Evidence That Angiotensin II and Lipoxygenase Products Activate c-Jun NH
            <sub>2</sub>
            -Terminal Kinase

Wen, Yeong-Ray; Scott, Stephen; Liu, Yaxia; Gonzales, Noe; Nadler, Jerry L.

doi:10.1161/01.res.81.5.651

Cited by 48 publications

(34 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is possible that, in this study, protein kinase C activation was also involved upstream of p38 MAPK. Earlier studies have indicated that 12(S)-HETE can activate members of the MAPK pathway in fibroblasts and VSMCs (43)(44)(45). However, p38 MAPK activation was not evaluated in those studies.…”

Section: Discussionmentioning

confidence: 99%

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

Reddy¹,

Thimmalapura²,

Lanting³

et al. 2002

Journal of Biological Chemistry

Self Cite

124

137

View full text Add to dashboard Cite

Growth factor-and cytokine-induced vascular smooth muscle cell proliferation, migration, hypertrophy, and matrix production have been shown to play important roles in the development of vascular disorders such as atherosclerosis, hypertension, and restenosis. Growth factors such as angiotensin II (AngII) 1 and platelet-derived growth factor (PDGF) activate intracellular phospholipases, leading to the formation of arachidonic acid, which can be further metabolized by cyclooxygenases, cytochrome P-450 oxygenases, and lipoxygenases (1). Lipoxygenase (LO) action leads to the formation of oxidized lipids such as 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE). LOs and their products of arachidonic acid and linoleic acid metabolism have been shown to mediate growth factor effects in vascular smooth muscle cells (VSMCs) as well as responses to vascular injury. Lipoxygenases are classified as 5-, 8-, 12-, and 15-lipoxygenases based on their ability to insert molecular oxygen at the corresponding carbon atom of arachidonic acid. Three major isoforms of 12-LO have been cloned. They are platelet-type 12-LO, leukocyte-type 12-LO, and epidermis-type 12-LO. These proteins are products of distinct genes and vary in tissue distribution (2, 3).Leukocyte 12-LO has been cloned from porcine and mouse leukocytes (4, 5). The presence of leukocyte-type 12-LO (also termed 12/15-LO) has also been demonstrated in various cell types and tissues, including VSMCs, adrenal cells, rat brain, and kidney (6 -11). Studies from this and other laboratories (12-21) have implicated the leukocyte-type 12-LO pathway in the pathogenesis of atherosclerosis and restenosis. 12-LO expression was demonstrated in atherosclerotic lesions (12). In vascular and mononuclear cells, growth factors and cytokines as well as high glucose stimulate both the activity and expression of 12-LO (6, 13-15). Furthermore, expression of 12-LO protein and mRNA is markedly increased in neointima of balloon-injured rat carotid arteries, and pretreatment with LO inhibitors reduces the rate of neointimal thickening in this model (16,17). We have demonstrated that treatment with a chimeric DNA-RNA hammerhead ribozyme targeted to cleave rat leukocyte-type 12-LO mRNA significantly reduces neointimal thickening in balloon-injured rat arteries (18). We have

show abstract

Section: Discussionmentioning

confidence: 99%

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

Reddy¹,

Thimmalapura²,

Lanting³

et al. 2002

Journal of Biological Chemistry

Self Cite

124

137

View full text Add to dashboard Cite

show abstract

“…Among the reported effects are activation of protein kinase C, 36 extracellular signal-regulated kinase, 37 or c-Jun N-terminal kinase 20,38 ; induction of immediate-early genes 14,36 ; and elevations in intracellular calcium 36 and formation of ROIs. 24 In this study, we also showed that Ang II in the same dose as was used in the above-mentioned studies generated ROIs.…”

Section: Discussionmentioning

confidence: 99%

“…[12][13][14][15] Both TNF-␣ and Ang II are implicated in reactive oxygen intermediates (ROIs). TNF-␣ exerts cytotoxic activity on some types of tumor cells, in part via the generation of ROIs, 16 -18 and Ang II causes hypertension in vivo 19 and c-Jun N-terminal kinase activation in cardiac myocytes, 20 in part via the generation of ROIs. ROIs are involved in many biological processes.…”

mentioning

confidence: 99%

Inhibitory Effects of Antioxidants on Neonatal Rat Cardiac Myocyte Hypertrophy Induced by Tumor Necrosis Factor-α and Angiotensin II

et al. 1998

View full text Add to dashboard Cite

Background-Tumor necrosis factor-␣ (TNF-␣) and angiotensin II (Ang II) modulate heart failure in part by provoking the hypertrophic response. Signal transduction pathways of those factors are implicated in reactive oxygen intermediates (ROIs). Therefore, we hypothesized that TNF-␣ and Ang II might cause myocyte hypertrophy via the generation of ROIs. Methods and Results-To test the hypothesis, we tested whether TNF-␣ and Ang II could induce the generation of ROIs and whether antioxidants such as butylated hydroxyanisole (BHA), vitamin E, and catalase might inhibit the hypertrophy in cultured neonatal rat cardiac myocytes. ROIs were measured by the ROI-specific probe 2Ј,7Ј-dichlorofluorescin diacetate in cultured cardiac myocytes. We demonstrated that TNF-␣ and Ang II induced the generation of ROIs in a dose-dependent manner. TNF-␣ (10 ng/mL) and Ang II (100 nmol/L) enlarged cardiac myocytes and increased [ 3 H]leucine uptake, and BHA (10 mol/L) significantly inhibited both effects. Other antioxidants, such as vitamin E (1 g/mL) and catalase (100 U/mL), also inhibited the enlargement of cardiac myocytes induced by TNF-␣. Conclusions-These

show abstract

“…12(S)-HETE can stimulate JNK/SAPK activation in ovary fibroblast cells and islet ␤ cells. 35,36 The lack of effect of 12(S)-HETE on JNK/SAPK activity in pancreatic cancer cells suggests that 12(S)-HETE-induced JNK/SAPK activation is also cell type-dependent.…”

Section: Genestein Abolished 12(s)-hete-induced Mapk Phosphorylationmentioning

confidence: 99%

12-lipoxygenase metabolite 12(S)-HETE stimulates human pancreatic cancer cell proliferationvia protein tyrosine phosphorylation and ERK activation

2001

View full text Add to dashboard Cite

We previously reported that inhibition of the 12-lipoxygenase pathway abolished proliferation and induced apoptosis in several pancreatic cancer cell lines. Furthermore, the 12-lipoxygenase product 12(S)-HETE stimulated pancreatic cancer cell proliferation and reversed 12-lipoxygenase inhibitorinduced growth inhibition. We investigated the underlying mechanism for 12(S)-HETE-induced pancreatic cancer cell proliferation, using 2 human pancreatic cancer cell lines, PANC-1 and HPAF. Cell proliferation was monitored by both thymidine incorporation and cell number. Key words: pancreatic cancer; mitogen-activated protein kinase; lipoxygenase; proliferation; 12(S)-HETEEpidemiologic and animal studies have linked pancreatic cancer growth with high fat intake, particularly unsaturated fats. 1-4 Concentration-dependent promotion of pancreatic cancer cell growth by linoleic acid has been demonstrated both in vivo and in vitro. 1,2,4 Furthermore, unsaturated fats in particular enhance carcinogen-induced pancreatic carcinogenesis in both hamsters and rats. [2][3][4] The 2 -6 polyunsaturated essential fatty acids, arachidonic and linoleic acid are substrates for 3 distinct enzymatic pathways: COX, LOX and epoxygenase. The LOX pathway catalyzes the incorporation of an oxygen molecule into polyunsaturated fatty acids containing the 1,4-cic,cis-pentadiene structure to yield a 1-hydroperoxy-2,4-trans,cis-pentadiene product. 5,6 Mammalian LOX possess regiospecificity for interaction with substrate and on that basis have been designated as arachidonate 5-, 12-and 15-LOX, which transiently produce 5(S)-, 12(S)-and 15(S)-HPETE and then 5(S)-, 12(S)-and 15(S)-HETE), respectively. 5,6 Several lines of evidence have shown the importance of LOX in regulating human cancer development and growth. [7][8][9][10][11][12] We previously reported that 12-LOX is expressed in several pancreatic cancer cell lines. 9 Blockade of 12-LOX markedly inhibits proliferation and induces apoptosis in human pancreatic cancer cells. 8,9 In contrast, the 12-LOX metabolite 12(S)-HETE directly stimulates pancreatic cancer cell proliferation. 8 The underlying mechanism by which 12(S)-HETE stimulates pancreatic cancer cell proliferation has not been investigated. The current study shows that 12(S)-HETE concentration-and time-dependently enhances pancreatic cancer cell proliferation by inducing tyrosine phosphorylation of multiple cellular proteins and activation of ERKs. Blockade of either tyrosine kinases or the MEK/ERK cascade inhibits the mitogenic effect of 12(S)-HETE. Furthermore, inhibition of tyrosine kinases blocked 12(S)-HETE-induced ERK phosphorylation, suggesting that cellular protein tyrosine phosphorylation is essential for 12(S)-HETE-induced ERK activation.

show abstract

Evidence That Angiotensin II and Lipoxygenase Products Activate c-Jun NH ₂ -Terminal Kinase

Cited by 48 publications

References 25 publications

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

Inhibitory Effects of Antioxidants on Neonatal Rat Cardiac Myocyte Hypertrophy Induced by Tumor Necrosis Factor-α and Angiotensin II

12-lipoxygenase metabolite 12(S)-HETE stimulates human pancreatic cancer cell proliferationvia protein tyrosine phosphorylation and ERK activation

Contact Info

Product

Resources

About

Evidence That Angiotensin II and Lipoxygenase Products Activate c-Jun NH 2 -Terminal Kinase

Cited by 48 publications

References 25 publications

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

The Oxidized Lipid and Lipoxygenase Product 12(S)-Hydroxyeicosatetraenoic Acid Induces Hypertrophy and Fibronectin Transcription in Vascular Smooth Muscle Cells via p38 MAPK and cAMP Response Element-binding Protein Activation

Inhibitory Effects of Antioxidants on Neonatal Rat Cardiac Myocyte Hypertrophy Induced by Tumor Necrosis Factor-α and Angiotensin II

12-lipoxygenase metabolite 12(S)-HETE stimulates human pancreatic cancer cell proliferationvia protein tyrosine phosphorylation and ERK activation

Contact Info

Product

Resources

About

Evidence That Angiotensin II and Lipoxygenase Products Activate c-Jun NH ₂ -Terminal Kinase