1) Bornstein P. Matricellular proteins: an overview. J Cell Commun Signal. 2009; 3: 163-5
|
|
|
2) Weber KT, Pick R, Jalil JE, et al. Patterns of myocardial fibrosis. J Mol Cell Cardiol. 1989; 21 Suppl 5: 121-31
|
|
|
3) Brilla CG, Weber KT. Reactive and reparative myocardial fibrosis in arterial hypertension in the rat. Cardiovasc Res. 1992; 26: 671-7
|
|
|
4) Dobaczewski M, Gonzalez-Quesada C, Fran-gogiannis NG. The extracellular matrix as a modulator of the inflammatory and reparative response following myocardial infarction. J Mol Cell Cardiol. 2009; 48: 504-11
|
|
|
5) Tran KT, Griffith L, Wells A. Extracellular matrix signaling through growth factor receptors during wound healing. Wound Repair Regen. 2004; 12: 262-8
|
|
|
6) Manabe I, Shindo T, Nagai R. Gene expression in fibroblasts and fibrosis: involvement in cardiac hypertrophy. Circ Res. 2002; 91: 1103-13
|
|
|
7) Baudino TA, Carver W, Giles W, et al. Cardiac fibroblasts: friend or foe? Am J Physiol Heart Circ Physiol. 2006; 291: H1015-26
|
|
|
8) Souders CA, Bowers SLK, Baudino TA. Cardiac fibroblast: the renaissance cell. Circ Res. 2009; 105: 1164-76
|
|
|
9) Spinale FG. Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. Physiol Rev. 2007; 87: 1285-342
|
|
|
10) Rocha R, Rudolph AE, Frierdich GE, et al. Aldosterone induces a vascular inflammatory phenotype in the rat heart. Am J Physiol. 2002; 283: H1802-10
|
|
|
11) Zhao W, Ahokas RA, Weber KT, et al. ANG II-induced cardiac molecular and cellular events: role of aldosterone. Am J Physiol Heart Circ Physiol. 2006; 291: H336-43
|
|
|
12) Berk BC, Fujiwara K, Lehoux S. ECM remodeling in hypertensive heart disease. J Clin Invest. 2007; 117: 568-75
|
|
|
13) Leask A. Potential therapeutic targets for cardiac fibrosis: TGFbeta, angiotensin, endothelin, CCN2, and PDGF, partners in fibroblast activation. Circ Res. 2010; 106: 1675-80
|
|
|
14) Wynn TA. Cellular and molecular mechanisms of fibrosis. J Pathol. 2008; 214: 199-210
|
|
|
15) Sage EH, Bornstein P. Extracellular proteins that modulate cell-matrix interactions. SPARC, tenascin, and thrombospondin. J Biol Chem. 1991; 266: 14831-4
|
|
|
16) Bornstein P. Diversity of function is inherent in matricellular proteins: an appraisal of thrombospondin 1. J Cell Biol. 1995; 130: 503-6
|
|
|
17) Murphy-Ullrich JE. The de-adhesive activity of matricellular proteins: is intermediate cell adhesion an adaptive state? J Clin Invest. 2001; 107: 785-90
|
|
|
18) Imanaka-Yoshida K, Hiroe M, Nishikawa T, et al. Tenascin-C modulates adhesion of cardiomyocytes to extracellular matrix during tissue remodeling after myocardial infarction. Lab Invest. 2001; 81: 1015-24
|
|
|
19) Liu A, Mosher DF, Murphy-Ullrich JE, et al. The counteradhesive proteins, thrombospondin 1 and SPARC/osteonectin, open the tyrosine phosphorylation-responsive paracellular pathway in pulmonary vascular endothelia. Microvasc Res. 2009; 77: 13-20
|
|
|
20) Midwood KS, Orend G. The role of tenascin-C in tissue injury and tumorigenesis. J Cell Commun Signal. 2009; 3: 287-310
|
|
|
21) Imanaka-Yoshida K, Hiroe M, Yoshida T. Interaction between cell and extracellular matrix in heart disease: multiple roles of tenascin-C in tissue remodeling. Histol Histopathol. 2004; 19: 517-25
|
|
|
22) Nishioka T, Onishi K, Shimojo N, et al. Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice. Am J Physiol Heart Circ Physiol. 2010; 298: H1072-8
|
|
|
23) Sato M, Toyozaki T, Odaka K, et al. Detection of experimental autoimmune myocarditis in rats by 111In monoclonal antibody specific for tenas-cin-C. Circulation. 2002; 106: 1397-402
|
|
|
24) Sato A, Aonuma K, Imanaka-Yoshida K, et al. Serum tenascin-C might be a novel predictor of left ventricular remodeling and prognosis after acute myocardial infarction. J Am Coll Cardiol. 2006; 47: 2319-25
|
|
|
25) Fujimoto N, Onishi K, Sato A, et al. Incremental prognostic values of serum tenascin-C levels with blood B-type natriuretic peptide testing at discharge in patients with dilated cardiomyopathy and decompensated heart failure. J Card Fail. 2009; 15: 898-905
|
|
|
26) Kyriakides TR, Maclauchlan S. The role of thrombospondins in wound healing, ischemia, and the foreign body reaction. J Cell Commun Signal. 2009; 3: 215-25
|
|
|
27) Tan K, Lawler J. The interaction of Thrombo-spondins with extracellular matrix proteins. J Cell Commun Signal. 2009; 3: 177-87
|
|
|
28) Bornstein P. Thrombospondins function as regulators of angiogenesis. J Cell Commun Signal. 2009; 3: 189-200
|
|
|
29) Frangogiannis NG, Ren G, Dewald O, et al. Critical role of endogenous thrombospondin-1 in preventing expansion of healing myocardial infarcts. Circulation. 2005; 111: 2935-42
|
|
|
30) Schellings MW, Pinto YM, Heymans S. Matricellular proteins in the heart: possible role during stress and remodeling. Cardiovasc Res. 2004; 64: 24-31
|
|
|
31) Bradshaw AD. The role of SPARC in extracellular matrix assembly. J Cell Commun Signal. 2009; 3: 239-46
|
|
|
32) McCurdy S, Baicu CF, Heymans S, et al. Cardiac extracellular matrix remodeling: fibrillar collagens and Secreted Protein Acidic and Rich in Cysteine (SPARC). J Mol Cell Cardiol. 2009; 48: 544-9
|
|
|
33) Schellings MW, Vanhoutte D, Swinnen M, et al. Absence of SPARC results in increased cardiac rupture and dysfunction after acute myocardial infarction. J Exp Med. 2009; 206: 113-23
|
|
|
34) Bradshaw AD, Baicu CF, Rentz TJ, et al. Pressure overload-induced alterations in fibrillar collagen content and myocardial diastolic function: role of secreted protein acidic and rich in cysteine (SPARC) in post-synthetic procollagen processing. Circulation. 2009; 119: 269-80
|
|
|
35) Lund SA, Giachelli CM, Scatena M. The role of osteopontin in inflammatory processes. J Cell Commun Signal. 2009; 3: 311-22
|
|
|
36) Singh M, Foster CR, Dalal S, et al. Osteopontin: role in extracellular matrix deposition and myocardial remodeling post-MI. J Mol Cell Cardiol. 2009; 48: 538-43
|
|
|
37) Chen CC, Lau LF. Functions and mechanisms of action of CCN matricellular proteins. Int J Biochem Cell Biol. 2009; 41: 771-83
|
|
|
38) Hilfiker-Kleiner D, Kaminski K, Kaminska A, et al. Regulation of proangiogenic factor CCN1 in cardiac muscle: impact of ischemia, pressure overload, and neurohumoral activation. Circulation. 2004; 109: 2227-33
|
|
|
39) Chuva De Sousa Lopes SM, Feijen A, Korving J, et al. Connective tissue growth factor expression and Smad signaling during mouse heart development and myocardial infarction. Dev Dyn. 2004; 231: 542-50
|
|
|
40) Kii I, Nishiyama T, Li M, et al. Incorporation of tenascin-C into the extracellular matrix by periostin underlies an extracellular meshwork architecture. J Biol Chem. 2010; 285: 2028-39
|
|
|
41) Norris RA, Moreno-Rodriguez R, Hoffman S, et al. The many facets of the matricelluar protein periostin during cardiac development, remodeling, and pathophysiology. J Cell Commun Signal. 2009; 3: 275-86
|
|
|
42) Oka T, Xu J, Kaiser RA, et al. Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling. Circ Res. 2007; 101: 313-21
|
|
|
43) Shimazaki M, Nakamura K, Kii I, et al. Periostin is essential for cardiac healing after acute myo-cardial infarction. J Exp Med. 2008; 205: 295-303
|
|
|