scholarly journals Transforming growth factor-β1 suppression of endotoxin-induced heme oxygenase-1 in macrophages involves activation of Smad2 and downregulation of Ets-2

2011 ◽  
Vol 227 (1) ◽  
pp. 351-360 ◽  
Author(s):  
Su Wol Chung ◽  
Min-Young Kwon ◽  
Young-Ho Kang ◽  
Hun-Taeg Chung ◽  
Seon-Jin Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Heme Oxygenase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Heme Oxygenase 1

Specificity protein 1 and Smad-dependent regulation of human heme oxygenase-1 gene by transforming growth factor-β1 in renal epithelial cells

2007 ◽  
Vol 293 (3) ◽  
pp. F885-F894 ◽  
Author(s):  
Amie Traylor ◽  
Thomas Hock ◽  
Nathalie Hill-Kapturczak
Keyword(s):  
Growth Factor ◽  
Heme Oxygenase ◽  
Transforming Growth Factor ◽  
Tissue Injury ◽  
Transforming Growth Factor Β1 ◽  
Molecular Regulation ◽  
Heme Oxygenase 1 ◽  
Specificity Protein 1 ◽  
Specificity Protein ◽  
Tgf Β1

Excess transforming growth factor-β1 (TGF-β1) in the kidney leads to increased cell proliferation and deposition of extracellular matrix, resulting in progressive kidney fibrosis. TGF-β1, however, stabilizes and attenuates tissue injury through the activation of cytoprotective proteins, including heme oxygenase-1 (HO-1). HO-1 catabolizes pro-oxidant heme into substances with anti-oxidant, anti-apoptotic, anti-fibrogenic, vasodilatory and immune modulatory properties. Little is known regarding the molecular regulation of human HO-1 induction by TGF-β1 except that it is dependent on de novo RNA synthesis and requires a group of structurally related proteins called Smads. It is not known whether other DNA binding proteins are required to initiate transcription of HO-1 and, furthermore, the promoter region(s) involved in TGF-β1-mediated induction of HO-1 has not been identified. The purpose of this study was to further delineate the molecular regulation of HO-1 by TGF-β1 in human renal proximal tubular cells. Actinomycin D and nuclear run-on studies demonstrate that TGF-β1 augments HO-1 expression by increased gene transcription and does not involve increased mRNA stability. Using transient transfection, mithramycin A, small interfering RNA, electrophoretic mobility shift assays, and decoy oligonucleotide experiments, a TGF-β1-responsive region is identified between 9.1 and 9.4 kb of the human HO-1 promoter. This ∼280-bp TGF-β1-responsive region contains a putative Smad binding element and specificity protein 1 binding sites, both of which are required for human HO-1 induction by TGF-β1.

scholarly journals Transforming growth factor β1 enhances heme oxygenase 1 expression in human synovial fibroblasts by inhibiting microRNA 519b synthesis

PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0176052 ◽  
Author(s):  
Shu-Jui Kuo ◽  
Wei-Hung Yang ◽  
Shan-Chi Liu ◽  
Chun-Hao Tsai ◽  
Horng-Chaung Hsu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Heme Oxygenase ◽  
Transforming Growth Factor ◽  
Synovial Fibroblasts ◽  
Transforming Growth Factor Β1 ◽  
Heme Oxygenase 1

scholarly journals Induction of Heme Oxygenase-1 During Endotoxemia Is Downregulated by Transforming Growth Factor-β1

1998 ◽  
Vol 83 (4) ◽  
pp. 396-403 ◽  
Author(s):  
Andrea Pellacani ◽  
Philippe Wiesel ◽  
Arunabh Sharma ◽  
Lauren C. Foster ◽  
Gordon S. Huggins ◽  
...  
Keyword(s):  
Growth Factor ◽  
Heme Oxygenase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Heme Oxygenase 1

scholarly journals Transforming Growth Factor-β Induces Transcription Factors MafK and Bach1 to Suppress Expression of the Heme Oxygenase-1 Gene

2013 ◽  
Vol 288 (28) ◽  
pp. 20658-20667 ◽  
Author(s):  
Yukari Okita ◽  
Atsushi Kamoshida ◽  
Hiroyuki Suzuki ◽  
Ken Itoh ◽  
Hozumi Motohashi ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Growth Factor ◽  
Heme Oxygenase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Heme Oxygenase 1

scholarly journals The association of genotype polymorphisms with vascular access patency in hemodialysis patients

2018 ◽  
Vol 20 (1_suppl) ◽  
pp. 24-30
Author(s):  
Chun-Fan Chen ◽  
Chih-Ching Lin
Keyword(s):  
Growth Factor ◽  
Vascular Access ◽  
Transforming Growth Factor ◽  
Coagulation Factors ◽  
Transforming Growth Factor Β1 ◽  
Hemodialysis Patients ◽  
Coagulation Cascade ◽  
Heme Oxygenase 1 ◽  
Methyl Transferase ◽  
Arteriovenous Access

Some hemodialysis patients suffer from repeat dysfunction of dialysis vascular access and need procedures of angioplasty, thrombectomy, and even temporary catheter use. Why these patients are vulnerable to vascular access dysfunction and how to improve its patency are imperative to be discovered. Traditional risk factors for vascular access function had been widely investigated but could not fully explain this question. Several genotype polymorphisms were demonstrated to increase the incidence of cardiovascular disease and might also be linked to higher risk of vascular access dysfunction. As the major causes of arteriovenous access thrombosis are hypercoagulable status and arteriovenous access stenosis, the investigated genes mainly focus on the mediators of the coagulation cascade, inflammatory process, and endothelial dysfunction. The reported polymorphisms of genes significantly associated with arteriovenous access dysfunction included genes encoding methylene tetrahydrofolate reductase, coagulation factors, heme oxygenase-1, matrix metalloproteinase, transforming growth factor-β1, tumor necrosis factor-α, vascular endothelial growth factor-A, renin-angiotensin-aldosterone system, and protein methyl transferase. However, further prospective study is indispensable to elucidate the association between the genotype polymorphisms and the outcome of vascular access. More and more therapeutic options that focus on genotype polymorphisms may generate a great benefit to the patency of vascular access of uremic patients.

scholarly journals Smad7-dependent Regulation of Heme Oxygenase-1 by Transforming Growth Factor-β in Human Renal Epithelial Cells

2000 ◽  
Vol 275 (52) ◽  
pp. 40904-40909 ◽  
Author(s):  
Nathalie Hill-Kapturczak ◽  
Leigh Truong ◽  
Vijayalakshmi Thamilselvan ◽  
Gary A. Visner ◽  
Harry S. Nick ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Heme Oxygenase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Heme Oxygenase 1 ◽  
Renal Epithelial Cells
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