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RISS 인기검색어
- 검색키워드
- 저자 : Margetts, Peter J. (검색결과 4 건)
- 무료
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Margetts, Peter J.,Bonniaud, Philippe,Liu, Limin,Hoff, Catherine M.,Holmes, Clifford J.,West-Mays, Judith A.,Kelly, Margaret M. American Society of Nephrology 2005 Journal of the American Society of Nephrology Vol.16 No.2
<P>Epithelial mesenchymal transition (EMT), a process involved in many growth and repair functions, has been identified in the peritoneal tissues of patients who undergo peritoneal dialysis. The sequence of changes in gene regulation and cellular events associated with EMT after TGF-beta1-induced peritoneal fibrosis is reported. Sprague-Dawley rats received an intraperitoneal injection of an adenovirus vector that transfers active TGF-beta1 (AdTGF-beta1) or control adenovirus, AdDL. Animals were killed 0 to 21 days after infection. Peritoneal effluent and tissue were analyzed for markers of EMT. In the animals that were treated with AdTGF-beta1, an increase in expression of genes associated with EMT and fibrosis, such as type I collagen A2, alpha-smooth muscle actin, and the zinc finger regulatory protein Snail, was identified. Transition of mesothelial cells 4 to 7 d after infection, with appearance of epithelial cells in the submesothelial zone 7 to 14 d after exposure to AdTGF-beta1, was demonstrated. This phase was associated with disruption of the basement membrane and increased expression of matrix metalloproteinase 2. By 14 to 21 d after infection, there was evidence of restoration of normal submesothelial architecture. These findings suggest that EMT occurs in vivo after TGF-beta1 overexpression in the peritoneum. Cellular changes and gene regulation associated with EMT are evident throughout the fibrogenic process and are not limited to early time points. This further supports the central role of TGF-beta1 in peritoneal fibrosis and provides an important model to study the sequence of events involved in TGF-beta1-induced EMT.</P>
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Transforming growth factor-beta and the glomerular ?ltration barrier
( Ayesha Ghayur ),( Peter J Margetts ) 대한신장학회 2013 Kidney Research and Clinical Practice Vol.32 No.1
The increasing burden of chronic kidney disease worldwide and recent advancements in the understanding of pathologic events leading to kidney injury have opened up new potential avenues for therapies to further diminish progression of kidney disease by targeting the glomerular ?ltration barrier and reducing proteinuria. The glomerular ?ltration barrier is affected by many different metabolic and immune-mediated injuries. Glomerular endothelial cells, the glomerular basement membrane, and podocytes-the three components of the ?ltration barrier-work together to prevent the loss of protein and at the same time allow passage of water and smaller molecules. Damage to any of the components of the ?ltration barrier can initiate proteinuria and renal ?brosis. Transforming growth factor-beta (TGF-b) is a pleiotropic cytokine strongly associated with the ?brogenic response. It has a known role in tubulointerstitial ?brosis. In this review we will highlight what is known about TGF-b and how it interacts with the components of glomerular ?ltration barrier and causes loss of function and proteinuria.
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Experimental systems to study the origin of the myofibroblast in peritoneal fibrosis
( Manreet Padwal ),( Peter J. Margetts ) 대한신장학회 2016 Kidney Research and Clinical Practice Vol.35 No.3
Peritoneal fibrosis is one of the major complications occurring in long-term peritoneal dialysis patients as a result of injury. Peritoneal fibrosis is characterized by submesothelial thickening and fibrosis which is associated with a decline in peritoneal membrane function. The myofibroblast has been identified as the key player involved in the development and progression of peritoneal fibrosis. Activation of the myofibroblast is correlated with expansion of the extracellular matrix and changes in peritoneal membrane integrity. Over the years, epithelial to mesenchymal transition (EMT) has been accepted as the predominant source of the myofibroblast. Peritoneal mesothelial cells have been described to undergo EMT in response to injury. Several animal and in vitro studies support the role of EMT in peritoneal fibrosis; however, emerging evidence from genetic fate-mapping studies has demonstrated that myofibroblasts may be arising from resident fibroblasts and pericytes/perivascular fibroblasts. In this review, we will discuss hypotheses currently surrounding the origin of the myofibroblast and highlight the experimental systems predominantly being used to investigate this.
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