All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
I Katsuragi, T Okeda, H Yoshimatsu, N Utsunomiya, K Ina, T Sakat. Transplantation of normal islets into the portal vein of Otsuka Long Evans Tokushima Fatty rats prevents diabetic progression. Experimental biology and medicine (Maywood, N.J.). vol 226. issue 7. 2001-07-19. PMID:11444104. immunohistochemical studies demonstrated that hypertrophic and fibrotic changes in pancreatic islets, together with mesangial proliferation of the glomerular matrix, an indicator for diabetic nephropathy, were attenuated predominantly in the it group at the late phase after transplantation compared with those in the corresponding phase of the so group. 2001-07-19 2023-08-12 rat
X Zhen, L Wei, Q Wu, Y Zhang, Q Che. Mitogen-activated protein kinase p38 mediates regulation of chondrocyte differentiation by parathyroid hormone. The Journal of biological chemistry. vol 276. issue 7. 2001-06-28. PMID:11098049. inhibition of p38 mapk in hypertrophic chondrocytes by either pth, sb303580, or both together leads to a decrease of hypertrophic marker type x collagen mrna and an increase of the expression of prehypertrophic marker cartilage matrix protein. 2001-06-28 2023-08-12 Not clear
F B Niessen, M P Andriessen, J Schalkwijk, L Visser, W Timen. Keratinocyte-derived growth factors play a role in the formation of hypertrophic scars. The Journal of pathology. vol 194. issue 2. 2001-06-21. PMID:11400150. in predisposed individuals, wound healing can lead to hypertrophic scar or keloid formation, characterized by an overabundant extracellular matrix. 2001-06-21 2023-08-12 Not clear
F B Niessen, M P Andriessen, J Schalkwijk, L Visser, W Timen. Keratinocyte-derived growth factors play a role in the formation of hypertrophic scars. The Journal of pathology. vol 194. issue 2. 2001-06-21. PMID:11400150. it is hypothesized that impaired production of keratinocyte-derived growth factors, such as il-1alpha, leads to a decrease in the catabolism of the dermal matrix, whereas augmented epidermal pdgf production leads to increased formation of the dermal matrix in hypertrophic scars. 2001-06-21 2023-08-12 Not clear
D Grimm, M Huber, H C Jabusch, M Shakibaei, S Fredersdorf, M Paul, G A Riegger, E P Krome. Extracellular matrix proteins in cardiac fibroblasts derived from rat hearts with chronic pressure overload: effects of beta-receptor blockade. Journal of molecular and cellular cardiology. vol 33. issue 3. 2001-06-14. PMID:11181017. left ventricular hypertrophy (lvh) is accompanied by progressive accumulations of extracellular matrix proteins. 2001-06-14 2023-08-12 rat
N A Trueblood, Z Xie, C Communal, F Sam, S Ngoy, L Liaw, A W Jenkins, J Wang, D B Sawyer, O H Bing, C S Apstein, W S Colucci, K Sing. Exaggerated left ventricular dilation and reduced collagen deposition after myocardial infarction in mice lacking osteopontin. Circulation research. vol 88. issue 10. 2001-06-14. PMID:11375279. osteopontin (opn), an extracellular matrix protein, is expressed in the myocardium with hypertrophy and failure. 2001-06-14 2023-08-12 mouse
M Alini, P J Roughle. Changes in leucine-rich repeat proteoglycans during maturation of the bovine growth plate. Matrix biology : journal of the International Society for Matrix Biology. vol 19. issue 8. 2001-06-07. PMID:11223340. at the message level, the expression of decorin shows a similar trend to that of protein abundance in the extracellular matrix, with its expression dropping markedly in the proliferative and hypertrophic zones. 2001-06-07 2023-08-12 cattle
P Chamiot-Clerc, J F Renaud, M E Safa. Pulse pressure, aortic reactivity, and endothelium dysfunction in old hypertensive rats. Hypertension (Dallas, Tex. : 1979). vol 37. issue 2. 2001-05-17. PMID:11230291. in old hypertensive rats, (1) increased kcl reactivity is endothelium independent but influenced by the map-dependent aortic hypertrophy with resulting increased vascular smooth muscle reactivity, whereas (2) increased ne reactivity is endothelium dependent in association with increased pp, altered endothelial function, and extracellular matrix, with resulting enhanced intrinsic arterial stiffness. 2001-05-17 2023-08-12 rat
K Kusafuka, Y Hiraki, C Shukunami, A Yamaguchi, T Kayano, T Takemur. Cartilage-specific matrix protein chondromodulin-I is associated with chondroid formation in salivary pleomorphic adenomas: immunohistochemical analysis. The American journal of pathology. vol 158. issue 4. 2001-05-03. PMID:11290564. in the growth plates of the long bones, chm-i was shown to be expressed in mature to upper hypertrophic chondrocytes, and to be deposited in the cartilage matrix. 2001-05-03 2023-08-12 Not clear
C M Tummalapalli, B J Heath, S C Tyag. Tissue inhibitor of metalloproteinase-4 instigates apoptosis in transformed cardiac fibroblasts. Journal of cellular biochemistry. vol 80. issue 4. 2001-04-26. PMID:11169735. the reduced levels of timp-4 elicit cellular transformation and may lead to adverse extracellular matrix degradation (remodeling), cardiac hypertrophy and failure. 2001-04-26 2023-08-12 human
W Weichert, A Paliege, A P Provoost, S Bachman. Upregulation of juxtaglomerular NOS1 and COX-2 precedes glomerulosclerosis in fawn-hooded hypertensive rats. American journal of physiology. Renal physiology. vol 280. issue 4. 2001-04-12. PMID:11249862. histopathological changes in fhh comprised focal segmental glomerulosclerosis (fsgs), focal matrix overexpression, and a moderate arteriolopathy with hypertrophy of the media, enhanced immunoreactivity for alpha-smooth muscle actin, and altered distribution of myofibrils. 2001-04-12 2023-08-12 rat
S Takeda, J P Bonnamy, M J Owen, P Ducy, G Karsent. Continuous expression of Cbfa1 in nonhypertrophic chondrocytes uncovers its ability to induce hypertrophic chondrocyte differentiation and partially rescues Cbfa1-deficient mice. Genes & development. vol 15. issue 4. 2001-04-05. PMID:11230154. despite the absence of osteoblasts in the rescued animals there were multinucleated, trap-positive cells resorbing the hypertrophic cartilage matrix. 2001-04-05 2023-08-12 mouse
H Uusitalo, A Hiltunen, M Söderström, H T Aro, E Vuori. Expression of cathepsins B, H, K, L, and S and matrix metalloproteinases 9 and 13 during chondrocyte hypertrophy and endochondral ossification in mouse fracture callus. Calcified tissue international. vol 67. issue 5. 2001-03-22. PMID:11136537. expression of cathepsins b, h, k, l, and s and matrix metalloproteinases 9 and 13 during chondrocyte hypertrophy and endochondral ossification in mouse fracture callus. 2001-03-22 2023-08-12 mouse
G L Brower, J S Janick. Contribution of ventricular remodeling to pathogenesis of heart failure in rats. American journal of physiology. Heart and circulatory physiology. vol 280. issue 2. 2001-03-22. PMID:11158966. the findings demonstrate an upper limit to lv hypertrophy and substantial increases in lv volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of chf. 2001-03-22 2023-08-12 rat
T Ohba, Y Ohba, K Moriyam. Synthesis of mRNAs for cathepsins L and K during development of the rat mandibular condylar cartilage. Cell and tissue research. vol 302. issue 3. 2001-03-15. PMID:11151446. furthermore, cathepsin l may play an important role in the degradation of the cartilaginous extracellular matrix in maturative and hypertrophic cell layers during successive developmental stages of the mandibular condyle. 2001-03-15 2023-08-12 rat
T Takao, T Iwaki, J Kondo, Y Hirak. Immunohistochemistry of chondromodulin-I in the human intervertebral discs with special reference to the degenerative changes. The Histochemical journal. vol 32. issue 9. 2001-03-08. PMID:11127975. it was detected in both the extracellular matrix and chondrocytes in the zone of hypertrophic cartilage, the zone of proliferative cartilage and the zone of resting cartilage in fetal discs. 2001-03-08 2023-08-12 human
R Tsou, J K Cole, A B Nathens, F F Isik, D M Heimbach, L H Engrav, N S Gibra. Analysis of hypertrophic and normal scar gene expression with cDNA microarrays. The Journal of burn care & rehabilitation. vol 21. issue 6. 2001-03-08. PMID:11194809. previous studies have suggested that hypertrophic scar formation results from altered gene expression of extracellular matrix molecules. 2001-03-08 2023-08-12 human
S L Zhang, C To, X Chen, J G Filep, S S Tang, J R Ingelfinger, S Carrière, J S Cha. Effect of renin-angiotensin system blockade on the expression of the angiotensinogen gene and induction of hypertrophy in rat kidney proximal tubular cells. Experimental nephrology. vol 9. issue 2. 2001-03-01. PMID:11150859. studies have shown that high levels of glucose and angiotensin ii (ang ii) stimulate hypertrophy and the expression of matrix protein genes in mouse proximal tubular cells in vitro. 2001-03-01 2023-08-12 mouse
K Ishizeki, T Naw. Further evidence for secretion of matrix metalloproteinase-1 by Meckel's chondrocytes during degradation of the extracellular matrix. Tissue & cell. vol 32. issue 3. 2001-02-15. PMID:11037790. these findings suggest that mmp-1 is present continuously in meckel's chondrocytes but that the active form, which degrades the extracellular matrix, is the mmp-1 that accumulates in the pericellular spaces around hypertrophic chondrocytes. 2001-02-15 2023-08-12 Not clear
C Colnot, S S Sidhu, N Balmain, F Poirie. Uncoupling of chondrocyte death and vascular invasion in mouse galectin 3 null mutant bones. Developmental biology. vol 229. issue 1. 2001-02-08. PMID:11133164. detailed histological and ultrastructural studies identified abnormalities in the cells of the proliferative, mature, and hypertrophic zones and in the extracellular matrix of the hypertrophic zone, as well as a reduction in the total number of hypertrophic chondrocytes. 2001-02-08 2023-08-12 mouse