Degradome Products of the Matricellular Protein CCN1 as Modulators of Pathological Angiogenesis in the Retina

Choi, Jinok; Lin, Ann; Shrier, Eric M.; Lau, Lester F.; Grant, Maria B.; Chaqour, Brahim

doi:10.1074/jbc.m113.475418

Cited by 29 publications

(38 citation statements)

References 59 publications

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“…To test whether enhanced expression of the endogenous CCN1 gene in miR-155 Ϫ/Ϫ mouse retina contributed to the vascular phenotype following OIR, mouse pup eyes were injected at P4 prior to OIR with a lentiviral vector encoding a mutant form of the CCN1 protein lacking the C-terminal domain. This mutant variant acts as a dominant negative form of the wild type protein and inhibits CCN1 activity (20). Retinal vessel sensitivity to hyperoxia at P12 was not affected by injection of lnv-CCN1-⌬CT because the degree of vaso-obliteration was similar to that of retinas from eyes injected with the control vector (data not shown).…”

Section: Microrna Expression Profile In the Retina Of Oir Mice-mentioning

confidence: 75%

“…A study by Roitbak et al (48) has demonstrated that interference with miR-155 in endothelial cells significantly enhances capillary tube formation, including the number of tubule branch points and tubular length. Interestingly, the direct effects of recombinant CCN1 on capillary tube formation recapitulate those of miR-155 inhibition (20,51). The CCN1 protein regulates several aspects of endothelial cell function, including adhesion, migration, proliferation, and survival.…”

Section: Discussionmentioning

confidence: 90%

“…The antiangiogenic functions of miR-155 correlate with the repression of CCN1, a secreted cysteine-rich and integrin-binding matricellular protein that positively regulates angiogenic signaling either directly by modulating endothelial cell function and behavior through integrin binding or indirectly by fine tuning the activity of growth factor receptors, such as vascular endothelial growth factor (VEGF) receptor (20,21). We report for the first time how miR-155-dependent suppression of CCN1 regulates both physiological and pathological angiogenesis, at least in part, by modulating the inflammatory response of the retina.…”

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confidence: 99%

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Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

Yan

Lee

Lazzaro

et al. 2015

Journal of Biological Chemistry

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Background: MicroRNA-155 is a proinflammatory small RNA, but its function in pathological angiogenesis is unknown. Results: MicroRNA-155 deficiency increases angiogenic protein CCN1 expression, which harnesses retinal neovascularization by reducing both microglia activation and inflammation. Conclusion: The microRNA-155/CCN1 regulatory axis regulates angiogenic and inflammatory responses in the retina. Significance: Modulation of microRNA-155 and CCN1 interaction is potentially beneficial in retinal neovascularization therapy.

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Section: Microrna Expression Profile In the Retina Of Oir Mice-mentioning

confidence: 75%

Section: Discussionmentioning

confidence: 90%

mentioning

confidence: 99%

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Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

Yan

Lee

Lazzaro

et al. 2015

Journal of Biological Chemistry

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“…Statistical analyses were performed using the Prism software for Windows Version 4 from GraphPad, as previously described (Choi et al, 2013;Liu et al, 2008).…”

Section: Statistical Analysesmentioning

confidence: 99%

The matricellular protein CCN1 controls retinal angiogenesis by targeting VEGF, Src homology 2 domain phosphatase-1 and Notch signaling

et al. 2015

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Physiological angiogenesis depends on the highly coordinated actions of multiple angiogenic regulators. CCN1 is a secreted cysteine-rich and integrin-binding matricellular protein required for proper cardiovascular development. However, our understanding of the cellular origins and activities of this molecule is incomplete. Here, we show that CCN1 is predominantly expressed in angiogenic endothelial cells (ECs) at the leading front of actively growing vessels in the mouse retina. Endothelial deletion of CCN1 in mice using a Cre-Lox system is associated with EC hyperplasia, loss of pericyte coverage and formation of dense retinal vascular networks lacking the normal hierarchical arrangement of arterioles, capillaries and venules.

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“…It is interesting to note that degradome products of this matricellular protein may modulate the pathological angiogenesis in the retina [20]. The PLAGL1 (pleiomorphic adenoma gene-like 1) gene encodes a C2H2 zinc finger protein, which is a transcriptional regulator with anti-proliferative properties [21,22].…”

Section: Experimental Researchmentioning

confidence: 99%

Expression of Endoplasmic Reticulum Stress Related Genes in Blood Cells of Obese Boys with and without Insulin Resistance

Minchenko¹

2015

Int J Biomed

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Objective: to study the changes in the expression level of the subset of genes, encoding for important cell growth factors and enzymes, which play an important role in the control of cellular growth and apoptosis, in blood cells of obese boys with and without insulin resistance for evaluation of its possible significance in the development of obesity and impaired insulin sensitivity. Material and Methods:We studied the expression of genes, which are responsible for control of cell growth and survival, in blood cells of obese boys with normal and impaired insulin sensitivity as compared to normal (control) individuals.Results: It was shown that the expression level of PLAGL, CYR61, ITGA5, and TFPI2 genes is increased, but the GADD45A gene is decreased in blood cells of obese children with normal insulin sensitivity as compared to the control group. Insulin resistance in obese boys leads to the up-regulation of PPP1R15A and PLAGL1 gene expressions as well as to the down-regulation of TFPI2, GADD45A, ALDH1A2, CYR61, and HSPA6 genes in blood cells as compared to obese patients with normal insulin sensitivity.Conclusion: Results of this study provide evidence that obesity affects the expression of the subset of genes related to the control of cell growth and survival in blood cells and that impaired insulin sensitivity in obesity is associated with changes in the expression level of PLAGL, CYR61, GADD45A, PPP1R15A, TFPI2, ALDH1A2, and HSPA6 genes, which possibly contributes to the development of obesity and its metabolic complications, including insulin resistance.

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Degradome Products of the Matricellular Protein CCN1 as Modulators of Pathological Angiogenesis in the Retina

Cited by 29 publications

References 59 publications

Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

The matricellular protein CCN1 controls retinal angiogenesis by targeting VEGF, Src homology 2 domain phosphatase-1 and Notch signaling

Expression of Endoplasmic Reticulum Stress Related Genes in Blood Cells of Obese Boys with and without Insulin Resistance

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