The role of oxygen tension in cell fate and regenerative medicine: implications of hypoxia/hyperoxia and free radicals

Rasouli, Mehdi; Fattahi, Roya; Nuoroozi, Ghader; Zarei-Behjani, Zeinab; Yaghoobi, Maliheh; Hajmohammadi, Zeinab; Hosseinzadeh, Simzar

doi:10.1007/s10561-023-10099-9

Cited by 5 publications

(2 citation statements)

References 173 publications

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“…The primary goal of current clinical treatment is to promote wound closure, in which the migration of epidermal cells from the edge of the wound to the center is a speed-limiting step. Oxygen has been confirmed to be associated with cell proliferation and differentiation [ 39 ]. Many studies have focused on providing oxygen to accelerate wound healing by promoting cell proliferation and migration and angiogenesis [ 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

Early short-term hypoxia promotes epidermal cell migration by activating the CCL2-ERK1/2 pathway and epithelial–mesenchymal transition during wound healing

Jin,

Zhou,

Zhao

et al. 2024

Burns &Amp; Trauma

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Background Due to vasculature injury and increased oxygen consumption, the early wound microenvironment is typically in a hypoxic state. We observed enhanced cell migration ability under early short-term hypoxia. CCL2 belongs to the CC chemokine family and was found to be increased in early hypoxic wounds and enriched in the extracellular signal-regulated kinase (ERK)1/2 pathway in our previous study. However, the underlying mechanism through which the CCL2-ERK1/2 pathway regulates wound healing under early short-term hypoxia remains unclear. Activation of epithelial–mesenchymal transition (EMT) is a key process in cancer cell metastasis, during which epithelial cells acquire the characteristics of mesenchymal cells and enhance cell motility and migration ability. However, the relationship between epithelial cell migration and EMT under early short-term hypoxia has yet to be explored. Methods HaCaT cells were cultured to verify the effect of early short-term hypoxia on migration through cell scratch assays. Lentiviruses with silenced or overexpressed CCL2 were used to explore the relationship between CCL2 and migration under short-term hypoxia. An acute full-thickness cutaneous wound rat model was established with the application of an ERK inhibitor to reveal the hidden role of the ERK1/2 pathway in the early stage of wound healing. The EMT process was verified in all the above experiments through western blotting. Results In our study, we found that short-term hypoxia promoted cell migration. Mechanistically, hypoxia promoted cell migration through mediating CCL2. Overexpression of CCL2 via lentivirus promoted cell migration, while silencing CCL2 via lentivirus inhibited cell migration and the production of related downstream proteins. In addition, we found that CCL2 was enriched in the ERK1/2 pathway, and the application of an ERK inhibitor in vivo and in vitro verified the upstream and downstream relationships between the CCL2 pathway and ERK1/2. Western blot results both in vivo and in vitro demonstrated that early short-term hypoxia promotes epidermal cell migration by activating the CCL2-ERK1/2 pathway and EMT during wound healing. Conclusions Our work demonstrated that hypoxia in the early stage serves as a stimulus for triggering wound healing through activating the CCL2-ERK1/2 pathway and EMT, which promote epidermal cell migration and accelerate wound closure. These findings provide additional detailed insights into the mechanism of wound healing and new targets for clinical treatment.

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Section: Discussionmentioning

confidence: 99%

Early short-term hypoxia promotes epidermal cell migration by activating the CCL2-ERK1/2 pathway and epithelial–mesenchymal transition during wound healing

Jin,

Zhou,

Zhao

et al. 2024

Burns &Amp; Trauma

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“…•− . An enzyme, termed superoxide dismutase (SOD), localized primarily in the matrix or inner membrane of the mitochondria, will convert this ROS to H 2 O 2 [16]. This nonradical can move across the mitochondrial membrane through specific aquaporin channels called peroxiporins [17,18].…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

An Overview of Reactive Oxygen Species Damage Occurring during In Vitro Bovine Oocyte and Embryo Development and the Efficacy of Antioxidant Use to Limit These Adverse Effects

Keane,

Ealy

2024

Animals

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The in vitro production (IVP) of bovine embryos has gained popularity worldwide and in recent years and its use for producing embryos from genetically elite heifers and cows has surpassed the use of conventional superovulation-based embryo production schemes. There are, however, several issues with the IVP of embryos that remain unresolved. One limitation of special concern is the low efficiency of the IVP of embryos. Exposure to reactive oxygen species (ROS) is one reason why the production of embryos with IVP is diminished. These highly reactive molecules are generated in small amounts through normal cellular metabolism, but their abundances increase in embryo culture because of oocyte and embryo exposure to temperature fluctuations, light exposure, pH changes, atmospheric oxygen tension, suboptimal culture media formulations, and cryopreservation. When uncontrolled, ROS produce detrimental effects on the structure and function of genomic and mitochondrial DNA, alter DNA methylation, increase lipid membrane damage, and modify protein activity. Several intrinsic enzymatic pathways control ROS abundance and damage, and antioxidants react with and reduce the reactive potential of ROS. This review will focus on exploring the efficiency of supplementing several of these antioxidant molecules on oocyte maturation, sperm viability, fertilization, and embryo culture.

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Hyperoxia and brain: the link between necessity and injury from a molecular perspective

Simon Machado,

Mathias,

Joaquim

et al. 2024

Neurotox Res

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The role of oxygen tension in cell fate and regenerative medicine: implications of hypoxia/hyperoxia and free radicals

Cited by 5 publications

References 173 publications

Early short-term hypoxia promotes epidermal cell migration by activating the CCL2-ERK1/2 pathway and epithelial–mesenchymal transition during wound healing

Early short-term hypoxia promotes epidermal cell migration by activating the CCL2-ERK1/2 pathway and epithelial–mesenchymal transition during wound healing

An Overview of Reactive Oxygen Species Damage Occurring during In Vitro Bovine Oocyte and Embryo Development and the Efficacy of Antioxidant Use to Limit These Adverse Effects

Hyperoxia and brain: the link between necessity and injury from a molecular perspective

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