@article{(Open Science Index):https://publications.waset.org/pdf/17118,
	  title     = {Tumor Necrosis Factor-α Regulates Heme Oxygenase-1 Expression in Endothelial Cells via the Phosphorylation of JNK/p38},
	  author    = {Chan-Jung Liang and  Shu-Huei Wang and  Pei-Jhen Wu and  Jaw-Shiun Tsai and  Chau-Chung Wu and  Yuh-Lien Chen},
	  country	= {},
	  institution	= {},
	  abstract     = {Heme oxygenase-1 (HO-1), an enzyme degrading heme to carbon monoxide, iron, and biliverdin, has been recognized as playing a crucial role in cellular defense against stressful conditions, not only related to heme release. In the present study, the effects of TNF-a on the expression of heme oxygenase-1 (HO-1) in human aortic endothelial cells (HAECs) as well as the related mechanisms were investigated. 10 ng/mL TNF-α treatment significantly increased HO-1 expression after 6h, then a further increase at 12h and declined at 24h. Treatment with 2 ng/mL of TNF-a after 12 h resulted in a significant increase in HO-1 expression, which peaked at 10 ng/mL, then declined at 20 ng/mL. TNF-α induced HO-1 expression and then HO-1 expression reduced  vascular cell adhesion molecule-1 (VCAM-1) expression. Phosphorylation studies of ERK1/2, JNK, and p38, three subgroups of mitogen-activated protein kinases (MAPKs) demonstrated TNF-α-induced ERK1/2, JNK, and p38 phosphorylation. The increase in HO-1 expression in response to TNF-α treatment was affected by pretreatment with SP600125 (a JNK inhibitor) and SB203580 (a p38 inhibitor), not with PD98059 (an ERK1/2 inhibitor). The expression of HO-1 was stronger in aortas of TNF-α-treated apo-E deficient mice when compared with control mice. These results suggest that low dose of TNF-α treatment notably induced HO-1 expression was mediated through JNK/p38 phosphorylation and may have a protective potential in cardiovascular diseases and inflammatory response through the regulation of HO-1 expression.
},
	    journal   = {International Journal of Medical and Health Sciences},
	  volume    = {7},
	  number    = {10},
	  year      = {2013},
	  pages     = {643 - 647},
	  ee        = {https://publications.waset.org/pdf/17118},
	  url   	= {https://publications.waset.org/vol/82},
	  bibsource = {https://publications.waset.org/},
	  issn  	= {eISSN: 1307-6892},
	  publisher = {World Academy of Science, Engineering and Technology},
	  index 	= {Open Science Index 82, 2013},
	}