scholarly journals A Thrombospondin-1 Antagonist of Transforming Growth Factor-β Activation Blocks Cardiomyopathy in Rats with Diabetes and Elevated Angiotensin II

2007 ◽  
Vol 171 (3) ◽  
pp. 777-789 ◽  
Author(s):  
Souad Belmadani ◽  
Juan Bernal ◽  
Chih-Chang Wei ◽  
Manuel A. Pallero ◽  
Louis Dell'Italia ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Thrombospondin 1

scholarly journals Expression of the Type-1 Repeats of Thrombospondin-1 Inhibits Tumor Growth Through Activation of Transforming Growth Factor-β

2004 ◽  
Vol 165 (2) ◽  
pp. 541-552 ◽  
Author(s):  
Karen O. Yee ◽  
Michael Streit ◽  
Thomas Hawighorst ◽  
Michael Detmar ◽  
Jack Lawler
Keyword(s):  
Growth Factor ◽  
Tumor Growth ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Thrombospondin 1

ANGIOTENSIN II TYPE 1 RECEPTOR ANTAGONIST (LOSARTAN) DOWN-REGULATES TRANSFORMING GROWTH FACTOR-β IN EXPERIMENTAL ACUTE PYELONEPHRITIS

2000 ◽  
Vol 164 (1) ◽  
pp. 186-191 ◽  
Author(s):  
ADLI KHALIL ◽  
KJELL TULLUS ◽  
MOIZ BAKHIET ◽  
LARS G. BURMAN ◽  
GEORG JAREMKO ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Receptor Antagonist ◽  
Acute Pyelonephritis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

Thrombospondin-1 promotes fibroblast-mediated collagen gel contraction caused by activation of latent transforming growth factor β-1

2003 ◽  
Vol 31 (2) ◽  
pp. 99-109 ◽  
Author(s):  
Kensuke Sakai ◽  
Yukio Sumi ◽  
Hisako Muramatsu ◽  
Ken-ichiro Hata ◽  
Takashi Muramatsu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Collagen Gel ◽  
Transforming Growth Factor Β ◽  
Collagen Gel Contraction ◽  
Thrombospondin 1

scholarly journals BMP-1 disrupts cell adhesion and enhances TGF-β activation through cleavage of the matricellular protein thrombospondin-1

2020 ◽  
Vol 13 (639) ◽  
pp. eaba3880 ◽  
Author(s):  
Cyril Anastasi ◽  
Patricia Rousselle ◽  
Maya Talantikite ◽  
Agnès Tessier ◽  
Caroline Cluzel ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Substantial Effect ◽  
Matricellular Protein ◽  
Matrix Assembly ◽  
Morphogenetic Protein ◽  
Thrombospondin 1

Bone morphogenetic protein 1 (BMP-1) is an important metalloproteinase that synchronizes growth factor activation with extracellular matrix assembly during morphogenesis and tissue repair. The mechanisms by which BMP-1 exerts these effects are highly context dependent. Because BMP-1 overexpression induces marked phenotypic changes in two human cell lines (HT1080 and 293-EBNA cells), we investigated how BMP-1 simultaneously affects cell-matrix interactions and growth factor activity in these cells. Increasing BMP-1 led to a loss of cell adhesion that depended on the matricellular glycoprotein thrombospondin-1 (TSP-1). BMP-1 cleaved TSP-1 between the VWFC/procollagen-like domain and the type 1 repeats that mediate several key TSP-1 functions. This cleavage induced the release of TSP-1 C-terminal domains from the extracellular matrix and abolished its previously described multisite cooperative interactions with heparan sulfate proteoglycans and CD36 on HT1080 cells. In addition, BMP-1–dependent proteolysis potentiated the TSP-1–mediated activation of latent transforming growth factor–β (TGF-β), leading to increased signaling through the canonical SMAD pathway. In primary human corneal stromal cells (keratocytes), endogenous BMP-1 cleaved TSP-1, and the addition of exogenous BMP-1 enhanced cleavage, but this had no substantial effect on cell adhesion. Instead, processed TSP-1 promoted the differentiation of keratocytes into myofibroblasts and stimulated production of the myofibroblast marker α-SMA, consistent with the presence of processed TSP-1 in human corneal scars. Our results indicate that BMP-1 can both trigger the disruption of cell adhesion and stimulate TGF-β signaling in TSP-1–rich microenvironments, which has important potential consequences for wound healing and tumor progression.

scholarly journals Lipid Accumulation and Transforming Growth Factor-β Upregulation in the Kidneys of Rats Administered Angiotensin II

Hypertension ◽  
2005 ◽  
Vol 46 (5) ◽  
pp. 1180-1185 ◽  
Author(s):  
Kan Saito ◽  
Nobukazu Ishizaka ◽  
Masumi Hara ◽  
Gen Matsuzaki ◽  
Masataka Sata ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Lipid Accumulation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

ANDROGEN-SENSITIVE THROMBOSPONDIN-1 REGULATES PROSTATE EPITHELIAL PROLIFERATION AND TRANSFORMING GROWTH FACTOR-β ACTIVATION IN THE MOUSE PROSTATE

2009 ◽  
Vol 181 (4S) ◽  
pp. 93-94
Author(s):  
Jennifer A. Doll ◽  
Chung Lee ◽  
Anders Bergh ◽  
Philip Fitchev ◽  
Mona Cornwell ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Epithelial Proliferation ◽  
Mouse Prostate ◽  
Thrombospondin 1

Ovine Fetal Adrenal Synthesis of Cortisol: Regulation by Adrenocorticotropic Angiotensin II and Transforming Growth Factor-β*

Endocrinology ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 1784-1791 ◽  
Author(s):  
WILLIAM E. RAINEY ◽  
KUNIHIKO OKA ◽  
RONALD R. MAGNESS ◽  
J. IAN MASON
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Ovine Fetal

scholarly journals TGF-β (Transforming Growth Factor-β) Signaling Protects the Thoracic and Abdominal Aorta From Angiotensin II-Induced Pathology by Distinct Mechanisms

2017 ◽  
Vol 37 (11) ◽  
pp. 2102-2113 ◽  
Author(s):  
Stoyan N. Angelov ◽  
Jie Hong Hu ◽  
Hao Wei ◽  
Nathan Airhart ◽  
Minghui Shi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Abdominal Aorta ◽  
Neutralizing Antibodies ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Specific Loss ◽  
Aortic Pathology ◽  
Thoracic And Abdominal

Objective— The role of TGF-β (transforming growth factor-β) signaling in abdominal aortic aneurysm (AAA) formation is controversial. Others reported that systemic blockade of TGF-β by neutralizing antibodies accelerated AAA development in angiotensin II-infused mice. This result is consistent with other studies suggesting that TGF-β signaling prevents AAA. Development of a therapy for AAA that exploits the protective actions of TGF-β would be facilitated by identification of the mechanisms through which TGF-β prevents AAA. We hypothesized that TGF-β signaling prevents AAA by its actions on aortic medial smooth muscle cells. Approach and Results— We compared the prevalence, severity, and histopathology of angiotensin II-induced AAA among control mice (no TGF-β blockade), mice with antibody-mediated systemic neutralization of TGF-β, and mice with genetically based smooth muscle–specific loss of TGF-β signaling. Surprisingly, we found that systemic—but not smooth muscle–specific—TGF-β blockade significantly increased the prevalence of AAA and tended to increase AAA severity, adventitial thickening, and aortic wall macrophage accumulation. In contrast, abdominal aortas of mice with smooth muscle–specific loss of TGF-β signaling differed from controls only in having a thinner media. We examined thoracic aortas of the same mice. Here we found that smooth muscle–specific loss of Tgfbr2 —but not systemic TGF-β neutralization—significantly accelerated development of aortic pathology, including increased prevalence of intramural hematomas, medial thinning, and adventitial thickening. Conclusion— Our results suggest that TGF-β signaling prevents both abdominal and thoracic aneurysmal disease but does so by distinct mechanisms. Smooth muscle extrinsic signaling protects the abdominal aorta and smooth muscle intrinsic signaling protects the thoracic aorta.

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