-
1
-
-
0030419494
-
Molecular insights into renal interstitial fibrosis
-
Eddy AA. Molecular insights into renal interstitial fibrosis. J Am Soc Nephrol 1996; 7:2495-2508.
-
(1996)
J Am Soc Nephrol
, vol.7
, pp. 2495-2508
-
-
Eddy, A.A.1
-
2
-
-
0028137068
-
Myofibroblasts, predictors of progression of mesangial IgA nephropathy?
-
Goumenos DS, Brown CB, Shortland J, El Nahas AM. Myofibroblasts, predictors of progression of mesangial IgA nephropathy? Nephrol Dial Transplant 1992; 9:1418-1425.
-
(1992)
Nephrol Dial Transplant
, vol.9
, pp. 1418-1425
-
-
Goumenos, D.S.1
Brown, C.B.2
Shortland, J.3
El Nahas, A.M.4
-
3
-
-
0031050172
-
Interstitial myofibroblasts: Predictors of progression in membranous nephropathy
-
Roberts IS, Burrows C, Shanks JH, et al. Interstitial myofibroblasts: predictors of progression in membranous nephropathy. J Clin Pathol 1997; 50:123-127.
-
(1997)
J Clin Pathol
, vol.50
, pp. 123-127
-
-
Roberts, I.S.1
Burrows, C.2
Shanks, J.H.3
-
4
-
-
0029074870
-
Interstitial myofibroblasts in experimental renal infection and scarring
-
Hewitson TD, Wu HL, Becker GJ, Interstitial myofibroblasts in experimental renal infection and scarring. Am J Nephrol 1995; 15:411-417.
-
(1995)
Am J Nephrol
, vol.15
, pp. 411-417
-
-
Hewitson, T.D.1
Wu, H.L.2
Becker, G.J.3
-
5
-
-
0029958887
-
Myofibroblasts differentiate from fibroblasts when plated at low density
-
Masur SK, Dewal HS, Dinh TT, et al. Myofibroblasts differentiate from fibroblasts when plated at low density. Proc Natl Acad Sci USA 1996; 93:4219-4223.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 4219-4223
-
-
Masur, S.K.1
Dewal, H.S.2
Dinh, T.T.3
-
6
-
-
7344251771
-
Local macrophage and myofibroblast proliferation in 5/6 nephretomised rat model
-
Yang N, Wu LL, Nickolic-Paterson DJ, et al. Local macrophage and myofibroblast proliferation in 5/6 nephretomised rat model. Nephrol Dial Transplant 1998; 13:1967-1974.
-
(1998)
Nephrol Dial Transplant
, vol.13
, pp. 1967-1974
-
-
Yang, N.1
Wu, L.L.2
Nickolic-Paterson, D.J.3
-
7
-
-
0029157019
-
Transformations between epithelium and mesenchyme: Normal, pathological, and experimentally induced
-
Hay ED, Zuk A. Transformations between epithelium and mesenchyme: normal, pathological, and experimentally induced. Am J Kidney Dis 1995; 26:678-690.
-
(1995)
Am J Kidney Dis
, vol.26
, pp. 678-690
-
-
Hay, E.D.1
Zuk, A.2
-
8
-
-
0029091682
-
Identification and characterization of a fibroblast marker: FSP1
-
Strutz F, Okada H, Lo CW, et al. Identification and characterization of a fibroblast marker: FSP1. J Cell Biol 1995; 130:393-405.
-
(1995)
J Cell Biol
, vol.130
, pp. 393-405
-
-
Strutz, F.1
Okada, H.2
Lo, C.W.3
-
9
-
-
0031682715
-
Tubular epithelial-myofibroblast transdifferentiation in progressive tubulointerstitial fibrosis in 5/6 nephrectomized rats
-
Ng YY, Huang TP, Yang WC, et al. Tubular epithelial-myofibroblast transdifferentiation in progressive tubulointerstitial fibrosis in 5/6 nephrectomized rats. Kidney Int 1998; 54:864-876
-
(1998)
Kidney Int
, vol.54
, pp. 864-876
-
-
Ng, Y.Y.1
Huang, T.P.2
Yang, W.C.3
-
10
-
-
0021355642
-
Expression of vimentin and cytokeratin types of intermediate filament proteins in developing and adult human kidneys
-
Holthofer H, Miettinen A, Lehto VP, et al. Expression of vimentin and cytokeratin types of intermediate filament proteins in developing and adult human kidneys. Lab Invest 1984; 50:552-559.
-
(1984)
Lab Invest
, vol.50
, pp. 552-559
-
-
Holthofer, H.1
Miettinen, A.2
Lehto, V.P.3
-
11
-
-
0026717771
-
Mechanism of the nephrogenic repair response: Studies on proliferation and vimentin expression after 35S-1,2-dichlorovinyl-L-cysteine nephrotoxicity in vivo and in cultured proximal tubule epithelial cells
-
Wallin A, Zhang G, Jones TW, et al. Mechanism of the nephrogenic repair response: studies on proliferation and vimentin expression after 35S-1,2-dichlorovinyl-L-cysteine nephrotoxicity in vivo and in cultured proximal tubule epithelial cells. Lab invest 1992; 66:474-484.
-
(1992)
Lab Invest
, vol.66
, pp. 474-484
-
-
Wallin, A.1
Zhang, G.2
Jones, T.W.3
-
12
-
-
0028273536
-
Localization of proliferating cell nuclear antigen, vimentin, c-Fos, and clusterin in the postischemic kidney: Evidence for a heterogenous genetic response among nephron segments, and a large pool of mitotically active and dedifferentiated cells
-
Witzgall R, Brown D, Schwarz C, Bonventre JV. Localization of proliferating cell nuclear antigen, vimentin, c-Fos, and clusterin in the postischemic kidney: evidence for a heterogenous genetic response among nephron segments, and a large pool of mitotically active and dedifferentiated cells. J Clin Invest 1994; 93:2175-2188.
-
(1994)
J Clin Invest
, vol.93
, pp. 2175-2188
-
-
Witzgall, R.1
Brown, D.2
Schwarz, C.3
Bonventre, J.V.4
-
13
-
-
0034219152
-
Connective tissue growth factor expression in the rat remnant kidney model and association with tubular epithelial cells undergoing transdifferentiation
-
Frazier KS, Paredes A, Dube P, Styer E. Connective tissue growth factor expression in the rat remnant kidney model and association with tubular epithelial cells undergoing transdifferentiation. Vet Pathol 2000; 37:328-335.
-
(2000)
Vet Pathol
, vol.37
, pp. 328-335
-
-
Frazier, K.S.1
Paredes, A.2
Dube, P.3
Styer, E.4
-
14
-
-
0032738399
-
Glomerular epithelial-myofibroblast transdifferentiation in the evolution of glomerular crescent formation
-
Ng YY, Fan J-M, Mu W, et al. Glomerular epithelial-myofibroblast transdifferentiation in the evolution of glomerular crescent formation. Nephrol Dial Transplant 1999; 14:2860-2872.
-
(1999)
Nephrol Dial Transplant
, vol.14
, pp. 2860-2872
-
-
Ng, Y.Y.1
Fan, J.-M.2
Mu, W.3
-
15
-
-
0034811585
-
Tubular phenotypic change in progressive tubulointerstitial fibrosis in human glomerulonephritis
-
Jinde K, Nikolic-Paterson DJ, Huang XR, et al. Tubular phenotypic change in progressive tubulointerstitial fibrosis in human glomerulonephritis. Am J Kidney Dis 2001; 38:761-769. This exciting study provides the first evidence for TEMT in progressive tubulointerstitial fibrosis in human glomerulonephritis and demonstrates that the transformed TECs with co-expression of cytokeratin and α-SMA are co-localized with upregulation of TGF-β and FGF-2 and collagen matrix production.
-
(2001)
Am J Kidney Dis
, vol.38
, pp. 761-769
-
-
Jinde, K.1
Nikolic-Paterson, D.J.2
Huang, X.R.3
-
16
-
-
0034785496
-
Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis
-
Yang J, Liu Y. Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis. Am J Pathol 2001; 159:1465-1475. This study dissects the process of TEMT involved in four key steps, including loss of epithelial phenotype, expression of α-SMA, destruction of TBM, and enhanced migration and invasion.
-
(2001)
Am J Pathol
, vol.159
, pp. 1465-1475
-
-
Yang, J.1
Liu, Y.2
-
17
-
-
0032842887
-
Transforming growth factor-beta regulates tubular epithelial-myofibroblast transdifferentiation in vitro
-
Fan JM, Ng YY, Hill PA, et al. Transforming growth factor-beta regulates tubular epithelial-myofibroblast transdifferentiation in vitro. Kidney Int 1999; 56:1455-1467.
-
(1999)
Kidney Int
, vol.56
, pp. 1455-1467
-
-
Fan, J.M.1
Ng, Y.Y.2
Hill, P.A.3
-
18
-
-
0035061819
-
Interleukin-1 induces tubular epithelial-myofibroblast transdifferentiation through a transforming growth factor-beta 1-dependent mechanism in vitro
-
Fan JM, Huang XR, Ng YY, et al. Interleukin-1 induces tubular epithelial-myofibroblast transdifferentiation through a transforming growth factor-beta 1-dependent mechanism in vitro. Am J Kidney Dis 2001; 37:820-831. This study identifies that interleukin-1 can induce TEMP via the TGF-β-dependent mechanism cells and describes the process of TEMP involving a loss of E-cadherin and de-novo expression of α-SMA in NRK52E.
-
(2001)
Am J Kidney Dis
, vol.37
, pp. 820-831
-
-
Fan, J.M.1
Huang, X.R.2
Ng, Y.Y.3
-
19
-
-
0036138824
-
Blockage of tubular epithelial to myofibroblast transition by hepatocyte growth factor prevents renal interstitial fibrosis
-
Yang J, Lui Y. Blockage of tubular epithelial to myofibroblast transition by hepatocyte growth factor prevents renal interstitial fibrosis. J Am Soc Nephrol 2002; 13:96-107. This study demonstrates that TGF-β-induced TEMT is inhibited by the addition of HGF both in vitro and in vivo, indicating that HGF is capable of counter-regulating TGF-β-induced TEMT.
-
(2002)
J Am Soc Nephrol
, vol.13
, pp. 96-107
-
-
Yang, J.1
Lui, Y.2
-
20
-
-
0034116268
-
Selective degradation of E-cadherin and dissolution of E-cadherin-catenin complexes in epithelial ischemia
-
Bush KT, Tsukamoto T, Nigam SK. Selective degradation of E-cadherin and dissolution of E-cadherin-catenin complexes in epithelial ischemia. Am J Physiol 2000; 278:F847-F852.
-
(2000)
Am J Physiol
, vol.278
-
-
Bush, K.T.1
Tsukamoto, T.2
Nigam, S.K.3
-
21
-
-
0028821380
-
A targeted mutation in the mouse E-cadherin gene results in defective preimplantation development
-
Riethmacher D, Brinkmann V, Birchmeier C. A targeted mutation in the mouse E-cadherin gene results in defective preimplantation development. Proc Natl Acad Sci USA 1995; 92:855-859.
-
(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 855-859
-
-
Riethmacher, D.1
Brinkmann, V.2
Birchmeier, C.3
-
22
-
-
0033784843
-
The transcription factor Snail controls epithelial-mesenchymal transitions by repressing E-cadherin expression
-
Cano A, Perez-Moreno MA, Rodrigo I, et al. The transcription factor Snail controls epithelial-mesenchymal transitions by repressing E-cadherin expression. Nat Cell Biol 2000; 2:76-83.
-
(2000)
Nat Cell Biol
, vol.2
, pp. 76-83
-
-
Cano, A.1
Perez-Moreno, M.A.2
Rodrigo, I.3
-
23
-
-
0034799176
-
Renal fibrosis: Collagen composition and assembly regulates epithelial-mesenchymal transdifferentiation
-
Zeisberg M, Bonner G, Maeshima Y, et al. Renal fibrosis: collagen composition and assembly regulates epithelial-mesenchymal transdifferentiation. Am J Pathol 2001; 159:1313-1321. This study describes the importance of TBM in the maintenance of epithelial phenotype and the critical role of TBM compositions in TGF-β and EMT in vitro.
-
(2001)
Am J Pathol
, vol.159
, pp. 1313-1321
-
-
Zeisberg, M.1
Bonner, G.2
Maeshima, Y.3
-
24
-
-
0036233040
-
Role of basic fibroblast growth factor-2 in epithelial-mesenchymal transformation
-
Strutz F, Zeisberg M, Ziyadeh FN, et al. Role of basic fibroblast growth factor-2 in epithelial-mesenchymal transformation. Kidney Int 2002; 61:1714-1728. This study demonstrates that FGF-2, like TGF-β, induces fibroblast-specific protein-1 and vimentin expression, but inhibits cytokeratin expression. The induction of matrix metalloproteinase-2 and 9 expression by FGF-2 indicates that FGF-2 makes an important contribution to EMT in vitro.
-
(2002)
Kidney Int
, vol.61
, pp. 1714-1728
-
-
Strutz, F.1
Zeisberg, M.2
Ziyadeh, F.N.3
-
26
-
-
0035661067
-
Advanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE)
-
Oldfield MD, Bach LA, Forbes JM, et al. Advanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE). J Clin Invest 2001; 108:1853-1863. This exciting study provides the first evidence that AGEs are able to induce TEMT via the receptor for advanced glycation end products-mediated, TGF-β-dependent mechanism in vitro, indicating that TEMT may play a pathogenic role in diabetic nephropathy.
-
(2001)
J Clin Invest
, vol.108
, pp. 1853-1863
-
-
Oldfield, M.D.1
Bach, L.A.2
Forbes, J.M.3
-
27
-
-
0012386003
-
SMAD signaling, a novel pathway of angiotensin II-induced renal fibrosis
-
Huang XR, Li JH, Chen YX, et al. SMAD signaling, a novel pathway of angiotensin II-induced renal fibrosis. J Am Soc Nephrol 2001; 12:465.
-
(2001)
J Am Soc Nephrol
, vol.12
, pp. 465
-
-
Huang, X.R.1
Li, J.H.2
Chen, Y.X.3
-
28
-
-
0036014928
-
Smad7 inhibits fibrotic effect of tgf-Beta on renal tubular epithelial cells by blocking smad2 activation
-
Li JH, Zhu HJ, Huang XR, et al. Smad7 inhibits fibrotic effect of tgf-Beta on renal tubular epithelial cells by blocking smad2 activation. J Am Soc Nephrol 2002; 13:1464-1472. This important study delineates the intracellular signaling pathway whereby TGF-β induces TEMT in vitro. TGF-β signals through Smad2 to mediate TEMT and collagen matrix production, which is blocked by overexpression of the inhibitory Smad7, indicating that Smad signaling plays a key role in TEMT.
-
(2002)
J Am Soc Nephrol
, vol.13
, pp. 1464-1472
-
-
Li, J.H.1
Zhu, H.J.2
Huang, X.R.3
-
29
-
-
0031911356
-
Smads: Mediators and regulators of TGF-β signaling
-
Kretzschmar M, Massague J. Smads: mediators and regulators of TGF-β signaling. Curr Opin Genet Dev 1998; 8:103-111.
-
(1998)
Curr Opin Genet Dev
, vol.8
, pp. 103-111
-
-
Kretzschmar, M.1
Massague, J.2
-
30
-
-
0034673972
-
Transforming growth factor B signaling mediators and regulators
-
Zimmerman CM, Padgett RW. Transforming growth factor B signaling mediators and regulators. Gene 2000; 249:17-30.
-
(2000)
Gene
, vol.249
, pp. 17-30
-
-
Zimmerman, C.M.1
Padgett, R.W.2
-
31
-
-
0030611757
-
Identification of Smad7, a TGF beta-inducible antagonist of TGF-beta signaling
-
Nakao A, Afrakhte M, Moren A, et al. Identification of Smad7, a TGF beta-inducible antagonist of TGF-beta signaling. Nature 1997; 389:631-635.
-
(1997)
Nature
, vol.389
, pp. 631-635
-
-
Nakao, A.1
Afrakhte, M.2
Moren, A.3
-
32
-
-
0032582672
-
Transforming growth factor-β1 induces nuclear export of inhibitory Smad7
-
Itoh S, Landström M, Hermansson A, et al. Transforming growth factor-β1 induces nuclear export of inhibitory Smad7. J Biol Chem 1998; 44:29195-29201.
-
(1998)
J Biol Chem
, vol.44
, pp. 29195-29201
-
-
Itoh, S.1
Landström, M.2
Hermansson, A.3
-
33
-
-
0034517389
-
Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation
-
Kavsak P, Rasmussen RK, Causing CG, et al. Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation. Mol Cell 2000; 6:1365-1375.
-
(2000)
Mol Cell
, vol.6
, pp. 1365-1375
-
-
Kavsak, P.1
Rasmussen, R.K.2
Causing, C.G.3
|