scholarly journals Neutrophil gelatinase–associated lipocalin mediates 13-cis retinoic acid–induced apoptosis of human sebaceous gland cells

2008 ◽  
Vol 118 (4) ◽  
pp. 1468-1478 ◽  
Author(s):  
Amanda M. Nelson ◽  
Wei Zhao ◽  
Kathryn L. Gilliland ◽  
Andrea L. Zaenglein ◽  
Wenlei Liu ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Sebaceous Gland ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Gland Cells ◽  
Induced Apoptosis ◽  
Neutrophil Gelatinase ◽  
Human Sebaceous Gland

scholarly journals Neutrophil gelatinase-associated lipocalin as a survival factor

2005 ◽  
Vol 391 (2) ◽  
pp. 441-448 ◽  
Author(s):  
Zhimin Tong ◽  
Xuli Wu ◽  
Dmitriy Ovcharenko ◽  
Jiuxiang Zhu ◽  
Ching-Shih Chen ◽  
...  
Keyword(s):  
Survival Function ◽  
A549 Cells ◽  
Specific Effect ◽  
Mrna Levels ◽  
Mcf7 Cells ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
A Cell ◽  
Induced Apoptosis ◽  
Neutrophil Gelatinase ◽  
Interfering Rna

NGAL (human neutrophil gelatinase-associated lipocalin) and its mouse analogue 24p3 are members of the lipocalin family of small secreted proteins. These proteins are up-regulated in a number of pathological conditions, including cancers, and may function as transporters of essential factors. Although previous publications have suggested that 24p3 has pro-apoptotic functions, other data are more suggestive of a survival function. The current study was designed to determine whether NGAL is pro- or anti-apoptotic. Apoptosis induced in human adenocarcinoma A549 cells by the 5-lipoxygenase-activating-protein inhibitor MK886, or several celecoxib-derived PDK1 (phosphoinositide-dependent kinase 1) inhibitors that are devoid of cyclo-oxygenase-2 inhibitory activity, was accompanied by a dose- and time-dependent increase of NGAL mRNA levels, as was reported previously with 24p3. A similar induction of NGAL mRNA was observed in human breast cancer MCF7 cells treated with MK886, indicating this was not a cell-specific effect. Treatment of A549 cells with up to 150 μg/106 cells of purified recombinant NGAL protein had no effect on viability, whereas antisera against the full-length NGAL protein induced apoptosis in these cells. The stable overexpression of NGAL in A549 cells had no effect on proliferation or viability. However, the cell death induced by a PDK1 inhibitor was reduced by 50% in NGAL-overexpressing cells. Decreasing NGAL mRNA and protein expression with siRNA (small interfering RNA) in A549 cells increased the toxicity of a PDK1 inhibitor by approx. 45%. These data indicate that, although the induction of NGAL correlates with apoptosis, this induction represents a survival response. Because NGAL is a secreted protein, it may play an extracellular role in cell defence against toxicants and/or facilitate the survival of the remaining cells.

scholarly journals Involvement of PPARγ in Oxidative Stress-Mediated Prostaglandin E2 Production in SZ95 Human Sebaceous Gland Cells

2006 ◽  
Vol 126 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Qiwei Zhang ◽  
Holger Seltmann ◽  
Christos C. Zouboulis ◽  
Raymond L. Konger
Keyword(s):  
Oxidative Stress ◽  
Prostaglandin E2 ◽  
Sebaceous Gland ◽  
Gland Cells ◽  
Human Sebaceous Gland
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