Injury-induced Platelet-derived Growth Factor Receptor-α Expression Mediated by Interleukin-1β (IL-1β) Release and Cooperative Transactivation by NF-κB and ATF-4

Zhang, Ning; Khachigian, Levon M.

doi:10.1074/jbc.m109.025742

Cited by 9 publications

(2 citation statements)

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“…In contrast, inhibitor of IκB kinase (IKK), an upstream activator of NF-κB, shows a significant inhibition of ICAM-1 expression in Müller cells exposed to HG, indicating that the NF-κB pathway is critical for HG-induced ICAM-1 upregulation ( 6 ). In mouse fibroblasts, ATF4 and NF-κB interact, occupy the promoter of platelet-derived growth factor receptor, and induce platelet-derived growth factor receptor transcription in a cooperative manner ( 36 ). Whether ATF4 affects NF-κB transcriptional activity and enhances ICAM-1 expression in retinal Müller cells remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Activation of Endoplasmic Reticulum Stress by Hyperglycemia Is Essential for Müller Cell–Derived Inflammatory Cytokine Production in Diabetes

et al. 2012

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Inflammation plays an important role in diabetes-induced retinal vascular leakage. The purpose of this study is to examine the role of endoplasmic reticulum (ER) stress and the signaling pathway of ER stress–induced activating transcription factor 4 (ATF4) in the regulation of Müller cell–derived inflammatory mediators in diabetic retinopathy. In diabetic animals, elevated ER stress markers, ATF4, and vascular endothelial growth factor (VEGF) expression were partially localized to Müller cells in the retina. In cultured Müller cells, high glucose induced a time-dependent increase of ER stress, ATF4 expression, and inflammatory factor production. Inducing ER stress or overexpressing ATF4 resulted in elevated intracellular adhesion molecule 1 and VEGF proteins in Müller cells. In contrast, alleviation of ER stress or blockade of ATF4 activity attenuated inflammatory gene expression induced by high glucose or hypoxia. Furthermore, we found that ATF4 regulated the c-Jun NH2-terminal kinase pathway resulting in VEGF upregulation. ATF4 was also required for ER stress–induced and hypoxia-inducible factor-1α activation. Finally, we showed that administration of chemical chaperone 4-phenylbutyrate or genetic inhibition of ATF4 successfully attenuated retinal VEGF expression and reduced vascular leakage in mice with STZ-induced diabetes. Taken together, our data indicate that ER stress and ATF4 play a critical role in retinal inflammatory signaling and Müller cell–derived inflammatory cytokine production in diabetes.

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Section: Discussionmentioning

confidence: 99%

Activation of Endoplasmic Reticulum Stress by Hyperglycemia Is Essential for Müller Cell–Derived Inflammatory Cytokine Production in Diabetes

et al. 2012

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“…HDACs play a central role in the epigenetic regulation of gene expression. Recent findings from our group indicate that IL-1␤ facilitates HDAC dissociation from the PDGF receptor ␣ promoter and that HDAC inhibition potentiates induction of PDGF receptor ␣ transcription (15).…”

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confidence: 99%

Histone Deacetylase-1 Is Enriched at the Platelet-derived Growth Factor-D Promoter in Response to Interleukin-1β and Forms a Cytokine-inducible Gene-silencing Complex with NF-κB p65 and Interferon Regulatory Factor-1

Liu

Khachigian

2009

Journal of Biological Chemistry

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Systemic protection through remote ischemic preconditioning is spread by platelet-dependent signaling in mice

Oberkofler¹,

Limani²,

Jang³

et al. 2014

Hepatology

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Remote ischemic preconditioning (RIPC), the repetitive transient mechanical obstruction of vessels at a limb remote to the operative site, is a novel strategy to mitigate distant organ injury associated with surgery. In the clinic, RIPC has demonstrated efficacy in protecting various organs against ischemia reperfusion (IR), but a common mechanism underlying the systemic protection has not been identified. Here, we reasoned that protection may rely on adaptive physiological reponses toward local stress, as is incurred through RIPC. Standardized mouse models of partial hepatic IR and of RIPC to the femoral vascular bundle were applied. The roles of platelets, peripheral serotonin, and circulating vascular endothelial growth factor (Vegf) were studied in thrombocytopenic mice, Tph1−/− mice, and through neutralizing antibodies, respectively. Models of interleukin‐10 (Il10) and matrix metalloproteinase 8 (Mmp8) deficiency were used to assess downstream effectors of organ protection. The protection against hepatic IR through RIPC was dependent on platelet‐derived serotonin. Downstream of serotonin, systemic protection was spread through up‐regulation of circulating Vegf. Both RIPC and serotonin‐Vegf induced differential gene expression in target organs, with Il10 and Mmp8 displaying consistent up‐regulation across all organs investigated. Concerted inhibition of both molecules abolished the protective effects of RIPC. RIPC was able to mitigate pancreatitis, indicating that it can protect beyond ischemic insults. Conclusions: We have identified a platelet‐serotonin‐Vegf‐Il10/Mmp8 axis that mediates the protective effects of RIPC. The systemic action, the conservation of RIPC effects among mice and humans, and the protection beyond ischemic insults suggest that the platelet‐dependent axis has evolved as a preemptive response to local stress, priming the body against impending harm. (Hepatology 2014;60:1409–1417)

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Injury-induced Platelet-derived Growth Factor Receptor-α Expression Mediated by Interleukin-1β (IL-1β) Release and Cooperative Transactivation by NF-κB and ATF-4

Cited by 9 publications

References 50 publications

Activation of Endoplasmic Reticulum Stress by Hyperglycemia Is Essential for Müller Cell–Derived Inflammatory Cytokine Production in Diabetes

Activation of Endoplasmic Reticulum Stress by Hyperglycemia Is Essential for Müller Cell–Derived Inflammatory Cytokine Production in Diabetes

Histone Deacetylase-1 Is Enriched at the Platelet-derived Growth Factor-D Promoter in Response to Interleukin-1β and Forms a Cytokine-inducible Gene-silencing Complex with NF-κB p65 and Interferon Regulatory Factor-1

Systemic protection through remote ischemic preconditioning is spread by platelet-dependent signaling in mice

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