| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Xiao-Fan Xie, Li-Xin He, Xiao-Feng Hao, Bi Chen, Chi-Yu Jia, Zhi-Gang Sun, Yu-Jue Cao, Dong Hai L. [Expression of matrix metalloproteinase-2, -9 and their inhibitor-1 in hypertrophic scars]. Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns. vol 23. issue 6. 2009-07-07. PMID:18457258. |
[expression of matrix metalloproteinase-2, -9 and their inhibitor-1 in hypertrophic scars]. |
2009-07-07 |
2023-08-12 |
Not clear |
| Xiao-Fan Xie, Li-Xin He, Xiao-Feng Hao, Bi Chen, Chi-Yu Jia, Zhi-Gang Sun, Yu-Jue Cao, Dong Hai L. [Expression of matrix metalloproteinase-2, -9 and their inhibitor-1 in hypertrophic scars]. Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns. vol 23. issue 6. 2009-07-07. PMID:18457258. |
to investigate the gene expression of matrix metalloproteinases (mmp-2, mmp-9) and tissue inhibitor of metalloproteinase-1 (timp-1) in proliferative and mature hypertrophic scars. |
2009-07-07 |
2023-08-12 |
Not clear |
| Franciszek Burdan, Justyna Szumiło, Agnieszka Korobowicz, Rabia Farooquee, Sagar Patel, Ankit Patel, Anjalee Dave, Michał Szumiło, Michał Solecki, Robert Klepacz, Jarosław Dudk. Morphology and physiology of the epiphyseal growth plate. Folia histochemica et cytobiologica. vol 47. issue 1. 2009-07-01. PMID:19419931. |
this multilayer structure is formed by the proliferation and hypertrophy of cells that synthesize the extracellular matrix composed of collagen (mainly type ii, ix, x, xi) and proteoglycans (aggrecan, decorin, annexin ii, v and vi). |
2009-07-01 |
2023-08-12 |
Not clear |
| Ezequiel J Molina, Jon Palma, Dipin Gupta, Denise Torres, John P Gaughan, Steven Houser, Mahender Mach. Reverse remodeling is associated with changes in extracellular matrix proteases and tissue inhibitors after mesenchymal stem cell (MSC) treatment of pressure overload hypertrophy. Journal of tissue engineering and regenerative medicine. vol 3. issue 2. 2009-06-15. PMID:19065545. |
reverse remodeling is associated with changes in extracellular matrix proteases and tissue inhibitors after mesenchymal stem cell (msc) treatment of pressure overload hypertrophy. |
2009-06-15 |
2023-08-12 |
rat |
| Ezequiel J Molina, Jon Palma, Dipin Gupta, Denise Torres, John P Gaughan, Steven Houser, Mahender Mach. Reverse remodeling is associated with changes in extracellular matrix proteases and tissue inhibitors after mesenchymal stem cell (MSC) treatment of pressure overload hypertrophy. Journal of tissue engineering and regenerative medicine. vol 3. issue 2. 2009-06-15. PMID:19065545. |
changes in ventricular extracellular matrix (ecm) composition of pressure overload hypertrophy determine clinical outcomes. |
2009-06-15 |
2023-08-12 |
rat |
| Xiang Wang, Fung Lan Chow, Tatsujiro Oka, Li Hao, Ana Lopez-Campistrous, Sandra Kelly, Stephan Cooper, Jeffrey Odenbach, Barry A Finegan, Richard Schulz, Zamaneh Kassiri, Gary D Lopaschuk, Carlos Fernandez-Patro. Matrix metalloproteinase-7 and ADAM-12 (a disintegrin and metalloproteinase-12) define a signaling axis in agonist-induced hypertension and cardiac hypertrophy. Circulation. vol 119. issue 18. 2009-06-09. PMID:19398663. |
matrix metalloproteinase-7 and adam-12 (a disintegrin and metalloproteinase-12) define a signaling axis in agonist-induced hypertension and cardiac hypertrophy. |
2009-06-09 |
2023-08-12 |
Not clear |
| Nadja Herbach, Irene Schairer, Andreas Blutke, Sabine Kautz, Angela Siebert, Burkhard Göke, Eckhard Wolf, Ruediger Wank. Diabetic kidney lesions of GIPRdn transgenic mice: podocyte hypertrophy and thickening of the GBM precede glomerular hypertrophy and glomerulosclerosis. American journal of physiology. Renal physiology. vol 296. issue 4. 2009-06-02. PMID:19211686. |
early renal changes of transgenic mice consisted of podocyte hypertrophy, reduced numerical volume density of podocytes in glomeruli, and homogenous thickening of the glomerular basement membrane, followed by renal and glomerular hypertrophy as well as mesangial expansion and matrix accumulation. |
2009-06-02 |
2023-08-12 |
mouse |
| Jung-Tak Kim, Sang-Heum Baek, Sang-Han Lee, Eui Kyun Park, Eun-Cheol Kim, In-Sook Kwun, Hong-In Shi. Zinc-deficient diet decreases fetal long bone growth through decreased bone matrix formation in mice. Journal of medicinal food. vol 12. issue 1. 2009-05-29. PMID:19298204. |
the fetal developing tibia of the zinc-deficient group showed marked shortening of diaphysis and a mild narrowing of the hypertrophic chondrocyte zone width with increased osteoclast number, but there was no influence on the mineralization of bone matrix. |
2009-05-29 |
2023-08-12 |
mouse |
| E J Mackie, Y A Ahmed, L Tatarczuch, K-S Chen, M Miram. Endochondral ossification: how cartilage is converted into bone in the developing skeleton. The international journal of biochemistry & cell biology. vol 40. issue 1. 2009-05-01. PMID:17659995. |
during endochondral ossification, chondrocytes proliferate, undergo hypertrophy and die; the cartilage extracellular matrix they construct is then invaded by blood vessels, osteoclasts, bone marrow cells and osteoblasts, the last of which deposit bone on remnants of cartilage matrix. |
2009-05-01 |
2023-08-12 |
Not clear |
| Denise L Cecil, C Thomas G Appleton, Monika D Polewski, John S Mort, Ann Marie Schmidt, Alison Bendele, Frank Beier, Robert Terkeltau. The pattern recognition receptor CD36 is a chondrocyte hypertrophy marker associated with suppression of catabolic responses and promotion of repair responses to inflammatory stimuli. Journal of immunology (Baltimore, Md. : 1950). vol 182. issue 8. 2009-04-23. PMID:19342682. |
multiple inflammatory mediators in osteoarthritis (oa) cartilage, including s100/calgranulin ligands of receptor for advanced glycation end products (rage), promote chondrocyte hypertrophy, a differentiation state associated with matrix catabolism. |
2009-04-23 |
2023-08-12 |
mouse |
| Denise L Cecil, C Thomas G Appleton, Monika D Polewski, John S Mort, Ann Marie Schmidt, Alison Bendele, Frank Beier, Robert Terkeltau. The pattern recognition receptor CD36 is a chondrocyte hypertrophy marker associated with suppression of catabolic responses and promotion of repair responses to inflammatory stimuli. Journal of immunology (Baltimore, Md. : 1950). vol 182. issue 8. 2009-04-23. PMID:19342682. |
however, cd36 transfection in normal human knee-immortalized chondrocytes (ch-8 cells) was associated with decreased capacity of s100a11 and tnf-alpha to induce chondrocyte hypertrophy and adamts-4 and matrix metalloproteinase 13 expression. |
2009-04-23 |
2023-08-12 |
mouse |
| Serafim M Oliveira, Isabel F Amaral, Mário A Barbosa, Cristina C Teixeir. Engineering endochondral bone: in vitro studies. Tissue engineering. Part A. vol 15. issue 3. 2009-04-16. PMID:18759672. |
ra treatment caused chondrocyte hypertrophy, characterized by the presence of type x collagen in the extracellular matrix and increased alkaline phosphatase activity. |
2009-04-16 |
2023-08-12 |
chicken |
| Luisa Lassová, Zeling Niu, Eleanor B Golden, Arthur J Cohen, Sherrill L Adam. Thyroid hormone treatment of cultured chondrocytes mimics in vivo stimulation of collagen X mRNA by increasing BMP 4 expression. Journal of cellular physiology. vol 219. issue 3. 2009-04-16. PMID:19170125. |
during endochondral bone formation, chondrocytes undergo terminal differentiation, during which the rate of proliferation decreases, cells become hypertrophic, and the extracellular matrix is altered by production of collagen x, as well as proteins required for matrix mineralization. |
2009-04-16 |
2023-08-12 |
Not clear |
| Konstantinos Tziomalos, Joshua M Har. Role of xanthine oxidoreductase in cardiac nitroso-redox imbalance. Frontiers in bioscience (Landmark edition). vol 14. 2009-04-07. PMID:19273066. |
within the heart, xor activity stimulates cardiomyocyte hypertrophy, apoptosis, and impairs matrix structure. |
2009-04-07 |
2023-08-12 |
Not clear |
| Narayana Anilkumar, Alexander Sirker, Ajay M Sha. Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure. Frontiers in bioscience (Landmark edition). vol 14. 2009-04-07. PMID:19273265. |
in particular, the tightly regulated generation of ros by nadph oxidases appears especially important in key signaling events that drive the development of cardiomyocyte hypertrophy, fibrosis, extracellular matrix remodelling and cell apoptosis. |
2009-04-07 |
2023-08-12 |
Not clear |
| Kristin Schram, Gary Sweene. Implications of myocardial matrix remodeling by adipokines in obesity-related heart failure. Trends in cardiovascular medicine. vol 18. issue 6. 2009-04-02. PMID:19185809. |
the events that these adipokines can regulate include alterations in myocardial metabolism, cardiomyocyte hypertrophy, cell death, and structure and composition of the extracellular matrix. |
2009-04-02 |
2023-08-12 |
Not clear |
| George Osol, Maurizio Mandal. Maternal uterine vascular remodeling during pregnancy. Physiology (Bethesda, Md.). vol 24. 2009-04-01. PMID:19196652. |
the process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. |
2009-04-01 |
2023-08-12 |
Not clear |
| S Tanriverdi-Akhisaroglu, A Menderes, G Okta. Matrix metalloproteinase-2 and -9 activities in human keloids, hypertrophic and atrophic scars: a pilot study. Cell biochemistry and function. vol 27. issue 2. 2009-03-30. PMID:19165813. |
matrix metalloproteinase-2 and -9 activities in human keloids, hypertrophic and atrophic scars: a pilot study. |
2009-03-30 |
2023-08-12 |
human |
| Hiroyuki Tsutsui, Shintaro Kinugawa, Shouji Matsushim. Mitochondrial oxidative stress and dysfunction in myocardial remodelling. Cardiovascular research. vol 81. issue 3. 2009-03-26. PMID:18854381. |
reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. |
2009-03-26 |
2023-08-12 |
Not clear |
| Kevin V Lemle. Diabetes and chronic kidney disease: lessons from the Pima Indians. Pediatric nephrology (Berlin, Germany). vol 23. issue 11. 2009-03-23. PMID:18320236. |
this population well illustrates the often inexorable progression from glomerular hyperfiltration to microalbuminuria to overt proteinuria and loss of glomerular filtration rate (gfr), paralleled by the accumulation of mesangial matrix and basement membrane, glomerular hypertrophy, loss of podocytes and eventual glomerular sclerosis and interstitial fibrosis. |
2009-03-23 |
2023-08-12 |
Not clear |