Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
C Tselepis, J A Hoyland, R E Barber, B H Thorp, A P Kwa. Expression and distribution of cartilage matrix macromolecules in avian tibial dyschondroplasia. Avian pathology : journal of the W.V.P.A. vol 25. issue 2. 2009-03-10. PMID:18645860. |
type x collagen in the normal hypertrophic cartilage showed strong pericellular and matrix distribution, whereas in td cartilage labelling for aggrecan, biglycan and collagen x was located intracellularly with a very low level of signal in the matrix. |
2009-03-10 |
2023-08-12 |
Not clear |
Abdi Ghaffari, Ruhangiz T Kilani, Aziz Ghahar. Keratinocyte-conditioned media regulate collagen expression in dermal fibroblasts. The Journal of investigative dermatology. vol 129. issue 2. 2009-02-27. PMID:18787532. |
excessive extracellular matrix (ecm) production during dermal wound healing often leads to fibrotic conditions such as keloids and hypertrophic scarring (hsc). |
2009-02-27 |
2023-08-12 |
human |
Muneyoshi Okada, Ryuta Kikuzuki, Toshiyuki Harada, Yasutomo Hori, Hideyuki Yamawaki, Yukio Har. Captopril attenuates matrix metalloproteinase-2 and -9 in monocrotaline-induced right ventricular hypertrophy in rats. Journal of pharmacological sciences. vol 108. issue 4. 2009-02-19. PMID:19057128. |
captopril attenuates matrix metalloproteinase-2 and -9 in monocrotaline-induced right ventricular hypertrophy in rats. |
2009-02-19 |
2023-08-12 |
rat |
Fuad N Ziyadeh, Gunter Wol. Pathogenesis of the podocytopathy and proteinuria in diabetic glomerulopathy. Current diabetes reviews. vol 4. issue 1. 2009-02-13. PMID:18220694. |
transforming growth factor-beta 1 (tgf-beta1) has emerged as an important downstream mediator for the development of renal hypertrophy and the accumulation of mesangial extracellular matrix components, but there is limited evidence to support its role in the development of albuminuria. |
2009-02-13 |
2023-08-12 |
Not clear |
Cyril Thouverey, Agnieszka Strzelecka-Kiliszek, Marcin Balcerzak, René Buchet, Slawomir Pikul. Matrix vesicles originate from apical membrane microvilli of mineralizing osteoblast-like Saos-2 cells. Journal of cellular biochemistry. vol 106. issue 1. 2009-02-13. PMID:19009559. |
in bone, mineralization is tightly regulated by osteoblasts and hypertrophic chondrocytes which release matrix vesicles (mvs) and control extracellular ionic conditions and matrix composition. |
2009-02-13 |
2023-08-12 |
Not clear |
Rudy F Duisters, Anke J Tijsen, Blanche Schroen, Joost J Leenders, Viola Lentink, Ingeborg van der Made, Veronica Herias, Rick E van Leeuwen, Mark W Schellings, Paul Barenbrug, Jos G Maessen, Stephane Heymans, Yigal M Pinto, Esther E Creemer. miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remodeling. Circulation research. vol 104. issue 2. 2009-02-12. PMID:19096030. |
the myocardium of the failing heart undergoes a number of structural alterations, most notably hypertrophy of cardiac myocytes and an increase in extracellular matrix proteins, often seen as primary fibrosis. |
2009-02-12 |
2023-08-12 |
human |
B D Boyan, Z Schwart. 1,25-Dihydroxy vitamin D3 is an autocrine regulator of extracellular matrix turnover and growth factor release via ERp60-activated matrix vesicle matrix metalloproteinases. Cells, tissues, organs. vol 189. issue 1-4. 2009-02-10. PMID:18765931. |
as growth plate chondrocytes mature and hypertrophy, they reorganize their proteoglycan-rich type ii collagen extracellular matrix (ecm), involving 1,25(oh)(2)d(3)-dependent regulation of matrix metalloproteinases (mmps). |
2009-02-10 |
2023-08-12 |
Not clear |
Angela Lorts, Jennifer A Schwanekamp, John W Elrod, Michelle A Sargent, Jeffery D Molkenti. Genetic manipulation of periostin expression in the heart does not affect myocyte content, cell cycle activity, or cardiac repair. Circulation research. vol 104. issue 1. 2009-02-10. PMID:19038863. |
following a pathological insult, the adult mammalian heart undergoes hypertrophic growth and remodeling of the extracellular matrix. |
2009-02-10 |
2023-08-12 |
mouse |
Keiji Isshiki, Zhiheng He, Yasuhiro Maeno, Ronald C Ma, Yutaka Yasuda, Tatsuya Kuroki, Gregory S White, Mary E Patti, Gordon C Weir, George L Kin. Insulin regulates SOCS2 expression and the mitogenic effect of IGF-1 in mesangial cells. Kidney international. vol 74. issue 11. 2009-01-19. PMID:19008912. |
renal hypertrophy and deposition of extracellular matrix proteins are consistent findings in diabetic nephropathy and these processes can be halted or reversed by euglycemic control. |
2009-01-19 |
2023-08-12 |
rat |
Fuad N Ziyade. Different roles for TGF-beta and VEGF in the pathogenesis of the cardinal features of diabetic nephropathy. Diabetes research and clinical practice. vol 82 Suppl 1. 2009-01-15. PMID:18842317. |
the fibrogenic cytokine transforming growth factor-beta (tgf-beta), through its smad3 signaling pathway, is the etiologic agent of renal hypertrophy and the accumulation of mesangial extracellular matrix components in diabetes. |
2009-01-15 |
2023-08-12 |
mouse |
Kimiko Ishiguro, Kaori Hayashi, Hiroyuki Sasamura, Yusuke Sakamaki, Hiroshi Ito. "Pulse" treatment with high-dose angiotensin blocker reverses renal arteriolar hypertrophy and regresses hypertension. Hypertension (Dallas, Tex. : 1979). vol 53. issue 1. 2009-01-08. PMID:19047581. |
our aim was to examine whether high-dose "pulse" treatment with a renin-angiotensin system inhibitor could cause regression of established hypertension and to link this action to reversal of arteriolar hypertrophy and changes in vascular matrix metalloproteinase activities. |
2009-01-08 |
2023-08-12 |
rat |
Kimiko Ishiguro, Kaori Hayashi, Hiroyuki Sasamura, Yusuke Sakamaki, Hiroshi Ito. "Pulse" treatment with high-dose angiotensin blocker reverses renal arteriolar hypertrophy and regresses hypertension. Hypertension (Dallas, Tex. : 1979). vol 53. issue 1. 2009-01-08. PMID:19047581. |
the 2-week angiotensin receptor blocker treatment induced a marked reversal of the arteriolar hypertrophy specifically in the small (30 to 100 microm) renal arterioles, together with increased expression and activity of matrix metalloproteinase-13. |
2009-01-08 |
2023-08-12 |
rat |
Kimiko Ishiguro, Kaori Hayashi, Hiroyuki Sasamura, Yusuke Sakamaki, Hiroshi Ito. "Pulse" treatment with high-dose angiotensin blocker reverses renal arteriolar hypertrophy and regresses hypertension. Hypertension (Dallas, Tex. : 1979). vol 53. issue 1. 2009-01-08. PMID:19047581. |
in conclusion, transient high-dose pulse treatment with angiotensin receptor blocker caused changes in vascular matrix metalloproteinase activity, specific reversal of renal arteriolar hypertrophy, and regression of hypertension in spontaneously hypertensive rats. |
2009-01-08 |
2023-08-12 |
rat |
Xiaoping Luo, Nasser Chegin. The expression and potential regulatory function of microRNAs in the pathogenesis of leiomyoma. Seminars in reproductive medicine. vol 26. issue 6. 2009-01-07. PMID:18951332. |
it is clear that ovarian steroids are essential for leiomyoma growth, and local expression of many autocrine/paracrine mediators serving as key regulators of cell-cycle progression, cellular hypertrophy, extracellular matrix accumulation, and apoptosis appear to play central roles in this capacity. |
2009-01-07 |
2023-08-12 |
Not clear |
B S Kasinath, M M Mariappan, K Sataranatarajan, M J Lee, G Ghosh Choudhury, D Felier. Novel mechanisms of protein synthesis in diabetic nephropathy--role of mRNA translation. Reviews in endocrine & metabolic disorders. vol 9. issue 4. 2009-01-05. PMID:18654857. |
recent work has revealed an important role for translation in hypertrophy, matrix protein synthesis, elaboration of growth factors in in vivo and in vitro models of diabetic nephropathy. |
2009-01-05 |
2023-08-12 |
Not clear |
Jane Chiu, Hana Farhangkhoee, Bing Ying Xu, Shali Chen, Biju George, Subrata Chakrabart. PARP mediates structural alterations in diabetic cardiomyopathy. Journal of molecular and cellular cardiology. vol 45. issue 3. 2008-12-31. PMID:18657544. |
our results indicate that hyperhexosemia caused upregulation of extracellular matrix proteins in association with increased transcriptional co-activator p300 levels, cardiomyocyte hypertrophy and increased oxidative stress. |
2008-12-31 |
2023-08-12 |
mouse |
Meenalakshmi M Mariappan, Megan Shetty, Kavithalakshmi Sataranatarajan, Goutam Ghosh Choudhury, Balakuntalam S Kasinat. Glycogen synthase kinase 3beta is a novel regulator of high glucose- and high insulin-induced extracellular matrix protein synthesis in renal proximal tubular epithelial cells. The Journal of biological chemistry. vol 283. issue 45. 2008-12-23. PMID:18701453. |
gsk3beta and eif2bepsilon play a role in augmented protein synthesis associated with high glucose- and high insulin-stimulated hypertrophy and matrix accumulation in renal disease in type 2 diabetes. |
2008-12-23 |
2023-08-12 |
mouse |
Sana Siddiqui, James G Marti. Structural aspects of airway remodeling in asthma. Current allergy and asthma reports. vol 8. issue 6. 2008-12-23. PMID:18940147. |
the histologic changes to the airways consist of epithelial proliferation and goblet cell differentiation, subepithelial fibrosis, airway smooth muscle (asm) growth, angiogenesis, matrix protein deposition, gland hyperplasia and hypertrophy, and nerve proliferation. |
2008-12-23 |
2023-08-12 |
Not clear |
Kristen A Johnson, David M Rose, Robert A Terkeltau. Factor XIIIA mobilizes transglutaminase 2 to induce chondrocyte hypertrophic differentiation. Journal of cell science. vol 121. issue Pt 13. 2008-12-22. PMID:18544639. |
externalization of guanine-nucleotide-bound tg2 drives chondrocyte maturation to hypertrophy, a state linked to matrix remodeling and calcification. |
2008-12-22 |
2023-08-12 |
human |
Y Zhang, L Kong, C S Carlson, C-J Li. Cbfa1-dependent expression of an interferon-inducible p204 protein is required for chondrocyte differentiation. Cell death and differentiation. vol 15. issue 11. 2008-12-12. PMID:18636074. |
overexpression of p204 accelerates chondrocyte hypertrophy, as revealed by enhanced expression of type x collagen and matrix metalloproteinase-13; however, knockdown of p204 via an sirna approach abolishes hypertrophic chondrocyte differentiation. |
2008-12-12 |
2023-08-12 |
Not clear |