International Journal of Molecular Sciences (Apr 2016)

Induction of Lipocalin2 in a Rat Model of Lung Irradiation

  • Sadaf Sultan,
  • Shakil Ahmad,
  • Margret Rave-Fränk,
  • Ihtzaz Ahmed Malik,
  • Clemens F. Hess,
  • Hans Christiansen,
  • Silke Cameron

DOI
https://doi.org/10.3390/ijms17050637
Journal volume & issue
Vol. 17, no. 5
p. 637

Abstract

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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.

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