Differential activity of pro-angiogenic CXC chemokines

Moldobaeva, Aigul; Baek, Amy E.; Eldridge, Lindsey; Wagner, Elizabeth M.

doi:10.1016/j.mvr.2010.01.011

Cited by 12 publications

(7 citation statements)

References 26 publications

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“…; Moldobaeva et al. ), results are consistent with a paracrine role of CD11b + interstitial macrophages for ischemia‐induced angiogenesis. Furthermore, coculture of macrophages with systemic endothelium but not pulmonary endothelial cells showed enhanced endothelial cell proliferation.…”

Section: Discussionsupporting

confidence: 76%

CD11b⁺ interstitial macrophages are required for ischemia-induced lung angiogenesis

et al. 2018

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The importance of myeloid cells in promoting neovascularization has been shown in a number of pathological settings in several organs. However, the specific role of macrophages in promoting systemic angiogenesis during pulmonary ischemia is not fully determined. Our past work suggested that cells of monocytic lineage contributed to systemic angiogenesis in the lung since clodronate‐induced depletion of all macrophages resulted in attenuated neovascularization. Our current goals were to define the population of macrophages important for systemic vessel growth into the lung after the onset of pulmonary ischemia in mice. Interstitial macrophages (CD64+ MerTK + CD11b+) increased significantly as did the percent of CD45+ Ly6G+ neutrophils 1 day after the induction of left lung ischemia, despite the fact there was limited cell recruitment due to complete obstruction of the left pulmonary artery in this ischemia model. Since both interstitial macrophages and neutrophils express CD11b, we used CD11b+ DTR mice and showed the critical role for these cells since CD11b+ depleted mice showed no systemic angiogenesis 7 days after the onset of ischemia when compared to control mice. Coculture of mouse aortic endothelial cells with macrophages showed increased proliferation relative to endothelial cells in culture without inflammatory cells, or pulmonary artery endothelial cells. We conclude that CD11b+ leukocytes, trapped within the lung at the onset of ischemia, contribute to growth factor release, and are critical for new blood vessel proliferation.

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Section: Discussionsupporting

confidence: 76%

CD11b⁺ interstitial macrophages are required for ischemia-induced lung angiogenesis

et al. 2018

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“…The key role of ELR + CXC chemokines in angiogenesis determines their fundamental position in the abnormal regulation of angiogenesis during the development of malignant tumors. This viewpoint is supported by a great number of studies (27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 83%

The effect of NFATc1 on vascular generation and the possible underlying mechanism in epithelial ovarian carcinoma

Duan

et al. 2016

International Journal of Oncology

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We investigated the effect of nuclear factor of activated T cells c1 (NFATc1) on the growth and vascular generation of human ovarian carcinoma SKOV3 cell-transplanted tumors in nude mice and explored the possible underlying mechanism. NFATc1 siRNA was transfected into the SKOV3 cells, which were then subjected to immunofluorescence tests and real-time reverse transcription polymerase chain reaction (RT-PCR) to determine the transfection-induced inhibition rate. The tumor volumes in the nude mice in all groups were measured to determine the in vivo antitumor effect of NFATc1 siRNA. Immunohistochemical (IHC) methods were employed to detect NFATc1 expression in tumor tissue, combined with cytokeratin (CK) staining to label the epithelial origin of the tumor tissue. CD34 and podoplanin were used as markers for labeling microvessels and microlymphatic vessels, respectively. The densities of microvessels and microlymphatic vessels in each group were calculated and statistically analyzed. RT-PCR and western blotting were performed to detect the protein and mRNA expression levels of NFATc1, the ELR+ CXC chemokine interleukin (IL)-8, fibroblast growth factor-2 (FGF-2), and platelet-derived growth factor BB (PDGF BB) in xenografted tumor tissue in all groups. NFATc1 was highly expressed in tumor tissue in the control groups. The intervention group exhibited a tumor growth inhibition rate of 57.08% and presented a lower tumor weight and volume compared with the two control groups. In the control groups, the microvessel densities were 12.00 ± 1.65 and 11.47 ± 0.32, respectively, and the microlymphatic vessel densities were 10.03 ± 0.96 and 9.95 ± 1.12; these values were significantly higher than in the intervention group. RT-PCR and western blot shows that NFATc1 siRNA could markedly suppress the expression of IL-8, FGF-2 and PDGF BB at the mRNA and the protein level. In conclusion, it was shown that NFATc1 siRNA significantly suppresses the growth and vascular generation of SKOV3 human ovarian carcinoma cell-transplanted tumors subcutaneously xenografted into nude mice. The downregulation of the expression of IL-8, FGF-2 and PDGF BB may be one of the mechanisms underlying the above inhibitory effects.

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“…Non-migrated cells were removed from the upper side of the membrane before the migrated cells of the lower chamber (bottom side of membrane) were fixed and stained (Diff-Quik stain set; Dade Behring). Membranes were mounted on slides and the migrated cells were counted under a microscope (20x objective) in five fields across each membrane and averaged (23). The effects of axitinib (0.1μM) on chemotaxis were evaluated by treating cells in the upper chamber immediately after plating.…”

Section: Methodsmentioning

confidence: 99%

Lymphangiogenesis in rat asthma model

et al. 2016

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Although bronchial angiogenesis has been well documented in allergic asthma, lymphangiogenesis has not been widely studied. Therefore, we evaluated changes in lung lymphatics in a rat model of allergen-induced asthma using house dust mite (Der p 1; 100 μg/challenge). Additionally, properties of isolated lung lymphatic endothelial cells (CD45−, CD141+, LYVE-1+, Prox-1+) were studied in vitro. Three weeks after the onset of intranasal allergen exposure (twice weekly), an increase in the number of lung lymphatic vessels was measured (34% increase) by lung morphometry. New lymphatic structures were seen predominantly in the peribronchial and periarterial interstitial space but also surrounding large airways. Isolated lymphatic endothelial cells from sensitized lungs showed enhanced proliferation (% Ki67+), chemotaxis, and tube formation (number and length) compared to lymphatic endothelial cells isolated from naïve rat lungs. This hyper-proliferative lymphangiogenic phenotype was preserved through multiple cell passages (2-8). Lymphatic endothelial cells isolated from naïve and HDM sensitized rats produced similar in vitro levels of VEGF-C, VEGF-D, and VEGFR3 protein, each recognized as critical lymphangiogenic factors. Inhibition with anti-VEGFR (axitinib, 0.1μM) blocked proliferation and chemotaxis. Results suggest that in vivo sensitization causes fundamental changes to lymphatic endothelium, which are retained in vitro, and may relate to VEGFR downstream signaling.

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Differential activity of pro-angiogenic CXC chemokines

Cited by 12 publications

References 26 publications

CD11b⁺ interstitial macrophages are required for ischemia-induced lung angiogenesis

CD11b⁺ interstitial macrophages are required for ischemia-induced lung angiogenesis

The effect of NFATc1 on vascular generation and the possible underlying mechanism in epithelial ovarian carcinoma

Lymphangiogenesis in rat asthma model

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Differential activity of pro-angiogenic CXC chemokines

Cited by 12 publications

References 26 publications

CD11b+ interstitial macrophages are required for ischemia-induced lung angiogenesis

CD11b+ interstitial macrophages are required for ischemia-induced lung angiogenesis

The effect of NFATc1 on vascular generation and the possible underlying mechanism in epithelial ovarian carcinoma

Lymphangiogenesis in rat asthma model

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Resources

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CD11b⁺ interstitial macrophages are required for ischemia-induced lung angiogenesis

CD11b⁺ interstitial macrophages are required for ischemia-induced lung angiogenesis