All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
Liju Yang, Paul G Scott, Carole Dodd, Abelardo Medina, Haiyan Jiao, Heather A Shankowsky, Aziz Ghahary, Edward E Tredge. Identification of fibrocytes in postburn hypertrophic scar. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 13. issue 4. 2005-12-23. PMID:16008729. we conclude that fibrocytes, which have been reported to be antigen-presenting cells, are recruited to wounds following extensive burn injury and could potentially upregulate the inflammatory response and synthesize collagen and other matrix macromolecules, thus contributing to the development of hypertrophic scarring. 2005-12-23 2023-08-12 Not clear
Kazi Sazzad Hossain, Norio Amizuka, Nobuyki Ikeda, Kayoko Nozawa-Inoue, Akiko Suzuki, Minqi Li, Kiichi Takeuchi, Megumi Aita, Yoshiro Kawano, Masaaki Hoshino, Kimimitsu Oda, Ritsuo Takagi, Takeyasu Maed. Histochemical evidences on the chronological alterations of the hypertrophic zone of mandibular condylar cartilage. Microscopy research and technique. vol 67. issue 6. 2005-12-12. PMID:16173089. the hypertrophic chondrocytes lack the ability to proliferate, thus permitting matrix mineralization as well as vascular invasion from the bone in both the mandibular condyle and the epiphyseal cartilage. 2005-12-12 2023-08-12 mouse
Edna D Lekgabe, Helen Kiriazis, Chongxin Zhao, Qi Xu, Xiao Lei Moore, Yidan Su, Ross A D Bathgate, Xiao-Jun Du, Chrishan S Samue. Relaxin reverses cardiac and renal fibrosis in spontaneously hypertensive rats. Hypertension (Dallas, Tex. : 1979). vol 46. issue 2. 2005-11-29. PMID:15967869. zymography was used to determine matrix metalloproteinase (mmp) expression and western blotting to determine proliferating cell nuclear antigen (pcna) expression and alpha-smooth muscle actin (alpha-sma)/myofibroblast expression, whereas cardiac hypertrophy was assessed by myocyte size and real-time polymerase chain reaction of associated genes. 2005-11-29 2023-08-12 rat
Nathalie Ortega, Danielle J Behonick, Céline Colnot, Douglas N W Cooper, Zena Wer. Galectin-3 is a downstream regulator of matrix metalloproteinase-9 function during endochondral bone formation. Molecular biology of the cell. vol 16. issue 6. 2005-11-21. PMID:15800063. deficiency of matrix metalloproteinase-9 (mmp-9) leads to an accumulation of late hypertrophic chondrocytes. 2005-11-21 2023-08-12 mouse
Nathalie Ortega, Danielle J Behonick, Céline Colnot, Douglas N W Cooper, Zena Wer. Galectin-3 is a downstream regulator of matrix metalloproteinase-9 function during endochondral bone formation. Molecular biology of the cell. vol 16. issue 6. 2005-11-21. PMID:15800063. we found that galectin-3, an in vitro substrate of mmp-9, accumulates in the late hypertrophic chondrocytes and their surrounding extracellular matrix in the expanded hypertrophic cartilage zone. 2005-11-21 2023-08-12 mouse
Filippo Renò, Maurizio Sabbatini, Maurizio Stella, Gilberto Magliacani, Mario Canna. Effect of in vitro mechanical compression on Epilysin (matrix metalloproteinase-28) expression in hypertrophic scars. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 13. issue 3. 2005-11-08. PMID:15953044. effect of in vitro mechanical compression on epilysin (matrix metalloproteinase-28) expression in hypertrophic scars. 2005-11-08 2023-08-12 Not clear
Takayoshi Suganami, Masashi Mukoyama, Kiyoshi Mori, Hideki Yokoi, Masao Koshikawa, Kazutomo Sawai, Shuji Hidaka, Ken Ebihara, Tomohiro Tanaka, Akira Sugawara, Hiroshi Kawachi, Charles Vinson, Yoshihiro Ogawa, Kazuwa Naka. Prevention and reversal of renal injury by leptin in a new mouse model of diabetic nephropathy. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. vol 19. issue 1. 2005-11-07. PMID:15496495. here, we show that a genetic model of lipoatrophic diabetes (a-zip/f-1 mice) manifests a typical renal injury observed in human diabetic nephropathy that is associated with glomerular hypertrophy, diffuse and pronounced mesangial widening, accumulation of extracellular matrix proteins, podocyte damage, and overt proteinuria. 2005-11-07 2023-08-12 mouse
S Corda, J L Samuel, L Rappapor. Extracellular matrix and growth factors during heart growth. Heart failure reviews. vol 5. issue 2. 2005-11-07. PMID:16228139. we describe here: 1) the main components of extracellular matrix within the cardiovascular system; 2) the role of integrins in the transmission of growth signals; 3) the shift in the expression of the components of the extracellular matrix (fibronectin and collagens) and the stimulation of the synthesis of metalloproteinases during normal and hypertrophic growth of the myocardium; 4) the effects of growth factors, such as angiotensin ii, fibroblast growth factors (fgf), transforming growth factor-beta (tgf-beta), on the synthesis of proteins of the extracellular matrix in the heart. 2005-11-07 2023-08-12 Not clear
S Jane-Lise, S Corda, C Chassagne, L Rappapor. The extracellular matrix and the cytoskeleton in heart hypertrophy and failure. Heart failure reviews. vol 5. issue 3. 2005-11-07. PMID:16228907. the extracellular matrix and the cytoskeleton in heart hypertrophy and failure. 2005-11-07 2023-08-12 Not clear
S Jane-Lise, S Corda, C Chassagne, L Rappapor. The extracellular matrix and the cytoskeleton in heart hypertrophy and failure. Heart failure reviews. vol 5. issue 3. 2005-11-07. PMID:16228907. we analyze here the nature and organization of extracellular matrix (ecm) proteins, cytoskeleton and integrins and their regulation by growth factors, such as angiotensin ii, in normal myocyte growth and in pathological growth (hypertrophy) of the myocardium and heart failure. 2005-11-07 2023-08-12 Not clear
Jaana Rysä, Hanna Leskinen, Mika Ilves, Heikki Ruskoah. Distinct upregulation of extracellular matrix genes in transition from hypertrophy to hypertensive heart failure. Hypertension (Dallas, Tex. : 1979). vol 45. issue 5. 2005-10-27. PMID:15837839. distinct upregulation of extracellular matrix genes in transition from hypertrophy to hypertensive heart failure. 2005-10-27 2023-08-12 rat
Jaana Rysä, Hanna Leskinen, Mika Ilves, Heikki Ruskoah. Distinct upregulation of extracellular matrix genes in transition from hypertrophy to hypertensive heart failure. Hypertension (Dallas, Tex. : 1979). vol 45. issue 5. 2005-10-27. PMID:15837839. our data show that transition from lv hypertrophy to diastolic hypertensive heart failure is almost exclusively associated with progressive remodeling of the extracellular matrix and provide new insights into the pathogenesis of hypertrophy by suggesting existence of novel regulators of lv remodeling. 2005-10-27 2023-08-12 rat
Seikoh Horiuchi, Yuka Unno, Hitomi Usui, Kenichi Shikata, Kaori Takaki, Wakako Koito, Yu-Ichiro Sakamoto, Ryoji Nagai, Kenji Makino, Akira Sasao, Jun Wada, Hirofumi Makin. Pathological roles of advanced glycation end product receptors SR-A and CD36. Annals of the New York Academy of Sciences. vol 1043. 2005-10-27. PMID:16037291. in terms of sr-a, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas sr-a-knockout mice showed reduced glomerular size and mesangial matrix area. 2005-10-27 2023-08-12 mouse
Céline Bouvet, Liz-Ann Gilbert, Daphné Girardot, Denis deBlois, Pierre Morea. Different involvement of extracellular matrix components in small and large arteries during chronic NO synthase inhibition. Hypertension (Dallas, Tex. : 1979). vol 45. issue 3. 2005-10-25. PMID:15655118. thus, in contrast to large artery hypertrophic remodeling, in which the contributions of cellular de-adhesion and matrix breakdown is manifest, the contribution of mmps in eutrophic remodeling appears less crucial. 2005-10-25 2023-08-12 rat
Zheng Feng, Anna Rita Plati, Qing-li Cheng, Mariana Berho, Anita Banerjee, Mylene Potier, Wen-che Jy, Andrew Koff, Liliane J Striker, Gary E Strike. Glomerular aging in females is a multi-stage reversible process mediated by phenotypic changes in progenitors. The American journal of pathology. vol 167. issue 2. 2005-09-29. PMID:16049323. the altered phenotype included increased extracellular matrix synthesis and decreased matrix metalloproteinase-2 levels as well as cell hypertrophy. 2005-09-29 2023-08-12 mouse
Gerold Untergasser, Stephan Madersbacher, Peter Berge. Benign prostatic hyperplasia: age-related tissue-remodeling. Experimental gerontology. vol 40. issue 3. 2005-08-25. PMID:15763388. prostate tissue-remodeling in the transition zone is characterized by: (i) hypertrophic basal cells, (ii) altered secretions of luminal cells leading to calcification, clogged ducts and inflammation, (iii) lymphocytic infiltration with production of proinflammatory cytokines, (iv) increased radical oxygen species (ros) production that damages epithelial and stromal cells, (v) increased basic fibroblast (bfgf) and transforming growth factor beta (tgf-beta 1) production leading to stromal proliferation, transdifferentiation and extracellular matrix production, (vi) altered autonomous innervation that decreases relaxation and leads to a high adrenergic tonus, (vii) and altered neuroendocine cell function and release of neuroendocrine peptides (nep). 2005-08-25 2023-08-12 human
Tetsuro Wakatsuki, Joseph Schlessinger, Elliot L Elso. The biochemical response of the heart to hypertension and exercise. Trends in biochemical sciences. vol 29. issue 11. 2005-08-23. PMID:15501680. chronic hypertension also causes hypertrophy, but in addition it causes an excessive increase in fibroblasts and extracellular matrix (fibrosis), death of cardiomyocytes and ultimately heart failure. 2005-08-23 2023-08-12 Not clear
Elena V Tchetina, Ginette Squires, A Robin Pool. Increased type II collagen degradation and very early focal cartilage degeneration is associated with upregulation of chondrocyte differentiation related genes in early human articular cartilage lesions. The Journal of rheumatology. vol 32. issue 5. 2005-08-09. PMID:15868625. articular cartilage degeneration in osteoarthritis (oa) involves excessive degradation of extracellular matrix (ecm) and chondrocyte differentiation (hypertrophy). 2005-08-09 2023-08-12 human
Kurt D Hankenson, Sheriar G Hormuzdi, Jeffrey A Meganck, Paul Bornstei. Mice with a disruption of the thrombospondin 3 gene differ in geometric and biomechanical properties of bone and have accelerated development of the femoral head. Molecular and cellular biology. vol 25. issue 13. 2005-08-02. PMID:15964815. thus, vascular invasion and ossification start in the femoral heads of tsp3-null mice at 9 weeks, whereas the wild-type femoral head is still composed of hypertrophic chondroctyes in a calcified matrix at 15 weeks. 2005-08-02 2023-08-12 mouse
Jürgen Pauluhn, Ulrich Moh. Experimental approaches to evaluate respiratory allergy in animal models. Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie. vol 56. issue 4-5. 2005-07-26. PMID:15816351. the pathology of asthma is associated with reversible narrowing of airways, associated with prominent features that involve structural changes in the airway walls and extracellular matrix remodeling including abnormalities of bronchial smooth muscle, eosinophilic inflammation of the bronchial wall, hyperplasia and hypertrophy of mucous glands. 2005-07-26 2023-08-12 human