scholarly journals Corrigendum: Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

2019 ◽  
Vol 10 ◽  
Author(s):  
Anup Bhusal ◽  
Md Habibur Rahman ◽  
In-Kyu Lee ◽  
Kyoungho Suk
Keyword(s):  
Lipocalin 2 ◽  
Diabetic Encephalopathy

scholarly journals Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

2019 ◽  
Vol 10 ◽  
Author(s):  
Anup Bhusal ◽  
Md Habibur Rahman ◽  
In-Kyu Lee ◽  
Kyoungho Suk
Keyword(s):  
Lipocalin 2 ◽  
Diabetic Encephalopathy

The critical biomechanical role of Lipocalin 2 in the crosstalk between endothelium and osteoblasts in unloading conditions.

2016 ◽  
Author(s):  
Vimal Veeriah ◽  
Mattia Capulli ◽  
Angelo Zanniti ◽  
Suvro Chatterjee ◽  
Nadia Rucci ◽  
...  
Keyword(s):  
Lipocalin 2

scholarly journals Iron-Bound Lipocalin-2 from Tumor-Associated Macrophages Drives Breast Cancer Progression Independent of Ferroportin

Metabolites ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 180
Author(s):  
Christina Mertens ◽  
Matthias Schnetz ◽  
Claudia Rehwald ◽  
Stephan Grein ◽  
Eiman Elwakeel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Progression ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Lung Metastases ◽  
Expression Profiles ◽  
The Cancer Genome Atlas ◽  
Lipocalin 2 ◽  
Tumor Associated Macrophages

Macrophages supply iron to the breast tumor microenvironment by enforced secretion of lipocalin-2 (Lcn-2)-bound iron as well as the increased expression of the iron exporter ferroportin (FPN). We aimed at identifying the contribution of each pathway in supplying iron for the growing tumor, thereby fostering tumor progression. Analyzing the expression profiles of Lcn-2 and FPN using the spontaneous polyoma-middle-T oncogene (PyMT) breast cancer model as well as mining publicly available TCGA (The Cancer Genome Atlas) and GEO Series(GSE) datasets from the Gene Expression Omnibus database (GEO), we found no association between tumor parameters and Lcn-2 or FPN. However, stromal/macrophage-expression of Lcn-2 correlated with tumor onset, lung metastases, and recurrence, whereas FPN did not. While the total iron amount in wildtype and Lcn-2−/− PyMT tumors showed no difference, we observed that tumor-associated macrophages from Lcn-2−/− compared to wildtype tumors stored more iron. In contrast, Lcn-2−/− tumor cells accumulated less iron than their wildtype counterparts, translating into a low migratory and proliferative capacity of Lcn-2−/− tumor cells in a 3D tumor spheroid model in vitro. Our data suggest a pivotal role of Lcn-2 in tumor iron-management, affecting tumor growth. This study underscores the role of iron for tumor progression and the need for a better understanding of iron-targeted therapy approaches.

scholarly journals Evidence for the Regulatory Role of Lipocalin 2 in High-Fat Diet-Induced Adipose Tissue Remodeling in Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3525-3538 ◽  
Author(s):  
Hong Guo ◽  
Merlijn Bazuine ◽  
Daozhong Jin ◽  
Merry M. Huang ◽  
Samuel W. Cushman ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Tissue Remodeling ◽  
Peroxisome Proliferator ◽  
Lipocalin 2 ◽  
Peroxisome Proliferator Activated Receptor ◽  
Adipose Tissue Remodeling ◽  
Fat Depot

Lipocalin 2 (Lcn2) has previously been characterized as an adipokine/cytokine playing a role in glucose and lipid homeostasis. In this study, we investigate the role of Lcn2 in adipose tissue remodeling during high-fat diet (HFD)-induced obesity. We find that Lcn2 protein is highly abundant selectively in inguinal adipose tissue. During 16 weeks of HFD feeding, the inguinal fat depot expanded continuously, whereas the expansion of the epididymal fat depot was reduced in both wild-type (WT) and Lcn2−/− mice. Interestingly, the depot-specific effect of HFD on fat mass was exacerbated and appeared more pronounced and faster in Lcn2−/− mice than in WT mice. In Lcn2−/− mice, adipocyte hypertrophy in both inguinal and epididymal adipose tissue was more profoundly induced by age and HFD when compared with WT mice. The expression of peroxisome proliferator-activated receptor-γ protein was significantly down-regulated, whereas the gene expression of extracellular matrix proteins was up-regulated selectively in epididymal adipocytes of Lcn2−/− mice. Consistent with these observations, collagen deposition was selectively higher in the epididymal, but not in the inguinal adipose depot of Lcn2−/− mice. Administration of the peroxisome proliferator-activated receptor-γ agonist rosiglitazone (Rosi) restored adipogenic gene expression. However, Lcn2 deficiency did not alter the responsiveness of adipose tissue to Rosi effects on the extracellular matrix expression. Rosi treatment led to the further enlargement of adipocytes with improved metabolic activity in Lcn2−/− mice, which may be associated with a more pronounced effect of Rosi treatment in reducing TGF-β in Lcn2−/− adipose tissue. Consistent with these in vivo observations, Lcn2 deficiency reduces the adipocyte differentiation capacity of stromal-vascular cells isolated from HFD-fed mice in these cells. Herein Rosi treatment was again able to stimulate adipocyte differentiation to a similar extent in WT and Lcn2−/− inguinal and epididymal stromal-vascular cells. Thus, combined, our data indicate that Lcn2 has a depot-specific role in HFD-induced adipose tissue remodeling.

scholarly journals The Role of Lipocalin 2 in the Regulation of Inflammation in Adipocytes and Macrophages

2008 ◽  
Vol 22 (6) ◽  
pp. 1416-1426 ◽  
Author(s):  
Jinhui Zhang ◽  
YingJie Wu ◽  
Yuanyuan Zhang ◽  
Derek LeRoith ◽  
David A. Bernlohr ◽  
...  
Keyword(s):  
Lipocalin 2

scholarly journals The role of lipocalin-2 serum levels in the diagnostics of endometrial cancer

2019 ◽  
Vol 24 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Aneta Cymbaluk-Płoska ◽  
Anita Chudecka-Głaz ◽  
Ewa Pius-Sadowska ◽  
Bogusław Machaliński ◽  
Agnieszka Sompolska-Rzechuła ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Serum Levels ◽  
Lipocalin 2

scholarly journals Role of glial metabolism in diabetic encephalopathy as detected by high resolution13C NMR

2003 ◽  
Vol 16 (67) ◽  
pp. 440-449 ◽  
Author(s):  
María A. García-Espinosa ◽  
María L. García-Martín ◽  
Sebastián Cerdán
Keyword(s):  
Diabetic Encephalopathy
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