Advanced glycation end products promote VEGF expression and thus choroidal neovascularization via Cyr61-PI3K/AKT signaling pathway

Sun, Lu; Huang, Tonglie; Xu, W.; Sun, Jiaxing; Lv, Yang; Wang, Yusheng

doi:10.1038/s41598-017-14015-6

Cited by 28 publications

(23 citation statements)

References 41 publications

(12 reference statements)

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“…It was observed that mangiferin administration in presence of cisplatin can upregulate the expression of Nrf-2 in the renal tissue via the activation of PI3K. Previous reports also showed that mangiferin exposure only alters the expression of p-PI3K without altering the expression of total PI3K ( Qi et al, 2017 ; Zou et al, 2017 ). Besides, p-PI3K can directly upregulate the expression of Nrf-2 and can significantly promote cell survival ( Saha et al, 2016c ).…”

Section: Discussionmentioning

confidence: 99%

Mangiferin Ameliorates Cisplatin Induced Acute Kidney Injury by Upregulating Nrf-2 via the Activation of PI3K and Exhibits Synergistic Anticancer Activity With Cisplatin

et al. 2018

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Occurrence of oxidative stress is the principal cause of acute kidney injury induced by cisplatin. Mangiferin, a naturally occurring antioxidant molecule, is found to ameliorate several oxidative stress mediated pathophysiological conditions including cancer. Cisplatin induced cytotoxicity was measured in NKE cells by MTT assay and microscopic analysis. Induction of oxidative stress and regulation of proapoptotic molecules were subsequently investigated by using different spectrophotometric analyses, FACS and immunocytochemistry. Induction of nephrotoxicity was determined by analyzing different serum biomarkers and histological parameters in vivo using swiss albino mice. Activation of NF-κB mediated pro-inflammatory and caspase dependent signaling cascades were investigated by semi-quantitative RT-PCR and immunoblotting. Mangiferin was found to ameliorate cisplatin induced nephrotoxicity in vitro and in vivo by attenuating the induction of oxidative stress and upregulating Nrf-2 mediated pro-survival signaling cascades via the activation of PI3K. Additionally, mangiferin showed synergistic anticancer activity with cisplatin in cancer cell lines (MCF-7 and SKRC-45) and EAC cell induced solid tumor bearing experimental mice. The ameliorative effect of mangiferin is primarily attributed to its anti-oxidant and anti-inflammatory properties. It acts differentially in normal tissue cells and tumor cells by modulating different cell survival regulatory signaling molecules. For the first time, the study reveals a mechanistic basis of mangiferin action against cisplatin induced nephrotoxicity. Since Mangiferin shows synergistic anticancer activity with cisplatin, it can be considered as a promising drug candidate, to be used in combination with cisplatin.

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Section: Discussionmentioning

confidence: 99%

Mangiferin Ameliorates Cisplatin Induced Acute Kidney Injury by Upregulating Nrf-2 via the Activation of PI3K and Exhibits Synergistic Anticancer Activity With Cisplatin

et al. 2018

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“…These three genes have an important role in the PI3K/AKT cell migration and proliferation related pathways. In fact, ENG and PECAM1 have a great influence over one another, and PECAM1 deficiently is associated with ENG reduction [ 56 , 57 ]. capping actin protein (CAPG) is also more highly expressed in SAT than in VAT.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Risk Factors and Differential Transcriptomic Profile of the Subcutaneous and Visceral Adipose Tissue and Their Resident Stem Cells

Arderiu

Lambert

Ballesta

et al. 2020

Cells

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Background: The increase in the incidence of obesity and obesity-related cardiovascular risk factors (CVRFs) over the last decades has brought attention on adipose tissue (AT) pathobiology. The expansion of AT is associated with the development of new vasculature needed to perfuse the tissue; however, not all fat depots have the same ability to induce angiogenesis that requires recruitment of their own endothelial cells. In this study we have investigated the effect of different CVRFs, on the angiogenic capacity of the subcutaneous (SAT) and visceral (VAT) adipose tissue and on the function of their mesenchymal cell reservoir. Methods: A transcriptomic approach was used to compare the different angiogenic and inflammatory profiles of the subcutaneous and visceral fat depots from individuals with obesity, as well as their resident stem cells (ASCs). Influence of other risk factors on fat composition was also measured. Finally, the microvesicles (MVs) released by ASCs were isolated and their regenerative potential analyzed by molecular and cellular methodologies. Results: Obesity decreases the angiogenic capacity of AT. There are differences between SAT and VAT; from the 21 angiogenic-related genes analyzed, only three were decreased in SAT compared with those decreased in VAT. ASCs isolated from both fat depots showed significant differences; there was a significant up-regulation of the VEGF-pathway on visceral derived ASCs. ASCs release MVs that stimulate endothelial cell migration and angiogenic capacity. Conclusions: In patients with obesity, SAT expresses a greater number of angiogenic molecules than VAT, independent of the presence of other CVRFs.

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“…; Sun et al . ). For immunoblots, lysates were separated on a 4–12% gradient sodium dodecyl sulfate‐polyacrylamide gel and transferred to a polyvinylidene fluoride membrane.…”

Section: Methodsmentioning

confidence: 97%

“…The following antibodies were selected for immunoblotting: rabbit anti-GluN1 (#G-8913, 1 : 1000; Sigma-Aldrich; RRID: AB_259978), rabbit anti-ERK1/2 (#4695, 1 : 1000; Cell Signaling Technology, Danvers, MA, USA; RRID: AB_390779), rabbit anti-p38 (#8690, 1 : 1000; Cell Signaling Technology; RRID: AB_10999090), and rabbit anti-SAPK/JNK (#9252, 1 : 1000; Cell Signaling Technology; RRID:AB_2250373). The specificity of these antibodies was validated in previous studies (Rudhard et al 2003;Brady et al 2017;Li et al 2017;Sun et al 2017). For immunoblots, lysates were separated on a 4-12% gradient sodium dodecyl sulfate-polyacrylamide gel and transferred to a polyvinylidene fluoride membrane.…”

Section: Co-immunoprecipitationmentioning

confidence: 99%

Mitogen‐activated protein kinase signaling mediates opioid‐induced presynaptic NMDA receptor activation and analgesic tolerance

Deng

Chen

Luo

et al. 2018

Journal of Neurochemistry

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Opioid-induced hyperalgesia and analgesic tolerance can lead to dose escalation and inadequate pain treatment with μ-opioid receptor agonists. Opioids cause tonic activation of glutamate NMDA receptors (NMDARs) at primary afferent terminals, increasing nociceptive input. However, the signaling mechanisms responsible for opioid-induced activation of presynaptic NMDARs in the spinal dorsal horn remain unclear. In the present study, we determined the role of mitogen-activated protein kinase (MAPK) signaling in opioid-induced presynaptic NMDAR activation caused by chronic morphine administration. Whole-cell recordings of excitatory postsynaptic currents (EPSCs) were performed on dorsal horn neurons in rat spinal cord slices. Chronic morphine administration markedly increased the frequency of miniature EPSCs, increased the amplitude of monosynaptic EPSCs evoked from the dorsal root, and reduced the paired-pulse ratio of evoked EPSCs. These changes were fully reversed by an NMDAR antagonist and normalized by inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2), p38, or c-Jun N-terminal kinase (JNK). Furthermore, intrathecal injection of a selective ERK1/2, p38, or JNK inhibitor blocked pain hypersensitivity induced by chronic morphine treatment. These inhibitors also similarly attenuated a reduction in morphine’s analgesic effect in rats. In addition, co-immunoprecipitation assays revealed that NMDARs formed a protein complex with ERK1/2, p38, and JNK in the spinal cord and that chronic morphine treatment increased physical interactions of NMDARs with these three MAPKs. Our findings suggest that opioid-induced hyperalgesia and analgesic tolerance are mediated by tonic activation of presynaptic NMDARs via three functionally interrelated MAPKs at the spinal cord level.

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Advanced glycation end products promote VEGF expression and thus choroidal neovascularization via Cyr61-PI3K/AKT signaling pathway

Cited by 28 publications

References 41 publications

Mangiferin Ameliorates Cisplatin Induced Acute Kidney Injury by Upregulating Nrf-2 via the Activation of PI3K and Exhibits Synergistic Anticancer Activity With Cisplatin

Mangiferin Ameliorates Cisplatin Induced Acute Kidney Injury by Upregulating Nrf-2 via the Activation of PI3K and Exhibits Synergistic Anticancer Activity With Cisplatin

Cardiovascular Risk Factors and Differential Transcriptomic Profile of the Subcutaneous and Visceral Adipose Tissue and Their Resident Stem Cells

Mitogen‐activated protein kinase signaling mediates opioid‐induced presynaptic NMDA receptor activation and analgesic tolerance

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