All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
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. 2004-12-06. PMID: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 2023-08-12 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. 2004-11-30. PMID: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 2023-08-12 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. 2004-11-19. PMID: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 2023-08-12 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. 2004-11-16. PMID:15358274. matrix metalloproteinase-dependent egf receptor activation in hypertension and left ventricular hypertrophy. 2004-11-16 2023-08-12 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. 2004-11-09. PMID: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 2023-08-12 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. 2004-11-02. PMID:15001995. dentin matrix protein 1 (dmp1) is an acidic phosphoprotein expressed in mineralized tissues including bone, tooth, and hypertrophic cartilage. 2004-11-02 2023-08-12 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. 2004-10-21. PMID:15056834. increased circulating matrix metalloproteinase-2 in patients with hypertrophic cardiomyopathy with systolic dysfunction. 2004-10-21 2023-08-12 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. 2004-10-21. PMID: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 2023-08-12 mouse
Stephan Rosenkran. TGF-beta1 and angiotensin networking in cardiac remodeling. Cardiovascular research. vol 63. issue 3. 2004-10-07. PMID: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 2023-08-12 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. 2004-09-16. PMID: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 2023-08-12 Not clear
Thaís P Amadeu, André S Braune, Luís C Porto, Alexis Desmoulière, Andréa M A Cost. Fibrillin-1 and elastin are differentially expressed in hypertrophic scars and keloids. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 12. issue 2. 2004-09-03. PMID:15086768. considering the importance of extracellular matrix elements in tissue repair, a morphological and quantitative analysis of the elastic system components (fibrillin-1 and elastin) was performed in normal skin, normal scars, hypertrophic scars, and keloids. 2004-09-03 2023-08-12 Not clear
Bernhard Schmitt, Jochen Ringe, Thomas Häupl, Michael Notter, Rudi Manz, Gerd-Rüdiger Burmester, Michael Sittinger, Christian Kap. BMP2 initiates chondrogenic lineage development of adult human mesenchymal stem cells in high-density culture. Differentiation; research in biological diversity. vol 71. issue 9-10. 2004-08-24. PMID:14686954. histologic staining of mineralized extracellular matrix with von kossa, immunostaining of type x collagen (typical for hypertrophic chondrocytes), and gene expression analysis of osteocalcin and adipocyte-specific fatty acid binding protein (ap2) further documented that bmp2 induced chondrogenic lineage development and not osteogenesis and/or adipogenesis in human mscs. 2004-08-24 2023-08-12 human
Sandro Goruppi, John M Kyriaki. The pro-hypertrophic basic helix-loop-helix protein p8 is degraded by the ubiquitin/proteasome system in a protein kinase B/Akt- and glycogen synthase kinase-3-dependent manner, whereas endothelin induction of p8 mRNA and renal mesangial cell hypertrophy require NFAT4. The Journal of biological chemistry. vol 279. issue 20. 2004-07-21. PMID:15016802. these changes include an excess deposition of extracellular matrix proteins into the glomerular basement membrane and renal mesangial cell hypertrophy. 2004-07-21 2023-08-12 human
Brian G Petrich, Yibin Wan. Stress-activated MAP kinases in cardiac remodeling and heart failure; new insights from transgenic studies. Trends in cardiovascular medicine. vol 14. issue 2. 2004-07-13. PMID:15030789. a far more complex picture has been provided by recent observations from both cellular and transgenic models that have not only challenged their role in hypertrophy and cell death but have also pointed out novel functions of sapks in different aspects of cardiac pathology, including contractile function, extracellular matrix remodeling, intercellular communication, and metabolic regulation. 2004-07-13 2023-08-12 Not clear
Marcy Wong, Mark Siegrist, Kelly Goodwi. Cyclic tensile strain and cyclic hydrostatic pressure differentially regulate expression of hypertrophic markers in primary chondrocytes. Bone. vol 33. issue 4. 2004-07-06. PMID:14555274. the goal of this study was to test this hypothesis by examining the expression of hypertrophic chondrocyte markers (transcription factor cbfa1, mmp-13, type x collagen, vegf, ctgf) and cartilage matrix proteins under cyclic tension and cyclic hydrostatic pressure. 2004-07-06 2023-08-12 Not clear
Young-Sook Kim, Marpadga A Reddy, Linda Lanting, Sharon G Adler, Rama Nataraja. Differential behavior of mesangial cells derived from 12/15-lipoxygenase knockout mice relative to control mice. Kidney international. vol 64. issue 5. 2004-06-24. PMID:14531803. the 12/15-lipoxygenase (12/15-lo) enzyme has been implicated in the pathogenesis of diabetic nephropathy since lipoxygenase products induce cellular hypertrophy and extracellular matrix deposition in mesangial cells. 2004-06-24 2023-08-12 mouse
Nan Jia, Hiroshi Okamoto, Toshihiro Shimizu, Satoru Chiba, Yutaka Matsui, Takeshi Sugawara, Masatoshi Akino, Akira Kitabatak. A newly developed angiotensin II type 1 receptor antagonist, CS866, promotes regression of cardiac hypertrophy by reducing integrin beta1 expression. Hypertension research : official journal of the Japanese Society of Hypertension. vol 26. issue 9. 2004-06-24. PMID:14620930. previous studies have demonstrated that integrins link the extracellular matrix to the hypertrophic response pathway of cardiac myocytes in vitro. 2004-06-24 2023-08-12 rat
Céline Colnot, Chuanyong Lu, Diane Hu, Jill A Helm. Distinguishing the contributions of the perichondrium, cartilage, and vascular endothelium to skeletal development. Developmental biology. vol 269. issue 1. 2004-06-14. PMID:15081357. during the initiation of endochondral ossification three events occur that are inextricably linked in time and space: chondrocytes undergo terminal differentiation and cell death, the skeletal vascular endothelium invades the hypertrophic cartilage matrix, and osteoblasts differentiate and begin to deposit a bony matrix. 2004-06-14 2023-08-12 mouse
Céline Colnot, Chuanyong Lu, Diane Hu, Jill A Helm. Distinguishing the contributions of the perichondrium, cartilage, and vascular endothelium to skeletal development. Developmental biology. vol 269. issue 1. 2004-06-14. PMID:15081357. endothelial cells residing within the perichondrium are the first cells to participate in the invasion of the hypertrophic cartilage matrix, followed by endothelial cells derived from the host environment. 2004-06-14 2023-08-12 mouse
Philippe H Tartaix, Marie Doulaverakis, Anne George, Larry W Fisher, William T Butler, Chunlin Qin, Erdjan Salih, Melin Tan, Yukiji Fujimoto, Lyudmila Spevak, Adele L Boske. In vitro effects of dentin matrix protein-1 on hydroxyapatite formation provide insights into in vivo functions. The Journal of biological chemistry. vol 279. issue 18. 2004-06-10. PMID:14769788. dentin matrix protein-1 (dmp1) is a mineralized tissue matrix protein synthesized by osteoblasts, hypertrophic chondrocytes, and ameloblasts as well as odontoblasts. 2004-06-10 2023-08-12 mouse