All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
A M Costa, S Peyrol, L C Pôrto, J P Comparin, J L Foyatier, A Desmoulièr. Mechanical forces induce scar remodeling. Study in non-pressure-treated versus pressure-treated hypertrophic scars. The American journal of pathology. vol 155. issue 5. 1999-11-30. PMID:10550323. our results show that, in hypertrophic scars, pressure therapy restores in part the extracellular matrix organization observed in normal scar and induces the disappearance of alpha-smooth muscle actin-expressing myofibroblasts, probably by apoptosis. 1999-11-30 2023-08-12 Not clear
M W Orth, J I Fenton, K A Chlebek-Brow. Biochemical characterization of cartilage degradation in embryonic chick tibial explant cultures. Poultry science. vol 78. issue 11. 1999-11-26. PMID:10560834. these results suggest that chondrocytes in the tibiae undergo hypertrophy, degrade the extracellular matrix, and die. 1999-11-26 2023-08-12 chicken
E B Hunziker, E Kapfinger, C Saage. Hypertrophy of growth plate chondrocytes in vivo is accompanied by modulations in the activity state and surface area of their cytoplasmic organelles. Histochemistry and cell biology. vol 112. issue 2. 1999-11-22. PMID:10460464. the rate of longitudinal bone growth is regulated primarily by modulations in the activity of epiphyseal plate hypertrophic chondrocytes, these being manifested as changes in cell and matrix volume. 1999-11-22 2023-08-12 rat
I Sato, M Sunohara, T Sat. Quantitative analysis of extracellular matrix proteins in hypertrophic layers of the mandibular condyle and temporal bone during human fetal development. Cells, tissues, organs. vol 165. issue 2. 1999-11-16. PMID:10516421. quantitative analysis of extracellular matrix proteins in hypertrophic layers of the mandibular condyle and temporal bone during human fetal development. 1999-11-16 2023-08-12 human
I Sato, M Sunohara, T Sat. Quantitative analysis of extracellular matrix proteins in hypertrophic layers of the mandibular condyle and temporal bone during human fetal development. Cells, tissues, organs. vol 165. issue 2. 1999-11-16. PMID:10516421. a computer image analysis of immunostained extracellular matrix (ecm) proteins (collagen types i, ii, iii and v, fibronectin and tenascin) in hypertrophic layers in the mandibular condyle and temporal bone of human fetuses, which ranged in gestational age from 12 to 32 weeks, was performed. 1999-11-16 2023-08-12 human
C Farquharson, D Lester, E Seawright, D Jefferies, B Housto. Microtubules are potential regulators of growth-plate chondrocyte differentiation and hypertrophy. Bone. vol 25. issue 4. 1999-11-02. PMID:10511106. a partial failure of chondrocyte hypertrophy was observed, although collagen type x immunoreactivity was noted within the interstitial matrix. 1999-11-02 2023-08-12 chicken
B Zerega, S Cermelli, P Bianco, R Cancedda, F D Cancedd. Parathyroid hormone [PTH(1-34)] and parathyroid hormone-related protein [PTHrP(1-34)] promote reversion of hypertrophic chondrocytes to a prehypertrophic proliferating phenotype and prevent terminal differentiation of osteoblast-like cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 14. issue 8. 1999-09-30. PMID:10457260. chick embryo hypertrophic chondrocytes maintained in suspension synthesized type ii and type x collagen and organized their extracellular matrix, forming a tissue highly reminiscent of true cartilage, which eventually mineralized. 1999-09-30 2023-08-12 chicken
B Zerega, S Cermelli, P Bianco, R Cancedda, F D Cancedd. Parathyroid hormone [PTH(1-34)] and parathyroid hormone-related protein [PTHrP(1-34)] promote reversion of hypertrophic chondrocytes to a prehypertrophic proliferating phenotype and prevent terminal differentiation of osteoblast-like cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 14. issue 8. 1999-09-30. PMID:10457260. hypertrophic chondrocytes cultured in adherent conditions in the presence of retinoic acid underwent further differentiation to osteoblast-like cells (i.e., they resumed cell proliferation, switched to type i collagen synthesis, and produced a mineralizing bone-like matrix). 1999-09-30 2023-08-12 chicken
B Zerega, S Cermelli, P Bianco, R Cancedda, F D Cancedd. Parathyroid hormone [PTH(1-34)] and parathyroid hormone-related protein [PTHrP(1-34)] promote reversion of hypertrophic chondrocytes to a prehypertrophic proliferating phenotype and prevent terminal differentiation of osteoblast-like cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 14. issue 8. 1999-09-30. PMID:10457260. these data indicate that pth/pthrp inhibit both the mineralization of a cartilage-like matrix and apoptosis (mimicked in the suspension culture) and the production of a mineralizing bone-like matrix, characterizing further differentiation of hypertrophic chondrocytes to osteoblasts like cells (mimicked in adhesion culture). 1999-09-30 2023-08-12 chicken
M Lajemi, S Gautier, A Beneto. [Rigidity of large arteries and cardiovascular risk. epidemiological aspects and genetic determinants]. Pathologie-biologie. vol 47. issue 6. 1999-09-23. PMID:10472072. aging, environmental and genetic factors are responsible for structural and functional changes of the arterial wall media (hypertrophy, extracellular matrix accumulation, calcium deposits) and of the vascular endothelium (decrease in the release of vasodilators and increased synthesis of vasoconstrictors), all that leading to a diminution of elasticity and increased stiffness. 1999-09-23 2023-08-12 human
N Nishijo, S Takamine, F Sugiyama, K Kimoto, K Taniguchi, H Horiguchi, T Ogata, K Murakami, A Fukamizu, K Yagam. Vascular remodeling in hypertensive transgenic mice. Experimental animals. vol 48. issue 3. 1999-09-23. PMID:10480026. they progressively developed remarkable vascular hypertrophy composed of dedifferentiation of vascular smooth muscle cells (vsmcs) and extracellular matrix accumulation in the thoracic aorta, and vsmc hyperplasia was predominant in the abdominal aorta. 1999-09-23 2023-08-12 mouse
M Polo, P D Smith, Y J Kim, X Wang, F Ko, M C Robso. Effect of TGF-beta2 on proliferative scar fibroblast cell kinetics. Annals of plastic surgery. vol 43. issue 2. 1999-09-20. PMID:10454327. keloids, hypertrophic scars, and burn hypertrophic scars are all forms of proliferative scarring characterized by overabundant matrix formation. 1999-09-20 2023-08-12 rat
A N Neely, C E Clendening, J Gardner, D G Greenhalgh, G D Warde. Gelatinase activity in keloids and hypertrophic scars. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 7. issue 3. 1999-09-10. PMID:10417752. ten hypertrophic scar samples, 9 keloid samples, and 10 donor skin samples were frozen, pulverized, homogenized, clarified by centrifugation, and analyzed for matrix metalloproteinases by quantitative zymography. 1999-09-10 2023-08-12 Not clear
A N Neely, C E Clendening, J Gardner, D G Greenhalgh, G D Warde. Gelatinase activity in keloids and hypertrophic scars. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 7. issue 3. 1999-09-10. PMID:10417752. however, matrix metalloproteinase-2 activity was significantly elevated in keloids and hypertrophic scars vs. donor samples: 2.6 and 3.9-fold increases for latent matrix metalloproteinase-2, 7.8 and 6.9-fold increases for active matrix metalloproteinase-2, respectively. 1999-09-10 2023-08-12 Not clear
A N Neely, C E Clendening, J Gardner, D G Greenhalgh, G D Warde. Gelatinase activity in keloids and hypertrophic scars. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 7. issue 3. 1999-09-10. PMID:10417752. we conclude that little matrix metalloproteinase-9 activity (the gelatinase involved in early tissue repair) is present in keloids and hypertrophic scars, while matrix metalloproteinase-2 activity (the gelatinase involved in prolonged tissue remodeling) is present in donor skin and is significantly increased in hypertrophic scars and keloids. 1999-09-10 2023-08-12 Not clear
A Salvetti, P Mattei, I Sudan. Renal protection and antihypertensive drugs: current status. Drugs. vol 57. issue 5. 1999-08-06. PMID:10353294. secondly, intrarenal actions on mechanisms such as glomerular hypertension and hypertrophy, proteinuria, mesangial cell proliferation, mesangial matrix production and probably endothelial dysfunction, which can cause and/or worsen renal failure, are relevant for the renal protective action of some drug classes. 1999-08-06 2023-08-12 Not clear
K M Hannan, P J Littl. Mechanisms regulating the vascular smooth muscle Na/H exchanger (NHE-1) in diabetes. Biochemistry and cell biology = Biochimie et biologie cellulaire. vol 76. issue 5. 1999-08-05. PMID:10353708. the pathology involves hypertrophy and proliferation of vascular smooth muscle cells and the production and modification of extracellular matrix. 1999-08-05 2023-08-12 Not clear
Y Nakamura, H Makino, R Morishit. [Distribution and function of angiotensin receptor subtypes in cardiovascular system]. Nihon rinsho. Japanese journal of clinical medicine. vol 57. issue 5. 1999-07-22. PMID:10361430. in adult, at1 is a dominant subtype in cardiovascular system, and mediates virtually all the previously known actions of aii, including vasoconstriction, production of growth factors, hypertrophy of smooth muscle and cardiomyocyte, proliferation of smooth muscle and fibroblast, production of extracellular matrix and so on. 1999-07-22 2023-08-12 Not clear
R Serra, A Karaplis, P Soh. Parathyroid hormone-related peptide (PTHrP)-dependent and -independent effects of transforming growth factor beta (TGF-beta) on endochondral bone formation. The Journal of cell biology. vol 145. issue 4. 1999-07-21. PMID:10330406. mouse embryonic metatarsal bone rudiments grown in organ culture were used to demonstrate that tgf-beta inhibits several stages of endochondral bone formation, including chondrocyte proliferation, hypertrophic differentiation, and matrix mineralization. 1999-07-21 2023-08-12 mouse
R Serra, A Karaplis, P Soh. Parathyroid hormone-related peptide (PTHrP)-dependent and -independent effects of transforming growth factor beta (TGF-beta) on endochondral bone formation. The Journal of cell biology. vol 145. issue 4. 1999-07-21. PMID:10330406. pthrp added to cultures inhibited hypertrophic differentiation and matrix mineralization but did not affect cell proliferation. 1999-07-21 2023-08-12 mouse