Bone morphogenic protein-7 inhibits progression of chronic renal fibrosis associated with two genetic mouse models.

@article{citeulike:2570965, abstract = {Tubulointerstitial fibrosis is a hallmark feature of chronic renal injury. Specific therapies to control the progression of renal fibrosis toward end-stage renal failure are limited. Previous studies have demonstrated that expression of endogenous bone morphogenic protein-7 (BMP-7) is reduced in the kidneys of several inducible mouse models of acute and chronic renal disease and that administration of exogenous recombinant human BMP-7 (rhBMP-7) has a beneficial effect on kidney function. Here we report that treatment with rhBMP-7 leads to improved renal function, histology, and survival in mice deficient in the alpha3-chain of type IV collagen and MRL/MpJlpr/lpr lupus mice, two genetic models for chronic renal injury and fibrosis. Such therapeutic benefit is also associated with a significant decrease in the expression of profibrotic molecules, such as type I collagen and fibronectin, in renal fibroblasts. Additionally, rhBMP-7 induces expression of active matrix metalloproteinase-2, which is potentially important for removal of fibrotic matrix. Collectively, these studies provide further evidence for rhBMP-7 as an important bone-associated protein with protective function against renal pathology.}, address = {Center for Matrix Biology, Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, USA.}, author = {Zeisberg, M. and Bottiglio, C. and Kumar, N. and Maeshima, Y. and Strutz, F. and M\"{u}ller, G. A. and Kalluri, R. }, citeulike-article-id = {2570965}, doi = {10.1152/ajprenal.00191.2002}, issn = {0363-6127}, journal = {Am J Physiol Renal Physiol}, month = {December}, number = {6}, posted-at = {2008-03-22 02:52:50}, priority = {2}, title = {Bone morphogenic protein-7 inhibits progression of chronic renal fibrosis associated with two genetic mouse models.}, url = {http://dx.doi.org/10.1152/ajprenal.00191.2002}, volume = {285}, year = {2003} }

TY - JOUR ID - citeulike:2570965 L3 - citeulike-article-id:2570965 TI - Bone morphogenic protein-7 inhibits progression of chronic renal fibrosis associated with two genetic mouse models. JF - Am J Physiol Renal Physiol VL - 285 IS - 6 AD - Center for Matrix Biology, Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, USA. SN - 0363-6127 N2 - Tubulointerstitial fibrosis is a hallmark feature of chronic renal injury. Specific therapies to control the progression of renal fibrosis toward end-stage renal failure are limited. Previous studies have demonstrated that expression of endogenous bone morphogenic protein-7 (BMP-7) is reduced in the kidneys of several inducible mouse models of acute and chronic renal disease and that administration of exogenous recombinant human BMP-7 (rhBMP-7) has a beneficial effect on kidney function. Here we report that treatment with rhBMP-7 leads to improved renal function, histology, and survival in mice deficient in the alpha3-chain of type IV collagen and MRL/MpJlpr/lpr lupus mice, two genetic models for chronic renal injury and fibrosis. Such therapeutic benefit is also associated with a significant decrease in the expression of profibrotic molecules, such as type I collagen and fibronectin, in renal fibroblasts. Additionally, rhBMP-7 induces expression of active matrix metalloproteinase-2, which is potentially important for removal of fibrotic matrix. Collectively, these studies provide further evidence for rhBMP-7 as an important bone-associated protein with protective function against renal pathology. AU - Zeisberg, M AU - Bottiglio, C AU - Kumar, N AU - Maeshima, Y AU - Strutz, F AU - Müller, GA AU - Kalluri, R PY - 2003/12// UR - http://dx.doi.org/10.1152/ajprenal.00191.2002 ER -