Epidermis–dermis junction as a novel location for bone marrow-derived cells to reside in response to ionizing radiation

Okano, Jun-ichi; Kojima, Hideto; Katagi, Munehiro; Nakae, Yuki; Terashima, Tomoya; Nakagawa, Takahiko; Kurakane, Takeshi; Okamoto, Naoki; Morohashi, Ken-ichirou; Maegawa, Hiroshi; Udagawa, Jun

doi:10.1016/j.bbrc.2015.04.094

Cited by 4 publications

(7 citation statements)

References 23 publications

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“…The preparation of the epidermal cell suspension from ear skin and the cell sorting were performed as previously described [16]. Briefly, split ventral and dorsal skin of the ear was incubated in 0.5% dispase (Roche, Basle, Switzerland) for 45 minutes at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Hyperglycemia Induces Skin Barrier Dysfunctions with Impairment of Epidermal Integrity in Non-Wounded Skin of Type 1 Diabetic Mice

et al. 2016

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Diabetes causes skin complications, including xerosis and foot ulcers. Ulcers complicated by infections exacerbate skin conditions, and in severe cases, limb/toe amputations are required to prevent the development of sepsis. Here, we hypothesize that hyperglycemia induces skin barrier dysfunction with alterations of epidermal integrity. The effects of hyperglycemia on the epidermis were examined in streptozotocin-induced diabetic mice with/without insulin therapy. The results showed that dye leakages were prominent, and transepidermal water loss after tape stripping was exacerbated in diabetic mice. These data indicate that hyperglycemia impaired skin barrier functions. Additionally, the distribution of the protein associated with the tight junction structure, tight junction protein-1 (ZO-1), was characterized by diffuse and significantly wider expression in the diabetic mice compared to that in the control mice. In turn, epidermal cell number was significantly reduced and basal cells were irregularly aligned with ultrastructural alterations in diabetic mice. In contrast, the number of corneocytes, namely, denucleated and terminally differentiated keratinocytes significantly increased, while their sensitivity to mechanical stress was enhanced in the diabetic mice. We found that cell proliferation was significantly decreased, while apoptotic cells were comparable in the skin of diabetic mice, compared to those in the control mice. In the epidermis, Keratin 5 and keratin 14 expressions were reduced, while keratin 10 and loricrin were ectopically induced in diabetic mice. These data suggest that hyperglycemia altered keratinocyte proliferation/differentiation. Finally, these phenotypes observed in diabetic mice were mitigated by insulin treatment. Reduction in basal cell number and perturbation of the proliferation/differentiation process could be the underlying mechanisms for impaired skin barrier functions in diabetic mice.

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Section: Methodsmentioning

confidence: 99%

Hyperglycemia Induces Skin Barrier Dysfunctions with Impairment of Epidermal Integrity in Non-Wounded Skin of Type 1 Diabetic Mice

et al. 2016

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“…Furthermore, we found that CCR4, the receptor of CCL17, was expressed in the basal cells 3 weeks after IR exposure, before BMDC migration to the EDJ. This is probably because of IR-induced inflammation and apoptosis in epidermal cells 5 . Consistently, CCR4 expression is also induced in epidermal cells by allergic skin inflammation, such as atopic dermatitis 5,23 .…”

Section: Discussionmentioning

confidence: 99%

“…This study has several limitations, one of which is the mechanical peeling method used to isolate target BMDCs located in EDJ 5 . We have previously demonstrated that this method is efficient in dissociating most of the BMDCs from EDJ while preparing epidermal sheets 5 . A major concern for this method is the contamination with macrophages, as BMDCs and macrophages share several cell surface markers (GFP + CD45 + MHCII + EpCAM + ).…”

Section: Discussionmentioning

confidence: 99%

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

Okano

Nakae

Nakagawa

et al. 2021

Sci Rep

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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.

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“…However, it is questionable whether BMT animals correspond to bona fide controls in skin research. This is because moderate-dose irradiation (∼9 Gy), necessary for the elimination of recipient BM cells, causes skin inflammation due to radiation injury ( Okano et al, 2015 ). Consequently, inflammation induces BMDCs migration, most of which involves immune cells derived from BM.…”

Section: Role Of Bmdcs In Organs At a Steady Statementioning

confidence: 99%

Plasticity of bone marrow-derived cell differentiation depending on microenvironments in the skin

Okano,

Nakagawa,

Kojima

2024

Front. Physiol.

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Bone marrow-derived cells (BMDCs) are heterogeneous populations in which not only pluripotent stem cells, namely, hematopoietic stem cells (HSCs), mesenchymal stem cells (MSC) but also endothelial progenitor cells (EPC) are involved. BMDCs contribute to the maintenance of homeostasis and recovery from disrupted homeostasis as the immune, endocrine, and nervous systems. The skin is the largest organ in which various tissues, such as the epidermis, dermis, skin appendages (i.e., hair follicles), fats, muscles, and vessels, are tightly and systematically packed. It functions as a physical barrier to block the invasion of harmful substances and pathogenic microorganisms and properly regulate water evaporation. The skin is exposed to injuries from external stimuli because it is the outermost layer and owing to its specificity. Recovery from physical injuries and DNA mutations occurs constantly in the skin, but medical treatments are required for impaired wound healing. Recently, conservative treatments utilizing scaffolds have attracted attention as alternatives to surgical therapy, which is highly invasive. Against this background, numerous scaffolds are available in a clinical setting, although they have not surpassed surgery because of their distinct disadvantages. Here, we discuss the plasticity of BMDCs in the skin to maintain homeostasis, in addition to their critical roles on recovery from disrupted homeostasis. We also share our perspective on how scaffolds can be developed to establish scaffolds beyond surgery to regenerate skin structure during wound healing by maximally utilizing the plasticity of BMDCs.

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Epidermis–dermis junction as a novel location for bone marrow-derived cells to reside in response to ionizing radiation

Cited by 4 publications

References 23 publications

Hyperglycemia Induces Skin Barrier Dysfunctions with Impairment of Epidermal Integrity in Non-Wounded Skin of Type 1 Diabetic Mice

Hyperglycemia Induces Skin Barrier Dysfunctions with Impairment of Epidermal Integrity in Non-Wounded Skin of Type 1 Diabetic Mice

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

Plasticity of bone marrow-derived cell differentiation depending on microenvironments in the skin

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