All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
C A Tozzi, S Thakker-Varia, S Y Yu, R F Bannett, B W Peng, G J Poiani, F J Wilson, D J Rile. Mast cell collagenase correlates with regression of pulmonary vascular remodeling in the rat. American journal of respiratory cell and molecular biology. vol 18. issue 4. 1998-04-30. PMID:9533937. pulmonary vascular remodeling, produced by cell hypertrophy and extracellular matrix protein synthesis in response to hemodynamic stress, regresses after reduction of blood pressure, possibly by proteolysis of structural proteins. 1998-04-30 2023-08-12 rat
F Pietruck, S Spleiter, A Daul, T Philipp, M Derwahl, H Schatz, W Siffer. Enhanced G protein activation in IDDM patients with diabetic nephropathy. Diabetologia. vol 41. issue 1. 1998-04-27. PMID:9498636. a consequence of the altered metabolic milieu in diabetes is the increased release of vasoactive and proliferative agonists which promote glomerular hyperfiltration, hypertrophy, enhanced matrix deposition, and, finally, glomerulosclerosis. 1998-04-27 2023-08-12 human
F R Bühle. Cardiovascular care with the new T-type calcium channel antagonist: possible role of attendant sympathetic nervous system inhibition. Journal of hypertension. Supplement : official journal of the International Society of Hypertension. vol 15. issue 5. 1998-03-26. PMID:9481610. these and other factors reduce smooth muscle cell proliferation, hypertrophy and matrix deposition. 1998-03-26 2023-08-12 Not clear
B Corman, M Duriez, P Poitevin, D Heudes, P Bruneval, A Tedgui, B I Lev. Aminoguanidine prevents age-related arterial stiffening and cardiac hypertrophy. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 3. 1998-03-11. PMID:9448326. the prevention of arterial stiffening and cardiac hypertrophy in the absence of changes in collagen and elastin content suggests that the effect of aminoguanidine is related to a decrease in the age-induced cross-linking of the extracellular matrix. 1998-03-11 2023-08-12 rat
N Boos, A G Nerlich, I Wiest, K von der Mark, M Aeb. Immunolocalization of type X collagen in human lumbar intervertebral discs during ageing and degeneration. Histochemistry and cell biology. vol 108. issue 6. 1998-02-25. PMID:9450629. immunohistochemically, a positive specific type x staining was observed in the hypertrophic zone of the growth plate and only in the interstitial matrix of juvenile (<2 years) nucleus pulposus. 1998-02-25 2023-08-12 human
B Johnstone, T M Hering, A I Caplan, V M Goldberg, J U Yo. In vitro chondrogenesis of bone marrow-derived mesenchymal progenitor cells. Experimental cell research. vol 238. issue 1. 1998-02-23. PMID:9457080. by 14 days of culture, there was also evidence for type x collagen present in the matrix and the cells morphologically resembled hypertrophic chondrocytes. 1998-02-23 2023-08-12 rabbit
L Rai. Nitric oxide in hypertension: relationship with renal injury and left ventricular hypertrophy. Hypertension (Dallas, Tex. : 1979). vol 31. issue 1 Pt 2. 1998-02-20. PMID:9453301. specifically, in the presence of hypertension, nitric oxide may work in the kidney by inhibiting both mesangial cell hypertrophy and hyperplasia as well as synthesis of extracellular matrix and in the heart and systemic vessels by modulating smooth muscle cell hypertrophy and hyperplasia. 1998-02-20 2023-08-12 rat
A C Pessina, A Sacchetto, G P Ross. Left ventricular anatomy and function in primary aldosteronism and renovascular hypertension. Advances in experimental medicine and biology. vol 432. 1998-02-17. PMID:9433512. compelling evidence suggests that both the renin-angiotensin system (ras) and the aldosterone excess play an important role in the pathogenesis of lvh, since experimentally angiotensin ii has been found to cause myocardial cells hypertrophy and/or hyperplasia and excess aldosterone has been related to extracellular matrix and collagen deposition and therefore to myocardial fibrosis. 1998-02-17 2023-08-12 Not clear
N Kergosien, J Sautier, N Fores. Gene and protein expression during differentiation and matrix mineralization in a chondrocyte cell culture system. Calcified tissue international. vol 62. issue 2. 1998-02-11. PMID:9437044. however, our culture conditions promoted extracellular matrix mineralization and cell differentiation towards the hypertrophic phenotype. 1998-02-11 2023-08-12 rat
M S Hirsch, L E Lunsford, V Trinkaus-Randall, K K Svobod. Chondrocyte survival and differentiation in situ are integrin mediated. Developmental dynamics : an official publication of the American Association of Anatomists. vol 210. issue 3. 1998-02-10. PMID:9389451. cephalic chondrocytes become hypertrophic and secrete type x collagen into the extracellular matrix prior to bone deposition. 1998-02-10 2023-08-12 chicken
E Bonucci, G Silvestrini, P Mocett. MC22-33F monoclonal antibody shows unmasked polar head groups of choline-containing phospholipids in cartilage and bone. European journal of histochemistry : EJH. vol 41. issue 3. 1998-01-26. PMID:9359029. the mc22-33f mab immunoreaction was found in the cytoplasm of maturing and hypertrophic and, to a lesser extent, proliferating and degenerating chondrocytes; it was strongly positive in matrix vesicles, at the periphery of calcification nodules, and at the periphery of calcified matrix. 1998-01-26 2023-08-12 Not clear
L J Zhou, M Inoue, I Ono, F Kanek. The mode of action of prostaglandin (PG) I1 analog, SM-10906, on fibroblasts of hypertrophic scars is similar to PGE1 in its potential role of preventing scar formation. Experimental dermatology. vol 6. issue 6. 1998-01-22. PMID:9412820. the effects of prostaglandin (pg) i1 analog, sm-10906 (sm-6) and pge1 on extracellular matrix formation and the release of cytokines by cultured normal human dermal fibroblasts (ndf) and hypertrophic scar fibroblasts (hsf) were compared in order to evaluate the clinical efficacy of pgs in preventing scar formation. 1998-01-22 2023-08-12 human
G J Breur, M D Lapierre, K Kazmierczak, K M Stechuchak, G P McCab. The domain of hypertrophic chondrocytes in growth plates growing at different rates. Calcified tissue international. vol 61. issue 5. 1998-01-21. PMID:9351885. in this study, we tested the hypotheses that (a) both the domain volume (volume of the cell and the matrix it has formed) and matrix volume of juxtametaphyseal hypertrophic chondrocytes in the growth plate is tightly controlled, and that (b) the domain volume of juxtametaphyseal hypertrophic chondrocytes is a strong determinant of the rate of bone length growth. 1998-01-21 2023-08-12 rat
G J Breur, M D Lapierre, K Kazmierczak, K M Stechuchak, G P McCab. The domain of hypertrophic chondrocytes in growth plates growing at different rates. Calcified tissue international. vol 61. issue 5. 1998-01-21. PMID:9351885. the data suggest that the domain volume of juxtametaphyseal hypertrophic chondrocytes, as well as the matrix volume produced per cell, may be tightly regulated. 1998-01-21 2023-08-12 rat
N Fujitsuka, A Kurogi, T Hattori, S Shind. [Effects of onpi-to (TJ-8117) and (-)epicatechin-3-O-gallate on the proliferating changes in glomeruli of 5/6 nephrectomized rats]. Nihon Jinzo Gakkai shi. vol 39. issue 7. 1998-01-20. PMID:9396236. in the present study, the effects of tj-8117 and (-)epicatechin-3-o-gallate (ecg), which is a component of rhei rhizoma, on glomerular cell proliferation, extracellular matrix accumulation and glomerular hypertrophy were investigated in 5/6 nephrectomized rats. 1998-01-20 2023-08-12 rat
W S Colucc. Molecular and cellular mechanisms of myocardial failure. The American journal of cardiology. vol 80. issue 11A. 1998-01-20. PMID:9412539. these alterations include hypertrophy and cellular apoptosis of myocytes, changes in the molecular phenotype of the myocardium with reinduction of a fetal gene program, and alterations in the quantity and composition of the extracellular matrix. 1998-01-20 2023-08-12 Not clear
H Yu, A M Gallagher, P M Garfin, M P Print. Prostacyclin release by rat cardiac fibroblasts: inhibition of collagen expression. Hypertension (Dallas, Tex. : 1979). vol 30. issue 5. 1997-12-10. PMID:9369254. cardiac fibroblasts, as the source of extracellular matrix for the left ventricle, subserve important functions to cardiac remodeling and fibrotic development following myocardial infarction or with pressure-overload cardiac hypertrophy. 1997-12-10 2023-08-12 rat
C Shukunami, K Ishizeki, T Atsumi, Y Ohta, F Suzuki, Y Hirak. Cellular hypertrophy and calcification of embryonal carcinoma-derived chondrogenic cell line ATDC5 in vitro. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 12. issue 8. 1997-11-20. PMID:9258747. during the process of endochondral bone formation, proliferating chondrocytes give rise to hypertrophic cells, which then deposit a mineralized matrix to form calcified cartilage prior to replacement by bone. 1997-11-20 2023-08-12 Not clear
H Ono, Y On. Nephrosclerosis and hypertension. The Medical clinics of North America. vol 81. issue 6. 1997-11-19. PMID:9356598. in the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of cholesterol, shows an increased mesangial matrix and hypertrophic vascular medial smooth muscle cells. 1997-11-19 2023-08-12 human
G Wolf, F N Ziyade. Renal tubular hypertrophy induced by angiotensin II. Seminars in nephrology. vol 17. issue 5. 1997-11-18. PMID:9316213. angiotensin ii (ang ii) is a prime agent that has been linked to the progression of renal disease by a host of mechanisms, including the induction of tubular epithelial hypertrophy and stimulation of extracellular matrix biosynthesis. 1997-11-18 2023-08-12 Not clear