A novel role for bone marrow-derived cells to recover damaged keratinocytes from radiation-induced injury

• Published in: Scientific reports Vol. 11; no. 1; pp. 5653 - 14
• Main Authors: Okano, Junko, Nakae, Yuki, Nakagawa, Takahiko, Katagi, Miwako, Terashima, Tomoya, Nagakubo, Daisuke, Nakayama, Takashi, Yoshie, Osamu, Suzuki, Yoshihisa, Kojima, Hideto
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 11.03.2021; Nature Publishing Group; Nature Portfolio
• Subjects: 631/136; 631/57; 631/61; 631/80; Animals; Apoptosis; Basal cells; Bone marrow; Bone Marrow Cells - pathology; Bone Marrow Cells - radiation effects; Bone Marrow Transplantation; CCL17 protein; Cell migration; Cell Movement - radiation effects; Cell proliferation; Cell Proliferation - radiation effects; Chemokine CCL17 - metabolism; Dermis; Dermis - pathology; Dermis - radiation effects; Epidermis; Epidermis - pathology; Epidermis - radiation effects; Gene Deletion; HaCaT Cells; Humanities and Social Sciences; Humans; Ionizing radiation; Keratinocytes; Keratinocytes - pathology; Keratinocytes - radiation effects; Macrophages - radiation effects; Mice; Mice, Inbred C57BL; Mice, Transgenic; multidisciplinary; Radiation Injuries - pathology; Radiation therapy; Radiation, Ionizing; Receptors, CCR4 - deficiency; Receptors, CCR4 - metabolism; Recovery (Medical); Science; Science (multidisciplinary); Signal Transduction - radiation effects; Skin; Skin - pathology; Skin - radiation effects
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-021-84818-1

Exposure to moderate doses of ionizing radiation (IR), which is sufficient for causing skin injury, can occur during radiation therapy as well as in radiation accidents. Radiation-induced skin injury occasionally recovers, although its underlying mechanism remains unclear. Moderate-dose IR is frequently utilized for bone marrow transplantation in mice; therefore, this mouse model can help understand the mechanism. We had previously reported that bone marrow-derived cells (BMDCs) migrate to the epidermis-dermis junction in response to IR, although their role remains unknown. Here, we investigated the role of BMDCs in radiation-induced skin injury in BMT mice and observed that BMDCs contributed to skin recovery after IR-induced barrier dysfunction. One of the important mechanisms involved the action of CCL17 secreted by BMDCs on irradiated basal cells, leading to accelerated proliferation and recovery of apoptosis caused by IR. Our findings suggest that BMDCs are key players in IR-induced skin injury recovery.