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Körbel, C.

Publications and source records attributed to Körbel, C..

2 recordsLinked to original sources

Micro-CT analyses of the lung in mice: Parameters influencing the radiation dose and acquisition quality

Microcomputed tomography (micro-CT) is a frequently used imaging tool for a wide spectrum of in-vivo mouse models in basic and translational research. To allow an accurate interpretation of micro-CT images, high spatial resolution is necessary. However, this may also lead to a high radiation exposure of the animals. Therefore, animal welfare requires exact information about the expected radiation doses for experimental planning. To gain this, a mouse cadaver was herein used for micro-CT analyses under different conditions. For each radiation dose measurement, the cadaver was labeled with thermoluminescent dosimeter chips around the thoracic skin surface. Micro-CT scans of the thorax were performed with spatial resolutions of 35 {micro}m, 18 {micro}m and 9 {micro}m in combination with Al0.5, Al1.0, CuAl and Cu filters. As a surrogate of image quality, the number of identifiable lung vessels was counted on a transversal micro-CT slice. Measured radiation doses varied from 0.09 Gy up to 5.18 Gy dependent on resolution and filter settings. A significant dose reduction of > 75% was achieved by a Cu filter when compared to an Al0.5 filter. However, this resulted in a markedly reduced image quality and interpretability of microstructures due to higher radiation shielding and lower spatial resolution. Thus, the right combination of distinct filters and several scan protocol settings adjusted to the individual requirements can significantly reduce the radiation dose of micro-CT leading to a higher animal welfare standard.

biophysics↗

Suppression of endothelial miR-22-3p mediates non-small cell lung cancer cell-induced angiogenesis

MicroRNAs (miRNAs) expressed in endothelial cells (ECs) are powerful regulators of angiogenesis, which is essential for tumor growth and metastasis. Here, we demonstrated that miR-22-3p (miR-22) is preferentially and highly expressed in ECs, while its endothelial level is significantly down-regulated in human non-small cell lung cancer (NSCLC) tissues when compared to matched non-tumor lung tissues. This reduction of endothelial miR-22 is induced by NSCLC cell-secreted tumor necrosis factor (TNF)- and interleukin (IL)-1{beta}. Endothelial miR-22 functions as a potent angiogenesis inhibitor that inhibits all the key angiogenic activities of ECs and consequently NSCLC growth through directly targeting sirtuin (SIRT) 1 and fibroblast growth factor receptor (FGFR) 1 in ECs, leading to inactivation of AKT/mammalian target of rapamycin (mTOR) signaling. These novel findings provide insight into the molecular mechanisms of NSCLC angiogenesis and indicate that endothelial miR-22 represents a potential target for the future anti-angiogenic treatment of NSCLC.

cancer biology↗