Effect of angiotensin II type 1 receptor blocker on 12-lipoxygenase activity and slit diaphragm protein expression in type 2 diabetic rat glomeruli

2016 ◽  
Vol 29 (6) ◽  
pp. 775-782 ◽  
Author(s):  
Hong-zhao Xu ◽  
Wan-ning Wang ◽  
Yuan-yuan Zhang ◽  
Yan-li Cheng ◽  
Zhong-gao Xu
Keyword(s):  
Angiotensin Ii ◽  
Protein Expression ◽  
Lipoxygenase Activity ◽  
Slit Diaphragm ◽  
Receptor Blocker ◽  
Diabetic Rat ◽  
12 Lipoxygenase ◽  
Type 2 Diabetic

scholarly journals Angiotensin II type 1 receptor expression is increased via 12-lipoxygenase in high glucose-stimulated glomerular cells and type 2 diabetic glomeruli

2008 ◽  
Vol 24 (6) ◽  
pp. 1744-1752 ◽  
Author(s):  
Z.-G. Xu ◽  
L.-N. Miao ◽  
Y.-C. Cui ◽  
Y. Jia ◽  
H. Yuan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
High Glucose ◽  
Receptor Expression ◽  
12 Lipoxygenase ◽  
Type 2 Diabetic

scholarly journals Amelioration of Cognitive Impairment in the Type-2 Diabetic Mouse by the Angiotensin II Type-1 Receptor Blocker Candesartan

Hypertension ◽  
2007 ◽  
Vol 50 (6) ◽  
pp. 1099-1105 ◽  
Author(s):  
Kana Tsukuda ◽  
Masaki Mogi ◽  
Jian-Mei Li ◽  
Jun Iwanami ◽  
Li-Juan Min ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Angiotensin Ii ◽  
Diabetic Mouse ◽  
Receptor Blocker ◽  
Type 2 Diabetic

Role of 12-lipoxygenase in decreasing P-cadherin and increasing angiotensin II type 1 receptor expression according to glomerular size in type 2 diabetic rats

2011 ◽  
Vol 300 (4) ◽  
pp. E708-E716 ◽  
Author(s):  
Qiao-Yan Guo ◽  
Li-Ning Miao ◽  
Bing Li ◽  
Fu-Zhe Ma ◽  
Nian Liu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Diabetic Rats ◽  
Ang Ii ◽  
Direct Infusion ◽  
Protein Expressions ◽  
12 Lipoxygenase ◽  
Type 2 Diabetic

12-lipoxygenase (12-LO) was implicated in the development of diabetic nephropathy (DN), in which the proteinuria was thought to be associated with a decreased expression of glomerular P-cadherin. Therefore, we investigated the role of 12-LO in the glomerular P-cadherin expression in type 2 diabetic rats according to the glomerular sizes. Rats fed with high-fat diet for 6 wk were treated with low-dose streptozotocin. Once diabetes onset, diabetic rats were treated with 12-LO inhibitor cinnamyl-3,4-dihydroxy-cyanocinnamate (CDC) for 8 wk. Then glomeruli were isolated from diabetic and control rats with a sieving method. RT-PCR, Western blotting, and immunofluorescent staining were used for mRNA and protein expressions of P-cadherin and angiotensin II (Ang II) type 1 receptor (AT1). We found that CDC did not affect the glucose levels but completely attenuated diabetic increases in glomerular volume and proteinuria. Diabetes significantly decreased the P-cadherin mRNA and protein expressions and increased the AT1 mRNA and protein expressions in the glomeruli. These changes were significantly prevented by CDC and recaptured by direct infusion of 12-LO product [12(S)-HETE] to normal rats for 7 days. The decreased P-cadherin expression was similar between large and small glomeruli, but the increased AT1 expression was significantly higher in the large than in the small glomeruli from diabetic and 12(S)-HETE-treated rats. Direct infusion of normal rats with Ang II for 14 days also significantly decreased the glomerular P-cadherin expression. These results suggest that diabetic proteinuria is mediated by the activation of 12-LO pathway that is partially attributed to the decreased glomerular P-cadherin expression.

scholarly journals Expression Pattern of 12-Lipoxygenase in Human Islets With Type 1 Diabetes and Type 2 Diabetes

2015 ◽  
Vol 100 (3) ◽  
pp. E387-E395 ◽  
Author(s):  
Wojciech J. Grzesik ◽  
Joseph L. Nadler ◽  
Yui Machida ◽  
Jerry L. Nadler ◽  
Yumi Imai ◽  
...  
Keyword(s):  
Outcome Measure ◽  
Islet Cells ◽  
Human Islets ◽  
Β Cells ◽  
Β Cell ◽  
Diabetes Development ◽  
12 Lipoxygenase ◽  
Type 2 Diabetic

Context: Inflammation in the pancreas can cause β-cell stress, leading to diabetes development. Access to human pancreas tissues via the Network for Pancreatic Organ Donors with Diabetes (nPOD) has allowed characterization of pathways leading to this inflammation. Objective: 12-Lipoxygenase (12-LO) induces inflammation and has been implicated in diabetes development. Our goal was to determine expression of 12-LO in human islets from control, autoantibody-positive, type 1 diabetic, and type 2 diabetic nPOD pancreas donors. Design: Pancreas tissues from nPOD donors were examined by immunohistochemistry and immunofluorescence for islet expression of 12-LO in different subsets of islet cells. Participants: Donor pancreas samples were obtained from nPOD based on disease status (control, n = 7; autoantibody-positive, n = 8; type 1 diabetic, n = 17; or type 2 diabetic donors, n = 15). Main Outcome Measure: Determination of 12-LO expression within human islets served as the main outcome measure, including distinguishing which types of islet cells expressed 12-LO. Results: Islets from control participants (nondiabetic) lacked islet expression of 12-LO. Of donors in the other groups, 25% to 37% expressed islet 12-LO with a clear inverse relation between the numbers of β-cells and 12-LO+ cells within islets of 12-LO+ cases. 12-LO expression was not seen within macrophages, endothelial cells, α-cells, or β-cells, but only within cells expressing low levels of pancreatic polypeptide (PP) and increased levels of vimentin. Conclusions: 12-LO expression colocalizes within a specific type of islet PP+ cell under prediabetic and diabetic conditions. The costaining of PP and vimentin suggests that 12-LO participates in the process leading to β-cell dedifferentiation in the islet.

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