| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Takashi Nishida, Kenji Emura, Satoshi Kubota, Karen M Lyons, Masaharu Takigaw. CCN family 2/connective tissue growth factor (CCN2/CTGF) promotes osteoclastogenesis via induction of and interaction with dendritic cell-specific transmembrane protein (DC-STAMP). Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 26. issue 2. 2011-04-28. PMID:20721934. |
the phenotype of ccn2 null mice, having an expanded hypertrophic zone, indicates that the resorption of the cartilage extracellular matrix is impaired therein. |
2011-04-28 |
2023-08-12 |
mouse |
| Emmanuelle David, Pierre Guihard, Bénédicte Brounais, Anne Riet, Céline Charrier, Séverine Battaglia, François Gouin, Stéphanie Ponsolle, Ronan Le Bot, Carl D Richards, Dominique Heymann, Françoise Rédini, Frédéric Blanchar. Direct anti-cancer effect of oncostatin M on chondrosarcoma. International journal of cancer. vol 128. issue 8. 2011-04-18. PMID:21344373. |
in two tested cell lines, osm induced a hypertrophic chondrocyte differentiation, with an induced cbfa1/sox9 ratio and induced coll10, matrix metalloproteinase 13 (mmp13) and rankl expression. |
2011-04-18 |
2023-08-12 |
rat |
| Kim Sergerie, Stefan Parent, Pierre-Francois Beauchemin, Irene Londoño, Florina Moldovan, Isabelle Villemur. Growth plate explants respond differently to in vitro static and dynamic loadings. Journal of orthopaedic research : official publication of the Orthopaedic Research Society. vol 29. issue 4. 2011-04-12. PMID:21337387. |
however, dynamic compressive loads preserved the proliferative and hypertrophic zones ratio and contributed to the synthesis of aggrecan and type ii collagen in the extracellular matrix. |
2011-04-12 |
2023-08-12 |
Not clear |
| Norifumi Fujita, Takehiko Matsushita, Kazunari Ishida, Seiji Kubo, Tomoyuki Matsumoto, Koji Takayama, Masahiro Kurosaka, Ryosuke Kurod. Potential involvement of SIRT1 in the pathogenesis of osteoarthritis through the modulation of chondrocyte gene expressions. Journal of orthopaedic research : official publication of the Orthopaedic Research Society. vol 29. issue 4. 2011-04-12. PMID:21337390. |
our observations suggest that sirt1 expression decreases with development of oa and the reduction of sirt1 in chondrocytes may cause chondrocyte hypertrophy and cartilage matrix loss. |
2011-04-12 |
2023-08-12 |
Not clear |
| Christoffer K Abrahamsson, Fan Yang, Hyoungshin Park, Jonathan M Brunger, Piia K Valonen, Robert Langer, Jean F Welter, Arnold I Caplan, Farshid Guilak, Lisa E Free. Chondrogenesis and mineralization during in vitro culture of human mesenchymal stem cells on three-dimensional woven scaffolds. Tissue engineering. Part A. vol 16. issue 12. 2011-04-07. PMID:20673022. |
in chondrogenic medium, cartilaginous tissue formed by day 21, and hypertrophic mineralization was observed in the newly formed extracellular matrix at the interface with underlying scaffold by day 45. |
2011-04-07 |
2023-08-12 |
human |
| Debby Gawlitta, Eric Farrell, Jos Malda, Laura B Creemers, Jacqueline Alblas, Wouter J A Dher. Modulating endochondral ossification of multipotent stromal cells for bone regeneration. Tissue engineering. Part B, Reviews. vol 16. issue 4. 2011-04-06. PMID:20131956. |
subsequent terminal differentiation (hypertrophy) of the chondrocytes initiates the formation of a mineralized matrix that will then be converted into bone. |
2011-04-06 |
2023-08-12 |
Not clear |
| Arash Haghikia, Britta Stapel, Melanie Hoch, Denise Hilfiker-Kleine. STAT3 and cardiac remodeling. Heart failure reviews. vol 16. issue 1. 2011-04-05. PMID:20407820. |
multiple in vitro and in vivo studies showed that the signal transducer and activator of transcription 3 (stat3) protein is involved in cardiomyocyte protection and hypertrophy and via paracrine pathways impacts on the non-myocyte compartment, i.e., the vasculature and the extracellular matrix. |
2011-04-05 |
2023-08-12 |
Not clear |
| Julian C Lui, Jeffrey Baro. Effects of glucocorticoids on the growth plate. Endocrine development. vol 20. 2011-03-31. PMID:21164272. |
glucocorticoids slow longitudinal bone growth by inhibiting chondrocyte proliferation, hypertrophy, and cartilage matrix synthesis. |
2011-03-31 |
2023-08-12 |
Not clear |
| Hiu-Wa Cheng, Keith D K Luk, Kenneth M C Cheung, Barbara P Cha. In vitro generation of an osteochondral interface from mesenchymal stem cell-collagen microspheres. Biomaterials. vol 32. issue 6. 2011-03-29. PMID:21093047. |
cells at the interface region are hypertrophic chondrocytes while the extracellular matrix in this region contains collagen type ii and x, calcium deposits and vertically running fibers. |
2011-03-29 |
2023-08-12 |
Not clear |
| Jessica Bertrand, Christoph Cromme, Daniel Umlauf, Svetlana Frank, Thomas Pa. Molecular mechanisms of cartilage remodelling in osteoarthritis. The international journal of biochemistry & cell biology. vol 42. issue 10. 2011-03-09. PMID:20603225. |
the loss of proteoglycans, the mineralization of the extracellular matrix (ecm) and the hypertrophic differentiation of the chondrocytes constitute hallmarks of the disease. |
2011-03-09 |
2023-08-12 |
Not clear |
| Julie A Williams, Maureen Kane, Takahiro Okabe, Motomi Enomoto-Iwamoto, Joseph L Napoli, Maurizio Pacifici, Masahiro Iwamot. Endogenous retinoids in mammalian growth plate cartilage: analysis and roles in matrix homeostasis and turnover. The Journal of biological chemistry. vol 285. issue 47. 2011-02-28. PMID:20843807. |
retinoid signaling was previously found to be nearly absent in ugp, but to be much stronger in lgp coincident with hypertrophy, extracellular matrix turnover and endochondral bone formation. |
2011-02-28 |
2023-08-12 |
rabbit |
| Ulrich Schotten, Sander Verheule, Paulus Kirchhof, Andreas Goett. Pathophysiological mechanisms of atrial fibrillation: a translational appraisal. Physiological reviews. vol 91. issue 1. 2011-02-28. PMID:21248168. |
aging, neurohumoral activation, and chronic atrial stretch due to structural heart disease activate a variety of signaling pathways leading to histological changes in the atria including myocyte hypertrophy, fibroblast proliferation, and complex alterations of the extracellular matrix including tissue fibrosis. |
2011-02-28 |
2023-08-12 |
Not clear |
| Meenalakshmi M Mariappan, Kristin D'Silva, Myung Ja Lee, Kavithalakshmi Sataranatarajan, Jeffrey L Barnes, Goutam Ghosh Choudhury, Balakuntalam S Kasinat. Ribosomal biogenesis induction by high glucose requires activation of upstream binding factor in kidney glomerular epithelial cells. American journal of physiology. Renal physiology. vol 300. issue 1. 2011-02-09. PMID:20943765. |
diabetes promotes protein synthesis to induce kidney hypertrophy and increase renal matrix proteins. |
2011-02-09 |
2023-08-12 |
mouse |
| Meenalakshmi M Mariappan, Kristin D'Silva, Myung Ja Lee, Kavithalakshmi Sataranatarajan, Jeffrey L Barnes, Goutam Ghosh Choudhury, Balakuntalam S Kasinat. Ribosomal biogenesis induction by high glucose requires activation of upstream binding factor in kidney glomerular epithelial cells. American journal of physiology. Renal physiology. vol 300. issue 1. 2011-02-09. PMID:20943765. |
renal cortex from type 1 diabetic rats and type 2 diabetic db/db mice showed increased phosphorylation of ubf, erk, and p70s6 kinase coinciding with renal hypertrophy and onset of matrix accumulation. |
2011-02-09 |
2023-08-12 |
mouse |
| Mona Hedayat, Mohammad Jafar Mahmoudi, Noel R Rose, Nima Rezae. Proinflammatory cytokines in heart failure: double-edged swords. Heart failure reviews. vol 15. issue 6. 2011-02-08. PMID:20405319. |
cardiac myocyte hypertrophy, contractile dysfunction, cardiac myocyte apoptosis, and extracellular matrix remodeling contribute enormously to the development and progression of chronic heart failure. |
2011-02-08 |
2023-08-12 |
Not clear |
| Riccardo Lacchini, Anna L B Jacob-Ferreira, Marcelo R Luizon, Fernanda B Coeli, Tatiane C Izidoro-Toledo, Sandra Gasparini, Maria C Ferreira-Sae, Roberto Schreiber, Wilson Nadruz, Jose E Tanus-Santo. Matrix metalloproteinase 9 gene haplotypes affect left ventricular hypertrophy in hypertensive patients. Clinica chimica acta; international journal of clinical chemistry. vol 411. issue 23-24. 2011-01-19. PMID:20707992. |
matrix metalloproteinase 9 gene haplotypes affect left ventricular hypertrophy in hypertensive patients. |
2011-01-19 |
2023-08-12 |
Not clear |
| S Giovannini, J Diaz-Romero, T Aigner, P Heini, P Mainil-Varlet, D Nesi. Micromass co-culture of human articular chondrocytes and human bone marrow mesenchymal stem cells to investigate stable neocartilage tissue formation in vitro. European cells & materials. vol 20. 2011-01-19. PMID:20925023. |
msc produced cartilage-specific matrix only in +t+d but underwent hypertrophy in all pellet cultures. |
2011-01-19 |
2023-08-12 |
human |
| Elizabeth Sweeney, Douglas Roberts, Tina Corbo, Olena Jacenk. Congenic mice confirm that collagen X is required for proper hematopoietic development. PloS one. vol 5. issue 3. 2011-01-11. PMID:20209091. |
disrupted function of collagen x, a major hypertrophic cartilage matrix protein, resulted in skeletal and hematopoietic defects in endochondrally derived tissues. |
2011-01-11 |
2023-08-12 |
mouse |
| Doris Allerstorfer, Stefano Longato, Christoph Schwarzer, Reiner Fischer-Colbrie, Alison R Hayman, Michael J F Blume. VEGF and its role in the early development of the long bone epiphysis. Journal of anatomy. vol 216. issue 5. 2011-01-05. PMID:20525089. |
epiphyseal development further involves maturation of the resting chondrocytes into hypertrophic ones, associated with the mineralization of the cartilage matrix and eventual death of the latter cells. |
2011-01-05 |
2023-08-12 |
mouse |
| Cecelia C Yates, Priya Krishna, Diana Whaley, Richard Bodnar, Timothy Turner, Alan Well. Lack of CXC chemokine receptor 3 signaling leads to hypertrophic and hypercellular scarring. The American journal of pathology. vol 176. issue 4. 2010-12-14. PMID:20203286. |
these in vivo studies establish that the absence of cxcr3(-/-) signaling network results in hypertrophic and hypercellular scarring characterized by on-going wound regeneration, cellular proliferation, and scars in which immature matrix components are undergoing increased turnover resulting in a chronic inflammatory process. |
2010-12-14 |
2023-08-12 |
mouse |