Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling
Accumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, in...
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MDPI AG
2021-08-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/16/8992 |
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| author | Islamy Rahma Hutami Takashi Izawa Tsendsuren Khurel-Ochir Takuma Sakamaki Akihiko Iwasa Eiji Tanaka |
| author_facet | Islamy Rahma Hutami Takashi Izawa Tsendsuren Khurel-Ochir Takuma Sakamaki Akihiko Iwasa Eiji Tanaka |
| author_sort | Islamy Rahma Hutami |
| collection | DOAJ |
| description | Accumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, inflammation. Hypoxic conditions generated at a wound site also strongly recruit macrophages and affect their function. Hypoxia inducible factor (HIF)-1α is a transcription factor that contributes to both glycolysis and the induction of inflammatory genes, while also being critical for macrophage activation. For the latter, HIF-1α regulates sphingosine 1-phosphate (S1P) to affect the migration, activation, differentiation, and polarization of macrophages. Recently, S1P and HIF-1α have received much attention, and various studies have been performed to investigate their roles in initiating and resolving inflammation via macrophages. It is hypothesized that the HIF-1α/S1P/S1P receptor axis is an important determinant of macrophage function under inflammatory conditions and during disease pathogenesis. Therefore, in this review, biological regulation of monocytes/macrophages in response to circulating HIF-1α is summarized, including signaling by S1P/S1P receptors, which have essential roles in wound healing. |
| first_indexed | 2024-03-10T08:43:51Z |
| format | Article |
| id | doaj.art-5d44d809d9cd4d7792d72b1134730c24 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T08:43:51Z |
| publishDate | 2021-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-5d44d809d9cd4d7792d72b1134730c242023-11-22T08:03:43ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-08-012216899210.3390/ijms22168992Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P SignalingIslamy Rahma Hutami0Takashi Izawa1Tsendsuren Khurel-Ochir2Takuma Sakamaki3Akihiko Iwasa4Eiji Tanaka5Department of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8504, JapanAccumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, inflammation. Hypoxic conditions generated at a wound site also strongly recruit macrophages and affect their function. Hypoxia inducible factor (HIF)-1α is a transcription factor that contributes to both glycolysis and the induction of inflammatory genes, while also being critical for macrophage activation. For the latter, HIF-1α regulates sphingosine 1-phosphate (S1P) to affect the migration, activation, differentiation, and polarization of macrophages. Recently, S1P and HIF-1α have received much attention, and various studies have been performed to investigate their roles in initiating and resolving inflammation via macrophages. It is hypothesized that the HIF-1α/S1P/S1P receptor axis is an important determinant of macrophage function under inflammatory conditions and during disease pathogenesis. Therefore, in this review, biological regulation of monocytes/macrophages in response to circulating HIF-1α is summarized, including signaling by S1P/S1P receptors, which have essential roles in wound healing.https://www.mdpi.com/1422-0067/22/16/8992HIF1M1/M2 macrophageS1Pwound healing |
| spellingShingle | Islamy Rahma Hutami Takashi Izawa Tsendsuren Khurel-Ochir Takuma Sakamaki Akihiko Iwasa Eiji Tanaka Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling International Journal of Molecular Sciences HIF1 M1/M2 macrophage S1P wound healing |
| title | Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling |
| title_full | Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling |
| title_fullStr | Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling |
| title_full_unstemmed | Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling |
| title_short | Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling |
| title_sort | macrophage motility in wound healing is regulated by hif 1α via s1p signaling |
| topic | HIF1 M1/M2 macrophage S1P wound healing |
| url | https://www.mdpi.com/1422-0067/22/16/8992 |
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