All Relations between hypertrophic and matrix compartment

Reference Sentence Publish Date Extraction Date Species
Anja Niehoff, Uwe G Kersting, Frank Zaucke, Michael M Morlock, Gert-Peter Br\\xc3\\xbcggeman. Adaptation of mechanical, morphological, and biochemical properties of the rat growth plate to dose-dependent voluntary exercise. Bone vol 35 issue 4 2005 15454097 osteonectin was located in the matrix of the upper hypertrophic zone in the ue group, whereas the le and con group showed more chondrocytes in the hypertrophic and lower proliferation zones stained for osteonectin, suggesting a higher level of mineralization in the growth plate of the ue group. 2005-02-02 2023-01-24 rat
Fraser D Russel. Emerging roles of urotensin-II in cardiovascular disease. Pharmacology & therapeutics vol 103 issue 3 2005 15464591 in vitro and in vivo studies show that under pathophysiological conditions, uii might contribute to cardiomyocyte hypertrophy, extracellular matrix production, enhanced vasoconstriction, vascular smooth muscle cell hyperplasia, and endothelial cell hyper-permeability. 2005-01-28 2023-01-24 human
Darren J Kelly, Yuan Zhang, Renae Gow, Richard E Gilber. Tranilast attenuates structural and functional aspects of renal injury in the remnant kidney model. Journal of the American Society of Nephrology : JASN vol 15 issue 10 2005 15466266 tranilast (n-[3,4-dimethoxycinnamoyl] anthranilic acid), an antifibrotic agent that is used to treat hypertrophic scars and scleroderma, has also been shown to inhibit tgf-beta-induced extracellular matrix synthesis in a range of cell types, including those of renal origin. 2005-01-27 2023-01-24 rat
Shona R Elshaw, Neil Henderson, Alan J Knox, Susan A Watson, David J Buttle, Simon R Johnso. Matrix metalloproteinase expression and activity in human airway smooth muscle cells. British journal of pharmacology vol 142 issue 8 2005 15265805 airway remodelling is a feature of chronic asthma comprising smooth muscle hypertrophy and deposition of extracellular matrix (ecm) proteins. 2005-01-26 2023-01-24 human
Florian Karreth, Astrid Hoebertz, Harald Scheuch, Robert Eferl, Erwin F Wagne. The AP1 transcription factor Fra2 is required for efficient cartilage development. Development (Cambridge, England) vol 131 issue 22 2005 15509771 the absence of fra2 in embryos and newborns leads to reduced zones of hypertrophic chondrocytes and impaired matrix deposition in femoral and tibial growth plates, probably owing to impaired differentiation into hypertrophic chondrocytes. 2005-01-18 2023-01-24 mouse
Rama Garimella, Xiahong Bi, Nancy Camacho, Joseph B Sipe, H Clarke Anderso. Primary culture of rat growth plate chondrocytes: an in vitro model of growth plate histotype, matrix vesicle biogenesis and mineralization. Bone vol 34 issue 6 2005 15193542 chondrocytes of growth plate undergo proliferation, maturation, hypertrophy, matrix vesicle (mv) biogenesis and programmed cell death (pcd, apoptosis). 2005-01-14 2023-01-24 rat
I Villemure, M A Chung, C S Seck, M H Kimm, J R Matyas, N A Dunca. The effects of mechanical loading on the mRNA expression of growth-plate cells. Studies in health technology and informatics vol 91 issue 2005 15457706 four key components were investigated: 18s (basic cell metabolism), type ii collagen (major extracellular matrix component), type x collagen (matrix component in hypertrophic zone) and pth-pthrp receptors (pre-hypertrophic chondrocytes). 2005-01-07 2023-01-24 rat
Dengshun Miao, Xiuying Bai, Dibyendu K Panda, Andrew C Karaplis, David Goltzman, Marc D McKe. Cartilage abnormalities are associated with abnormal Phex expression and with altered matrix protein and MMP-9 localization in Hyp mice. Bone vol 34 issue 4 2004 15050894 in addition, growth plate osteocalcin and bone sialoprotein levels were decreased, while osteonectin was increased, in hypertrophic chondrocytes and cartilage matrix in hyp mice. 2004-12-22 2023-01-24 mouse
Dengshun Miao, Xiuying Bai, Dibyendu K Panda, Andrew C Karaplis, David Goltzman, Marc D McKe. Cartilage abnormalities are associated with abnormal Phex expression and with altered matrix protein and MMP-9 localization in Hyp mice. Bone vol 34 issue 4 2004 15050894 these findings suggest that phex may control mineralization and removal of hypertrophic chondrocytes and cartilage matrix in growth plate by regulating the synthesis and deposition of certain bone matrix proteins and proteases such as mmp-9. 2004-12-22 2023-01-24 mouse
Darren J Kelly, Alison J Cox, Renae M Gow, Yuan Zhang, Bruce E Kemp, Richard E Gilber. Platelet-derived growth factor receptor transactivation mediates the trophic effects of angiotensin II in vivo. Hypertension (Dallas, Tex. : 1979) vol 44 issue 2 2004 15197170 the findings of attenuation of vascular hypertrophy and matrix deposition by imatinib indicate that transactivation of the pdgfr in vivo contributes to the growth factor-like effects of ang ii, independent of its hemodynamic effects or its ability to induce tgf-beta gene expression. 2004-12-21 2023-01-24 rat
Damiano Rizzoni, Gian Paolo Rossi, Enzo Porteri, Daniele Sticchi, Luigi Rodella, Rita Rezzani, Intissar Sleiman, Carolina De Ciuceis, Silvia Paiardi, Rossella Bianchi, G G Nussdorfer, Enrico Agabiti-Rose. Bradykinin and matrix metalloproteinases are involved the structural alterations of rat small resistance arteries with inhibition of ACE and NEP. Journal of hypertension vol 22 issue 4 2004 15126918 increased vascular resistance is a hallmark of hypertension and involves structural alterations, which may entail smooth muscle cell hypertrophy or hyperplasia, or qualitative or quantitative changes in extracellular matrix (ecm) proteins. 2004-12-06 2023-01-24 rat
Victoria Polyakova, Stefan Hein, Sawa Kostin, Tibor Ziegelhoeffer, Jutta Schape. Matrix metalloproteinases and their tissue inhibitors in pressure-overloaded human myocardium during heart failure progression. Journal of the American College of Cardiology vol 44 issue 8 2004 15489093 we studied the role of matrix metalloproteinases (mmps) and their tissue inhibitors (timps) in fibrosis formation in the transition from hypertrophy to heart failure (hf) as well as the cellular source of mmps and timps. 2004-11-30 2023-01-24 human
D Fraccarollo, P Galuppo, J Bauersach. Mineralocorticoid receptor antagonism and cardiac remodeling in ischemic heart failure. Current medicinal chemistry. Cardiovascular and hematological agents vol 2 issue 4 2004 15320779 while reduction of excessive extracellular matrix turnover leading to decreased fibrosis appears to be the most important effect of mineralocorticoid receptor antagonism in heart failure, other mechanisms such as regression of hypertrophy, improvement of endothelial function, reduction of superoxide formation, and enhanced renal sodium excretion may contribute. 2004-11-19 2023-01-24 rat
Bukhtiar H Shah, Kevin J Cat. Matrix metalloproteinase-dependent EGF receptor activation in hypertension and left ventricular hypertrophy. Trends in endocrinology and metabolism: TEM vol 15 issue 6 2004 15358274 matrix metalloproteinase-dependent egf receptor activation in hypertension and left ventricular hypertrophy. 2004-11-16 2023-01-24 Not clear
I S Shormano. [Structural remodeling of the renal vascular bed in experimental stenosis of the pulmonary trunk]. Morfologiia (Saint Petersburg, Russia) vol 125 issue 1 2004 15083578 this process included the hyperplasia and hypertrophy of the smooth myocytes in the media of the vascular wall as well as migration of these cells into the intima with the formation of specialized structures, regulating the hemodynamics, as well as the accumulation of the extracellular matrix in the walls of renal arteries and veins. 2004-11-09 2023-01-24 Not clear
Satoru Toyosawa, Yasuhiko Tomita, Mitsunobu Kishino, Jun Hashimoto, Takafumi Ueda, Takahiro Tsujimura, Katsuyuki Aozasa, Naokuni Ijuhin, Toshihisa Komor. Expression of dentin matrix protein 1 in tumors causing oncogenic osteomalacia. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc vol 17 issue 5 2004 15001995 dentin matrix protein 1 (dmp1) is an acidic phosphoprotein expressed in mineralized tissues including bone, tooth, and hypertrophic cartilage. 2004-11-02 2023-01-24 Not clear
Yoshihiro Noji, Masami Shimizu, Hidekazu Ino, Toshinori Higashikata, Masato Yamaguchi, Atsushi Nohara, Takahiro Horita, Kuniyoshi Shimizu, Yuji Ito, Takeshi Matsuda, Masanobu Namura, Hiroshi Mabuch. Increased circulating matrix metalloproteinase-2 in patients with hypertrophic cardiomyopathy with systolic dysfunction. Circulation journal : official journal of the Japanese Circulation Society vol 68 issue 4 2004 15056834 increased circulating matrix metalloproteinase-2 in patients with hypertrophic cardiomyopathy with systolic dysfunction. 2004-10-21 2023-01-24 Not clear
Sheldon Chen, Brenda B Hoffman, Joseph S Lee, Yuki Kasama, Belinda Jim, Jeffrey B Kopp, Fuad N Ziyade. Cultured tubule cells from TGF-beta1 null mice exhibit impaired hypertrophy and fibronectin expression in high glucose. Kidney international vol 65 issue 4 2004 15086458 to firmly establish the role of the transforming growth factor-beta1 (tgf-beta1) isoform in the pathophysiology of diabetic tubulointerstitial hypertrophy and fibrosis, we examined how the total absence of tgf-beta1 would alter the effect of high glucose on cellular hypertrophy and matrix expression in tubuloepithelial cells cultured from tgf-beta1 null mice. 2004-10-21 2023-01-24 mouse
Stephan Rosenkran. TGF-beta1 and angiotensin networking in cardiac remodeling. Cardiovascular research vol 63 issue 3 2004 15276467 tgf-beta induces the proliferation of cardiac fibroblasts and their phenotypic conversion to myofibroblasts, the deposition of extracellular matrix (ecm) proteins such as collagen, fibronectin, and proteoglycans, and hypertrophic growth of cardiomyocytes, and thereby mediates ang ii-induced structural remodeling of the ventricular wall in an auto-/paracrine manner. 2004-10-07 2023-01-24 Not clear
Masatoshi Takahara, Takuji Naruse, Michiaki Takagi, Hiroshi Orui, Toshihiko Ogin. Matrix metalloproteinase-9 expression, tartrate-resistant acid phosphatase activity, and DNA fragmentation in vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones. Journal of orthopaedic research : official publication of the Orthopaedic Research Society vol 22 issue 5 2004 15304278 recently it has been shown that matrix metalloproteinase-9 (mmp-9)/gelatinase b is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. 2004-09-16 2023-01-24 Not clear