Differential role of reactive oxygen species in the activation of mitogen‐activated protein kinases and Akt by key receptors on B‐lymphocytes: CD40, the B cell antigen receptor, and CXCR4

Lee, Rosaline L.; Westendorf, Jens; Gold, Michael R.

doi:10.1007/s12079-007-0006-y

Cited by 35 publications

(23 citation statements)

References 103 publications

(142 reference statements)

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“…SDF-1 is a member of the C-X-C chemokine subfamily and the only known ligand for the G protein-coupled receptor CXCR4 [17,18]. It has been shown that CXCR4 is expressed in malignant tumors and the SDF-1/CXCR4 interaction is involved in tumor progression, particularly brain and breast cancers [19]. Binding of SDF-1 to CXCR4 leads to stimulation of intracellular signaling that involves activation of multiple targets, including ERK1/2, MAPK, JNK, and AKT effectors [20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Role of the stromal-derived factor-1 (SDF-1)–CXCR4 axis in the interaction between hepatic stellate cells and cholangiocarcinoma

Gentilini

Rombouts

Galastri

et al. 2012

Journal of Hepatology

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Section: Introductionmentioning

confidence: 99%

Role of the stromal-derived factor-1 (SDF-1)–CXCR4 axis in the interaction between hepatic stellate cells and cholangiocarcinoma

Gentilini

Rombouts

Galastri

et al. 2012

Journal of Hepatology

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“…Upon SDF-1 binding to the CXCR4 receptor, there is a signaling pathway that involves transient production of ROS and the activation of phosphoinositide 3-kinase (PI3K) to eventually promote cell migration and survival. 24,25 Cells in culture increase intracellular ROS within seconds when stimulated with SDF-1. 27 The activation of RAGE increases levels of ROS in the cell 28 and signals mDia1, an intracellular signaling partner to RAGE, which has been implicated in smooth muscle cell migration and expansion.…”

Section: Discussionmentioning

confidence: 99%

“…12 Thus, ROS is a common intracellular messenger in the signaling pathways activated by CXCR4 and RAGE. On the one hand, the ROS spike is integral to the SDF-1 signaling pathway, 24,25 and on the other hand, AGE binding to RAGE increases ROS levels. 28 Since the site of ROS generation in both cases is in the cytosol, 24,28 it is plausible that the two pathways intersect in a negative way.…”

Section: Discussionmentioning

confidence: 99%

“…SDF-1 triggers a burst in ROS, which is critical to propagate the signal downstream to eventually cause cell migration. 24,25 We therefore investigated the ability of SDF-1 to increase ROS levels in HL-60 cells after preincubation in normoglycemic versus hyperglycemic conditions. For this purpose, after 24 h of preincubation in normal glucose, highglucose, glucose decoy, or high-glucose + sRAGE conditions, HL-60 cells were stained with the superoxide-sensitive dye DHE.…”

Section: Hyperglycemia Impairs Sdf-1-mediated Signaling Which Is Resmentioning

confidence: 99%

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Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments

Olekson

Faulknor

Hsia

et al. 2016

Advances in Wound Care

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Objective: In diabetes, hyperglycemia causes the accumulation of advanced glycation end products (AGEs) that trigger reactive oxygen species (ROS) generation through binding the receptor for AGEs (RAGE). Because exogenous growth factors have had little success in enhancing chronic wound healing, we investigated whether hyperglycemia-induced AGEs interfere with cellular responses to extracellular signals. We used stromal cell-derived factor-1 (SDF-1), an angiogenic chemokine also known to promote stem cell recruitment in skin wounds. Approach: Human leukemia-60 (HL-60) cells and mouse peripheral blood mononuclear cells (PBMCs), which express the SDF-1 receptor CXCR-4, were incubated for 24 h in medium supplemented with 25 mM d-glucose. Soluble RAGE (sRAGE) was used to block RAGE activation. Response to SDF-1 was measured in cellular migration and ROS assays. A diabetic murine excisional wound model measured SDF-1 liposome and sRAGE activity in vivo. Results: Hyperglycemia led to significant accumulation of AGEs, decreased SDF-1-directed migration, and elevated baseline ROS levels; it suppressed the ROS spike normally triggered by SDF-1. sRAGE decreased the ROS baseline and restored both the SDF-1-mediated spike and cell migration. Topically applied sRAGE alone promoted healing and enhanced the effect of exogenous SDF-1 on diabetic murine wounds. Innovation: While there is interest in using growth factors to improve wound healing, this strategy is largely ineffective in diabetic wounds. We show that sRAGE may restore signaling, thus potentiating the effect of exogenously applied growth factors. Conclusion: Blocking RAGE with sRAGE restores SDF-1-mediated cellular responses in hyperglycemic environments and may potentiate the effectiveness of SDF-1 applied in vivo.

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“…This pathway is triggered by HBO 2 in localized vasculogenic stem cells, which augments VEGF and SDF-1 synthesis, enhancing neovascularization (115,116). Subsequent signaling between SDF-1 and its cognate cellular receptor, CXCR4, also involves ROS (89). Likely a synergistic process, lactate can also mediate HIF stabilization in endothelial cells by metabolic conversion to pyruvate that inhibits prolyl hydroxylases (160).…”

Section: Oxygen and Wound Healingmentioning

confidence: 99%

Hyperbaric Oxygen, Vasculogenic Stem Cells, and Wound Healing

Fosen

Thom²

2014

Antioxidants & Redox Signaling

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Significance: Oxidative stress is recognized as playing a role in stem cell mobilization from peripheral sites and also cell function. Recent Advances: This review focuses on the impact of hyperoxia on vasculogenic stem cells and elements of wound healing. Critical Issues: Components of the wound-healing process in which oxidative stress has a positive impact on the various cells involved in wound healing are highlighted. A slightly different view of woundhealing physiology is adopted by departing from the often used notion of sequential stages: hemostatic, inflammatory, proliferative, and remodeling and instead organizes the cascade of wound healing as overlapping events or waves pertaining to reactive oxygen species, lactate, and nitric oxide. This was done because hyperoxia has effects of a number of cell signaling events that converge to influence cell recruitment/chemotaxis and gene regulation/ protein synthesis responses which mediate wound healing. Future Directions: Our alternative perspective of the stages of wound healing eases recognition of the multiple sites where oxidative stress has an impact on wound healing. This aids the focus on mechanistic events and the interplay among various cell types and biochemical processes. It also highlights the areas where additional research is needed.

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Differential role of reactive oxygen species in the activation of mitogen‐activated protein kinases and Akt by key receptors on B‐lymphocytes: CD40, the B cell antigen receptor, and CXCR4

Cited by 35 publications

References 103 publications

Role of the stromal-derived factor-1 (SDF-1)–CXCR4 axis in the interaction between hepatic stellate cells and cholangiocarcinoma

Role of the stromal-derived factor-1 (SDF-1)–CXCR4 axis in the interaction between hepatic stellate cells and cholangiocarcinoma

Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments

Hyperbaric Oxygen, Vasculogenic Stem Cells, and Wound Healing

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