Ingunn Hanson

• Hanson, Ingunn; Pitman, Kathinka Elinor; Altanerova, Ursula; Altaner, Čestmír; Malinen, Eirik & Edin, Nina Frederike Jeppesen (2022). Low-Dose-Rate Radiation-Induced Secretion of TGF-B3 Together with an Activator in Small Extracellular Vesicles Modifies Low-Dose Hyper-Radiosensitivity through ALK1 Binding. International Journal of Molecular Sciences. ISSN 1661-6596. 23(15). doi: 10.3390/%20ijms23158147.
• Arous, Delmon; Schrunner, Stefan; Hanson, Ingunn; Edin, Nina Frederike Jeppesen & Malinen, Eirik (2022). Principal component-based image segmentation: a new approach to outline in vitro cell colonies. Computer Methods in Biomechanics and Biomedical Engineering: Imaging & Visualization. ISSN 2168-1163. doi: 10.1080/21681163.2022.2035822.
• Sulheim, Einar; Hanson, Ingunn; Snipstad, Sofie; Vikedal, Krister; Mørch, Ýrr Asbjørg & Boucher, Yves [Show all 7 contributors for this article] (2021). Sonopermeation with nanoparticle-stabilized microbubbles reduces solid stress and improves nanomedicine delivery to tumors. Advanced therapeutics. ISSN 2366-3987. 4(10). doi: 10.1002/adtp.202100147. Full text in Research Archive

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• Hanson, Ingunn & Edin, Nina Frederike Jeppesen (2022). The role of TGF-β3 in modification of radiation response.
• Hanson, Ingunn & Edin, Nina Frederike Jeppesen (2022). Shielding of the femur reduces the severity of the gastrointestinal subsyndrome of ARS and increases survival in mice.
• Hanson, Ingunn; Pitman, Kathinka Elinor; Thiede, Bernd; Cai, Yiqing & Edin, Nina Frederike Jeppesen (2021). Proteomic Analysis of Low Dose-Rate Primed Cells and Extracellular Exosomes.
• Hanson, Ingunn; Edin, Nina Frederike J; Thiede, Bernd & Altanerova, Ursula (2020). Communication of radioprotective efects by TGF-β3.
• Hanson, Ingunn; Altanerova, Ursula; Thiede, Bernd & Edin, Nina Frederike J (2020). Radioprotector TGF-β3 is secreted in exosomes and activated by LDR priming. Show summary

  The biological effects of ionizing radiation in the low-dose region is important for diagnostic imaging, healthy tissue in radiation therapy and environmental radiation. For a majority of tested cell lines, the low dose hyper-radiosensitive (HRS) response has been shown to be default. We have previously shown that cells primed with a low dose-rate (⁓0.3 Gy/h) ionizing radiation permanently loses the HRS response. We have also shown that the transforming growth factor (TGF)-β3 is responsible for this effect. Here, we investigated the secretion mechanism of TGF-β3 from LDR primed cells, and theorize regarding the way it is activated. Exosomes were isolated from LDR primed cells, and were shown to remove HRS in reporter cells when co-cultured with these. Adding a TGF-β3 inhibitor to the medium restored the HRS response in reporter cells, confirming that TGF-β3 was the factor in the exosomes responsible for removing HRS. Mass spectrometry was performed on the content of exosomes from primed and control cells. Proteomic analysis confirmed the presence of exosome-specific proteins in exosomes from primed and control groups. TGF-β3 along with latency-associated protein (LAP), the protein that TGF-β3 is bound to in its inactive form, was present in similar amounts in both groups, indicating that TGF-β3 was secreted in its inactive form, regardless of LDR priming. Three proteins were significantly upregulated in the primed exosomes. These proteins will be investigated further in future experiments. We conclude that TGF-β3 is secreted in its inactive form in exosomes from LDR primed and unprimed cells, and that the priming is responsible for its activation. We will further investigate three significantly upregulated proteins with regards to their role in the activation of TGF-β3.

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