| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| A K Rosenthal, D Heinkel, C M Goh. Thyroxine stimulates transglutaminase activity in articular chondrocytes. Osteoarthritis and cartilage. vol 11. issue 6. 2003-08-12. PMID:12801486. |
hypertrophic chondrocytes are responsible for extracellular matrix mineralization, with formation of bone mineral in growth plate cartilage and pathologic calcium crystals in aging articular cartilage. |
2003-08-12 |
2023-08-12 |
Not clear |
| Tsutomu Yoshikaw. [Alterations in sympathoadrenal system in congestive heart failure]. Nihon rinsho. Japanese journal of clinical medicine. vol 61. issue 5. 2003-08-08. PMID:12754996. |
mechanisms underlying such adverse effects involve multiple biological events including production of oxygen free radicals, cytokines, matrix metalloproteinase, apoptosis, cardiac hypertrophy, and chamber remodeling as well as energy expenditure. |
2003-08-08 |
2023-08-12 |
mouse |
| E Grimaud, F Blanchard, C Charrier, F Gouin, F Redini, D Heyman. Leukaemia inhibitory factor (lif) is expressed in hypertrophic chondrocytes and vascular sprouts during osteogenesis. Cytokine. vol 20. issue 5. 2003-08-01. PMID:12550107. |
avascular cartilage is replaced by highly vascularized bone tissue during endochondral ossification, a process involving capillary invasion of calcified hypertrophic cartilage in association with apoptosis of hypertrophic chondrocytes, degradation of cartilage matrix and deposition of bone matrix. |
2003-08-01 |
2023-08-12 |
human |
| Sanja Ivkovic, Byeong S Yoon, Steven N Popoff, Fayez F Safadi, Diana E Libuda, Robert C Stephenson, Aaron Daluiski, Karen M Lyon. Connective tissue growth factor coordinates chondrogenesis and angiogenesis during skeletal development. Development (Cambridge, England). vol 130. issue 12. 2003-07-31. PMID:12736220. |
ctgf deficiency leads to skeletal dysmorphisms as a result of impaired chondrocyte proliferation and extracellular matrix composition within the hypertrophic zone. |
2003-07-31 |
2023-08-12 |
mouse |
| Sanja Ivkovic, Byeong S Yoon, Steven N Popoff, Fayez F Safadi, Diana E Libuda, Robert C Stephenson, Aaron Daluiski, Karen M Lyon. Connective tissue growth factor coordinates chondrogenesis and angiogenesis during skeletal development. Development (Cambridge, England). vol 130. issue 12. 2003-07-31. PMID:12736220. |
decreased expression of specific extracellular matrix components and matrix metalloproteinases suggests that matrix remodeling within the hypertrophic zones in ctgf mutants is defective. |
2003-07-31 |
2023-08-12 |
mouse |
| Miriam S Domowicz, Melissa M Mueller, Todd E Novak, Lauren E Schwartz, Nancy B Schwart. Developmental expression of the HNK-1 carbohydrate epitope on aggrecan during chondrogenesis. Developmental dynamics : an official publication of the American Association of Anatomists. vol 226. issue 1. 2003-07-29. PMID:12508223. |
this finding was verified by using an aggrecan-deficient mutant, the nanomelic chick, which lacks hnk-1 immunostaining in the extracellular matrix of dividing and hypertrophic chondrocytes as late as embryonic day 12. |
2003-07-29 |
2023-08-12 |
chicken |
| Miriam S Domowicz, Melissa M Mueller, Todd E Novak, Lauren E Schwartz, Nancy B Schwart. Developmental expression of the HNK-1 carbohydrate epitope on aggrecan during chondrogenesis. Developmental dynamics : an official publication of the American Association of Anatomists. vol 226. issue 1. 2003-07-29. PMID:12508223. |
localization changes with development and the hnk-1-aggrecan matrix becomes restricted to dividing and hypertrophic chondrocytes and is particularly concentrated in the intraterritorial matrix. |
2003-07-29 |
2023-08-12 |
chicken |
| Nathalie Ortega, Danielle Behonick, Dominique Stickens, Zena Wer. How proteases regulate bone morphogenesis. Annals of the New York Academy of Sciences. vol 995. 2003-07-22. PMID:12814943. |
apoptosis of the terminal hypertrophic chondrocytes, degradation of the cartilage matrix, and deposition of bone matrix by osteoblasts accompanies neovascularization of the growth plate. |
2003-07-22 |
2023-08-12 |
mouse |
| Russell L Prewitt, Darian C Rice, Anca D Dobria. Adaptation of resistance arteries to increases in pressure. Microcirculation (New York, N.Y. : 1994). vol 9. issue 4. 2003-07-16. PMID:12152105. |
during the development of hypertension, hypertrophy of smooth muscle cells and deposition of extracellular matrix thicken the walls of large arteries without reducing the size of the lumen. |
2003-07-16 |
2023-08-12 |
Not clear |
| Christopher J Babbitt, Shaw-Yung Shai, Alice E Harpf, Can G Pham, Robert S Ros. Modulation of integrins and integrin signaling molecules in the pressure-loaded murine ventricle. Histochemistry and cell biology. vol 118. issue 6. 2003-07-14. PMID:12483308. |
extracellular matrix is altered in the myocardium during hypertrophic induction and the transition to heart failure. |
2003-07-14 |
2023-08-12 |
Not clear |
| Dajun Wang, Suzanne Oparil, Ji An Feng, Peng Li, Gilbert Perry, Lan Bo Chen, Meiru Dai, Simon W M John, Yiu-Fai Che. Effects of pressure overload on extracellular matrix expression in the heart of the atrial natriuretic peptide-null mouse. Hypertension (Dallas, Tex. : 1979). vol 42. issue 1. 2003-07-11. PMID:12756220. |
this study tested the hypothesis that atrial natriuretic peptide has direct antihypertrophic actions on the heart by modulating expression of genes involved in cardiac hypertrophy and extracellular matrix production. |
2003-07-11 |
2023-08-12 |
mouse |
| Dajun Wang, Suzanne Oparil, Ji An Feng, Peng Li, Gilbert Perry, Lan Bo Chen, Meiru Dai, Simon W M John, Yiu-Fai Che. Effects of pressure overload on extracellular matrix expression in the heart of the atrial natriuretic peptide-null mouse. Hypertension (Dallas, Tex. : 1979). vol 42. issue 1. 2003-07-11. PMID:12756220. |
atrial natriuretic peptide-null mice demonstrated cardiac hypertrophy at baseline and an exaggerated hypertrophic response to transverse aortic constriction associated with increased expression of the extracellular matrix molecules periostin, osteopontin, collagen i and iii, and thrombospondin, as well as the extracellular matrix regulatory proteins, matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-3, and the novel growth factor pleiotrophin compared with wild-type controls. |
2003-07-11 |
2023-08-12 |
mouse |
| Dajun Wang, Suzanne Oparil, Ji An Feng, Peng Li, Gilbert Perry, Lan Bo Chen, Meiru Dai, Simon W M John, Yiu-Fai Che. Effects of pressure overload on extracellular matrix expression in the heart of the atrial natriuretic peptide-null mouse. Hypertension (Dallas, Tex. : 1979). vol 42. issue 1. 2003-07-11. PMID:12756220. |
these results support the hypothesis that atrial natriuretic peptide protects against pressure overload-induced cardiac hypertrophy and remodeling by negative modulation of genes involved in extracellular matrix deposition. |
2003-07-11 |
2023-08-12 |
mouse |
| Kristen A Johnson, Deborah van Etten, Nisha Nanda, Robert M Graham, Robert A Terkeltau. Distinct transglutaminase 2-independent and transglutaminase 2-dependent pathways mediate articular chondrocyte hypertrophy. The Journal of biological chemistry. vol 278. issue 21. 2003-07-07. PMID:12606540. |
altered chondrocyte differentiation, including development of chondrocyte hypertrophy, mediates osteoarthritis and pathologic articular cartilage matrix calcification. |
2003-07-07 |
2023-08-12 |
mouse |
| Marpadga A Reddy, Young-Sook Kim, Linda Lanting, Rama Nataraja. Reduced growth factor responses in vascular smooth muscle cells derived from 12/15-lipoxygenase-deficient mice. Hypertension (Dallas, Tex. : 1979). vol 41. issue 6. 2003-06-27. PMID:12707289. |
we recently showed that products of the 12/15-lipoxygenase pathway play an important role in mediating hypertrophy, matrix protein production, and inflammatory gene expression in vascular smooth muscle cells (vsmc) through activation of mitogen activated protein kinases and key transcription factors. |
2003-06-27 |
2023-08-12 |
mouse |
| Raymond D Adelma. Obesity and renal disease. Current opinion in nephrology and hypertension. vol 11. issue 3. 2003-06-20. PMID:11981264. |
these substances may individually or interactively affect glomerular hyperfiltration, mesangial cell hypertrophy and matrix production, and the production of collagen, fibronectin, transforming growth factor-beta and other fibrogenic mediators of change. |
2003-06-20 |
2023-08-12 |
Not clear |
| Sanja Zoricic, Ivana Maric, Dragica Bobinac, Slobodan Vukicevi. Expression of bone morphogenetic proteins and cartilage-derived morphogenetic proteins during osteophyte formation in humans. Journal of anatomy. vol 202. issue Pt 3. 2003-06-09. PMID:12713267. |
immunoreactivity for bmp-2 was observed in fibrous tissue matrix as well as in osteoblasts; bmp-3 was mainly present in osteoblasts; bmp-6 was restricted to young osteocytes and bone matrix; bmp-7 was observed in hypertrophic chondrocytes, osteoblasts and young osteocytes of both endochondral and intramembranous bone formation sites. |
2003-06-09 |
2023-08-12 |
human |
| Louise A Aquila-Pastir, Nicholas R DiPaola, Rosalia G Matteo, Nicholas G Smedira, Patrick M McCarthy, Christine Schomisch Morave. Quantitation and distribution of beta-tubulin in human cardiac myocytes. Journal of molecular and cellular cardiology. vol 34. issue 11. 2003-06-05. PMID:12431450. |
increasing evidence suggests that derangements of cytoskeletal proteins contribute to alterations in intracellular signaling, myocyte function, and the coupling of myocytes to the extracellular matrix during cardiac hypertrophy and failure. |
2003-06-05 |
2023-08-12 |
human |
| Marc de Gaspar. Angiotensin II and nitric oxide interaction. Heart failure reviews. vol 7. issue 4. 2003-06-04. PMID:12379820. |
through its at(1) receptor, ang ii stimulates the long-term increase of several membrane component of nadph oxidase such as p(22) phox or nox-1 and causes an increased activity of nadph oxidase with inactivation of no leading to impaired endothelium-dependent vasorelaxation, vascular smooth muscle cell hypertrophy, proliferation and migration, extracellular matrix formation, thrombosis, cellular infiltration and inflammatory reaction. |
2003-06-04 |
2023-08-12 |
Not clear |
| Suresh C Tyagi, Brian D Hoi. Metalloproteinase in myocardial adaptation and maladaptation. Journal of cardiovascular pharmacology and therapeutics. vol 7. issue 4. 2003-06-04. PMID:12490970. |
ventricular remodeling is a compensatory response that comprises the processes of apoptosis, muscle cell hypertrophy, and rearrangement of the extracellular matrix fibers connecting the muscles. |
2003-06-04 |
2023-08-12 |
Not clear |