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Int. J. Mol. Sci. 2016, 17(5), 637; doi:10.3390/ijms17050637

Induction of Lipocalin2 in a Rat Model of Lung Irradiation

1
Clinic for Gastroenterology and Endocrinology, University Medical Center Göttingen, Robert-Koch-Str. 40, D-37075 Göttingen, Germany
2
Clinic for Radiotherapy and Radiation Oncology, University Medical Center Göttingen, Robert-Koch-Str. 40, D-37075 Göttingen, Germany
These authors contributed equally to this work.
Department of Cardiology and Pneumology, University Medical Center, Robert-Koch-Str. 40, D-37075 Goettingen, Germany
§
Department of Radiotherapy, Hannover Medical School (MHH), Carl-Neuberg-Str. 1, 30625 Hannover, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Terrence Piva
Received: 29 December 2015 / Revised: 8 April 2016 / Accepted: 20 April 2016 / Published: 28 April 2016
(This article belongs to the Collection Radiation Toxicity in Cells)
View Full-Text   |   Download PDF [12356 KB, uploaded 28 April 2016]   |  

Abstract

Previously, we showed that lipocalin2 (LCN2) serum levels increased after liver irradiation and during acute-phase conditions. Here, we evaluate LCN2 expression and serum levels after single-dose lung irradiation with 25 Gy, percutaneously administered to the lung of randomly-paired male Wistar rats. Due to the concave anatomy of the lung recesses, the irradiation field included the upper part of the liver. No rat died due to irradiation. In control tissue, lung immunohistochemistry showed a high constitutive expression of LCN2+ granulocytes. LCN2 mRNA levels in lung tissue increased up to 24 h (9 ± 2.3-fold) after irradiation. However, serum LCN2 levels remained undetectable after lung irradiation. LCN2 expression in the upper part of the liver increased up to 4.2-fold after lung irradiation, but the lower liver showed an early decrease. Acute-phase cytokines (IL-1β and TNF-α) showed a significant increase on transcript level in both lung and upper liver, whilst the lower liver did not show any considerable increase. In conclusion, constitutive expression of LCN2 in local immune cells demonstrates its local role during stress conditions in the lung. The absence of LCN2 in the serum strengthens our previous findings that the liver is the key player in secreting LCN2 during stress conditions with liver involvement. View Full-Text
Keywords: lung irradiation; lipocalin2; upper and lower part of the liver lung irradiation; lipocalin2; upper and lower part of the liver
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Sultan, S.; Ahmad, S.; Rave-Fränk, M.; Malik, I.A.; Hess, C.F.; Christiansen, H.; Cameron, S. Induction of Lipocalin2 in a Rat Model of Lung Irradiation. Int. J. Mol. Sci. 2016, 17, 637.

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