Evaluation of the Antiangiogenic Effect of Kringle 1-5 in a Rat Glioma Model

Lin, Yuan-Mao; Tsai, Ming-Tzu; Lo, Ming-Jei; Chang, Shao-En; Shih, Yang-Hsin; Lee, Meng-Jen; Kuo, Huai-Sheng; Kuo, Wen-Chun; Huang, Wen Cheng; Cheng, Henrich; Huang, Miller

doi:10.1227/neu.0b013e31822f3aea

Cited by 4 publications

(3 citation statements)

References 45 publications

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“…C6-1 cell clones have been used in our laboratory and other laboratories to form aggressive glioma in rat brains. 17,19,20 In this study, the transplantation of 1× 10 6 cells of the 2 C6 clones into rat cerebral cortex was carried out to compare the tumorigenicity of C6-1 with C6-2. The median survival of C6-1 tumor-bearing rats was 12 days after implantation (dpi) (Fig.…”

Section: Proliferation and Tumorigenicity Of C6-1 And C6-2 Glioma Cellsmentioning

confidence: 99%

Induced interleukin-33 expression enhances the tumorigenic activity of rat glioma cells

et al. 2013

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Section: Proliferation and Tumorigenicity Of C6-1 And C6-2 Glioma Cellsmentioning

confidence: 99%

Induced interleukin-33 expression enhances the tumorigenic activity of rat glioma cells

et al. 2013

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“…C6 cultures were maintained in ATCC-formulated F-12 K Medium supplemented with 2.5% FBS and 12.5% horse serum during cell expansion. C6 glioma were adapted to DMEM + 10% FBS one passage before cDNA transfection experiments and thereafter [28]. …”

Section: Methodsmentioning

confidence: 99%

Cytoprotective and anti-inflammatory effects of PAL31 overexpression in glial cells

et al. 2014

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BackgroundAcute spinal cord injury (SCI) leads to a series of reactive changes and causes severe neurological deficits. A pronounced inflammation contributes to secondary pathology after SCI. Astroglia respond to SCI by proliferating, migrating, and altering phenotype. The impact of reactive gliosis on the pathogenesis of SCI is not fully understood. Our previous study has identified an inflammatory modulating protein, proliferation related acidic leucine-rich protein (PAL31) which is upregulated in the microglia/macrophage of injured cords. Because PAL31 participates in cell cycle progression and reactive astroglia often appears in the injured cord, we aim to examine whether PAL31 is involved in glial modulation after injury.ResultsEnhanced PAL31 expression was shown not only in microglia/macrophages but also in spinal astroglia after SCI. Cell culture study reveal that overexpression of PAL31 in mixed glial cells or in C6 astroglia significantly reduced LPS/IFNγ stimulation. Further, enhanced PAL31 expression in C6 astroglia protected cells from H2O2 toxicity; however, this did not affect its proliferative activity. The inhibiting effect of PAL31 on LPS/IFNγ stimulation was observed in glia or C6 after co-culture with neuronal cells. The results demonstrated that the overexpressed PAL31 in glial cells protected neuronal damages through inhibiting NF-kB signaling and iNOS.ConclusionsOur data suggest that PAL31upregulation might be beneficial after spinal cord injury. Reactive gliosis might become a good target for future therapeutic interventions.

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“…Kringle domain exists extensively in plasminogen and apolipoprotein, veri ed to play a key role in the inhibition of angiogenesis ,especially Kringle (K ). [7][8][9][10][11] Plasminogen Kringe is con rmed to suppress angiogenesis in gastric cancer, hepatocellular carcinoma and corneal neovascularization. [12][13][14] And Don J.…”

Section: Introductionmentioning

confidence: 99%

Exosome-Mediated Delivery of an Anti-Angiogenic Peptide Inhibits Corneal Neovascularization via VDAC1 and Autophagy

Chen

2022

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Background: Angiogenesis is a crucial reason for the poor prognosis of corneal diseases. KV11, an undecanoic peptide from Kringle Ⅴ domain derived from apolipoprotein(a) is identified to inhibit angiogenesis significantly. Given the poor permeability and instability of small peptide, we aim to use exosome and its anchoring peptide CP05 to deliver KV11 to alkali-burn cornea tissue and inhibit corneal neovascularization.Methods: In vitro, we tested the effect of EXO-KV11 on inhibition of angiogenesis with the method of tube formation, transwell migration assay and CCK-8. In vivo, we used subconjunctival injection of EXO-KV11 to the alkali-burn cornea-induced corneal neovascularization rat model and fluorescent angiography to directly detect the impact on corneal neovascularization. We also revealed the underlying mechanism by western blot.Results: EXO-KV11 was verified to suppress endothelial cells tube formation, migration and proliferation in vitro by tube formation assay, transwell migration assay and CCK-8 assy. EXO-KV11 was more efficiently delivered to cornea tissue and suppressed more corneal neovascularization in alkali burn-induced corneal neovascularization model. Furthermore, VDAC1 might be potential receptor for KV11 and KV11 stimulated PERK and blocked up autography flux.Conclusions: We used exosomes to delivery KV11 into cells and cornea tissue. We reported that EXO-KV11 could inhibit angiogenesis more than KV11 both in vitro and in vivo. Thus exosome-CP05 drug delivery system has promising prospect in the future.

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Evaluation of the Antiangiogenic Effect of Kringle 1-5 in a Rat Glioma Model

Abstract: Kringle 1-5 effectively reduces the growth of malignant gliomas in the rat. Although still far from translation in humans, K1-5 might be a possible future alternative treatment option for patients with gliomas.

Cited by 4 publications

References 45 publications

Induced interleukin-33 expression enhances the tumorigenic activity of rat glioma cells

Induced interleukin-33 expression enhances the tumorigenic activity of rat glioma cells

Cytoprotective and anti-inflammatory effects of PAL31 overexpression in glial cells

Exosome-Mediated Delivery of an Anti-Angiogenic Peptide Inhibits Corneal Neovascularization via VDAC1 and Autophagy

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