Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo.

Angiolillo, Anne; Sgadari, Cecilia; Taub, D.; Liao, Fang; Farber, Joshua M.; Maheshwari, S.; Kleinman, Hynda K.; Reaman, Gregory H.; Tosato, Giovanna

doi:10.1084/jem.182.1.155

Cited by 637 publications

(428 citation statements)

References 27 publications

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“…This possibility is raised by the recently reported capacity of human IP -10 for inhibiting endothelial cell growth, although the expression of the IP-10 receptor CXCR3 by normal and transformed endothelial cells is still a matter of controversy. 27,51,52 H5V cell cultures failed to express CXCR3 and were not sensitive to the MVMpmediated production of IP-10 (present work and Ref. [27 ]).…”

Section: Discussionsupporting

confidence: 56%

“…27,51,52 H5V cell cultures failed to express CXCR3 and were not sensitive to the MVMpmediated production of IP-10 (present work and Ref. [27 ]). Hence, the CXCR3 expression detected in H5V tumors in vivo can tentatively be assigned to infiltrating activated T and NK cells.…”

Section: Discussionsupporting

confidence: 56%

“…20 -26 Although the mechanism of IP -10 -induced tumor suppression has not yet been fully elucidated, both antiangiogenic and immune system -mediated effects appear to be essential to the antitumor activity of this chemokine in vivo. 27,28 Interestingly, IP-10 can act as an inverse agonist of the G -protein -coupled receptor homologue encoded by Kaposi's sarcoma -associated HHV-8, and thereby inhibit the constitutive signaling occurring in transformed cells 29 These facts prompted us to attempt to combine, in a recombinant vector MVMp /IP -10, the immunomodulating /angiostatic properties of IP -10 with the oncotropic / oncostatic features of MVMp, and to test the protective effect of MVMp / IP-10 against malignant hemangiosarcoma (H5V ) implanted into syngeneic immunocompetent mice. In the present preclinical study, wild -type MVMp was found to inhibit H5V tumor progression, provided that infection was carried out ex vivo to ensure that most cancer cells were hit.…”

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confidence: 99%

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Suppression of metastatic hemangiosarcoma by a parvovirus MVMp vector transducing the IP-10 chemokine into immunocompetent mice

et al. 2002

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We have previously shown that the growth of human tumor xenografts in immunodeficient mice can be efficiently suppressed upon infection with the autonomous parvovirus H -1 or with cytokine -transducing derivatives thereof. To further evaluate the benefits of implementing parvoviruses in cancer gene therapy, we have created a new recombinant vector, MVMp / IP -10, transducing the immunoactive, antiangiogenic chemokine IP -10, and used this virus to treat syngeneic tumors grown in immunocompetent mice. Intratumoral / intraperitoneal administration of only 3Â10 7 replication units of MVMp / IP -10 per animal strongly inhibited the progression of established H5V cell -induced vascular tumors, a highly malignant mouse model for human cavernous hemangioma and Kaposi's sarcoma. Retardation of recurrent tumor growth and suppression of life -threatening metastatic dissemination to internal organs were accompanied by a striking delay in hemangioma -associated mortality. Parental MVMp did not have a significant effect under these conditions up to the dose of 10 10 infectious units / animal, but had strong antihemangiosarcoma activity when used to infect H5V cells ex vivo prior to implantation. In all cases, virus therapy was very well tolerated. Virus -induced suppression of hemangiosarcoma was dependent on host T cells and associated with intratumoral persistence of IFN -expressing cytotoxic lymphocytes, and led to the reduced expression of hepatic plasminogen activator inhibitor -1 ( PAI -1 ), a metastasis -linked marker. This proof of principle study demonstrates that MVMp / IP -10 can aid the treatment of vascular tumors and that autonomous parvovirus -based vectors can be considered potent tools for cancer gene therapy purposes.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionsupporting

confidence: 56%

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confidence: 99%

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Suppression of metastatic hemangiosarcoma by a parvovirus MVMp vector transducing the IP-10 chemokine into immunocompetent mice

et al. 2002

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“…CXCL10 inhibits angiogenesis151, 152, 153 and preferentially recruits Th1154 through CXCR3. The actions of the detrimental inflammatory cytokines are also summarized in Table 2.…”

Section: Roles Of Inflammatory Cytokines In Sci Repairmentioning

confidence: 99%

Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents

et al. 2018

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The balance of inflammation is critical to the repair of spinal cord injury (SCI), which is one of the most devastating traumas in human beings. Inflammatory cytokines, the direct mediators of local inflammation, have differential influences on the repair of the injured spinal cord. Some inflammatory cytokines are demonstrated beneficial to spinal cord repair in SCI models, while some detrimental. Various animal researches have revealed that local delivery of therapeutic agents efficiently regulates inflammatory cytokines and promotes repair from SCI. Quite a few clinical studies have also shown the promotion of repair from SCI through regulation of inflammatory cytokines. However, local delivery of a single agent affects only a part of the inflammatory cytokines that need to be regulated. Meanwhile, different individuals have differential profiles of inflammatory cytokines. Therefore, future studies may aim to develop personalized strategies of locally delivered therapeutic agent cocktails for effective and precise regulation of inflammation, and substantial functional recovery from SCI.

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“…CXCL10 inhibits bone marrow colony formation by CD34 + cells in the presence of stem cell growth factor (SCGF), colony stimulating factor 2 (granulocyte-macrophage) (CSF2; GM-CSF), or a combination of SCGF and erythropoietin (EPO). Moreover, CXCL10 has antitumor activity in vivo and is a potent inhibitor of angiogenesis [26]. This antitumor activity appears to be mediated by the ability of CXCL10 to recruit lymphocytes, neutrophils, and monocytes into inflammatory infiltrates.…”

Section: Introductionmentioning

confidence: 99%

Identification of genes differentially expressed in T cells following stimulation with the chemokines CXCL12 and CXCL10

Smith

Shaw

et al. 2004

BMC Immunol

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BackgroundChemokines are involved in many biological activities ranging from leukocyte differentiation to neuronal morphogenesis. Despite numerous reports describing chemokine function, little is known about the molecular changes induced by cytokines.MethodsWe have isolated and identified by differential display analysis 182 differentially expressed cDNAs from CXCR3-transfected Jurkat T cells following treatment with CXCL12 or CXCL10. These chemokine-modulated genes were further verified using quantitative RT-PCR and Western blot analysis.ResultsOne hundred and forty-six of the cDNAs were successfully cloned, sequenced, and identified by BLAST. Following removal of redundant and non-informative clones, seventeen mRNAs were found to be differentially expressed post treatment with either chemokine ligand with several representing known genes with established functions. Twenty-one genes were upregulated in these transfected Jurkat cells following both CXCL12 and CXCL10, four genes displayed a discordant response and seven genes were downregulated upon treatment with either chemokine. Identified genes include geminin (GEM), thioredoxin (TXN), DEAD/H box polypeptide 1 (DDX1), growth hormone inducible transmembrane protein (GHITM), and transcription elongation regulator 1 (TCERG1). Subsequent analysis of several of these genes using semi-quantitative PCR and western blot analysis confirmed their differential expression post ligand treatment.ConclusionsTogether, these results provide insight into chemokine-induced gene activation and identify potentially novel functions for known genes in chemokine biology.

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Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo.

Cited by 637 publications

References 27 publications

Suppression of metastatic hemangiosarcoma by a parvovirus MVMp vector transducing the IP-10 chemokine into immunocompetent mice

Suppression of metastatic hemangiosarcoma by a parvovirus MVMp vector transducing the IP-10 chemokine into immunocompetent mice

Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents

Identification of genes differentially expressed in T cells following stimulation with the chemokines CXCL12 and CXCL10

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