org/10.1016/j.archoralbio.2020.104843.

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Patra, Debabrata, Elizabeth DeLassus, Guosheng Liang, and Linda J. Sandell. "Cartilage-Specific Ablation of Site-1 Protease in Mice Results in the Endoplasmic Reticulum Entrapment of Type IIB Procollagen and Down-Regulation of Cholesterol and Lipid Homeostasis." PLoS ONE 9, no. 8 (2014): e105674. http://dx.doi.org/10.1371/journal.pone.0105674.

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Cotti, Silvia, Ann Huysseune, Wolfgang Koppe, et al. "More Bone with Less Minerals? The Effects of Dietary Phosphorus on the Post-Cranial Skeleton in Zebrafish." International Journal of Molecular Sciences 21, no. 15 (2020): 5429. http://dx.doi.org/10.3390/ijms21155429.

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Dietary phosphorus (P) is essential for bone mineralisation in vertebrates. P deficiency can cause growth retardation, osteomalacia and bone deformities, both in teleosts and in mammals. Conversely, excess P supply can trigger soft tissue calcification and bone hypermineralisation. This study uses a wide range of complementary techniques (X-rays, histology, TEM, synchrotron X-ray tomographic microscopy, nanoindentation) to describe in detail the effects of dietary P on the zebrafish skeleton, after two months of administering three different diets: 0.5% (low P, LP), 1.0% (regular P, RP), and 1

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