| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Akiho Tsuchiya, Masato Yano, Jiraporn Tocharus, Hisae Kojima, Manabu Fukumoto, Masashi Kawaichi, Chio Ok. Expression of mouse HtrA1 serine protease in normal bone and cartilage and its upregulation in joint cartilage damaged by experimental arthritis. Bone. vol 37. issue 3. 2006-02-03. PMID:15993670. |
htra1 may, therefore, promote degeneration of cartilage by inducing terminal hypertrophic chondrocyte differentiation and by digesting cartilage matrix though its tgf-beta inhibitory activity and protease activity, respectively. |
2006-02-03 |
2023-08-12 |
mouse |
| Yves Gorin, Karen Block, James Hernandez, Basant Bhandari, Brent Wagner, Jeffrey L Barnes, Hanna E Abbou. Nox4 NAD(P)H oxidase mediates hypertrophy and fibronectin expression in the diabetic kidney. The Journal of biological chemistry. vol 280. issue 47. 2006-02-03. PMID:16135519. |
renal hypertrophy and extracellular matrix accumulation are early features of diabetic nephropathy. |
2006-02-03 |
2023-08-12 |
rat |
| Pamela S Howard, Umberto Kucich, Douglas E Coplen, Yuling H. Transforming growth factor-beta1-induced hypertrophy and matrix expression in human bladder smooth muscle cells. Urology. vol 66. issue 6. 2006-01-26. PMID:16360482. |
transforming growth factor-beta1-induced hypertrophy and matrix expression in human bladder smooth muscle cells. |
2006-01-26 |
2023-08-12 |
human |
| C Carda, G Silvestrini, M E Gomez de Ferraris, A Peydró, E Bonucc. Osteoprotegerin (OPG) and RANKL expression and distribution in developing human craniomandibular joint. Tissue & cell. vol 37. issue 3. 2006-01-20. PMID:15899507. |
the main results were: opg and rankl mrna and protein were co-localized in the same cell types; opg and rankl were specially immunolocated in osteogenic cells; immunolabeling was often seen in the nucleus and cytoplasm of otherwise negative hypertrophic chondrocytes; ihc and ish labeling decreased from proliferative to hypertrophic chondrocytes; early osteocytes showed dual protein expression and some of the mature osteocytes were ish-negative; periosteal osteoclasts and chondroclasts were mostly stained by ihc and variably labeled by ish; the new bone matrix and trabecular borders showed intense immunolabeling. |
2006-01-20 |
2023-08-12 |
human |
| Akiko Kirimoto, Yuzo Takagi, Keiichi Ohya, Hitoyata Shimokaw. Effects of retinoic acid on the differentiation of chondrogenic progenitor cells, ATDC5. Journal of medical and dental sciences. vol 52. issue 3. 2006-01-12. PMID:16350840. |
in this study, we show that ra suppresses the cell growth, cartilage nodule formation, accumulation of proteoglycan, alkaline phosphatase (alpase) activity and mineralization and that ra dose dependently upregulates the levels of type x collagen and matrix metalloproteinase-13 (mmp-13) mrna which are marker proteins of hypertrophic chondrocytes, in atdc5 cells. |
2006-01-12 |
2023-08-12 |
Not clear |
| Ola Nilsson, Rose Marino, Francesco De Luca, Moshe Phillip, Jeffrey Baro. Endocrine regulation of the growth plate. Hormone research. vol 64. issue 4. 2005-12-30. PMID:16205094. |
within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis. |
2005-12-30 |
2023-08-12 |
human |
| 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 |