All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
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
James Melrose, Susan Smith, Sarah Knox, John Whiteloc. Perlecan, the multidomain HS-proteoglycan of basement membranes, is a prominent pericellular component of ovine hypertrophic vertebral growth plate and cartilaginous endplate chondrocytes. Histochemistry and cell biology. vol 118. issue 4. 2003-06-03. PMID:12376823. in contrast to the aforementioned matrix components, ha, habps and perlecan were localised strongly to the pericellular matrices of the hypertrophic vgp and cep chondrocytes apparently indicating an important role for these components in terminal chondrocyte differentiation. 2003-06-03 2023-08-12 Not clear
Wilfried Briest, Alexander Hölzl, Beate Rassler, Alexander Deten, Hideo A Baba, Heinz-Gerd Zimme. Significance of matrix metalloproteinases in norepinephrine-induced remodelling of rat hearts. Cardiovascular research. vol 57. issue 2. 2003-04-29. PMID:12566110. norepinephrine (ne) induced hypertrophy and remodelling of the extracellular matrix (ecm) in the left ventricle (lv) of the rat heart with resulting fibrosis. 2003-04-29 2023-08-12 rat
Si-Kwang Li. Metabolic disease in animals. Seminars in musculoskeletal radiology. vol 6. issue 4. 2003-04-22. PMID:12541191. rickets is a metabolic bone disorder characterized by osteopenic changes resulting from the failure of calcification of the osteoid matrix and absent mineralization of hypertrophic cartilage cells at the epiphyseal growth plates in growing primates, herbivores, swine, carnivores, and birds. 2003-04-22 2023-08-12 Not clear
J Kitagaki, M Iwamoto, J-G Liu, Y Tamamura, M Pacifci, M Enomoto-Iwamot. Activation of beta-catenin-LEF/TCF signal pathway in chondrocytes stimulates ectopic endochondral ossification. Osteoarthritis and cartilage. vol 11. issue 1. 2003-04-21. PMID:12505485. recently, we found that beta-catenin-lef/tcf-dependent wnt signaling stimulates chondrocyte maturation and hypertrophy and extracellular matrix calcification in vitro, events normally associated with cartilage-to-bone transition during skeletogenesis. 2003-04-21 2023-08-12 Not clear
Z i-Jun Zhang, James Huckle, Clair A Francomano, Richard G S Spence. The influence of pulsed low-intensity ultrasound on matrix production of chondrocytes at different stages of differentiation: an explant study. Ultrasound in medicine & biology. vol 28. issue 11-12. 2003-04-16. PMID:12498950. however, plius did not induce hypertrophy in hyaline cartilage; moreover, increased matrix synthesis indicates a potential role in cartilage repair. 2003-04-16 2023-08-12 chicken
C Henningsen, G Zahner, F Thais. High glucose induces type 1 hexokinase gene expression in isolated glomeruli of diabetic rats and in mesangial cells. Nephron. Physiology. vol 93. issue 3. 2003-04-11. PMID:12660493. diabetic nephropathy, which is characterized by renal hypertrophy and accumulation of extracellular matrix, is one of the leading causes for end-stage renal disease. 2003-04-11 2023-08-12 rat
Ze'ev Hochber. Mechanisms of steroid impairment of growth. Hormone research. vol 58 Suppl 1. 2003-03-17. PMID:12373012. direct effects at the growth plate include the suppression of multiple gene expression, chondrocyte proliferation and matrix proteoglycan synthesis, sulfation, release and mineralization as well as the augmentation of hypertrophic cell apoptosis. 2003-03-17 2023-08-12 Not clear