Role of macrophages in inflammatory lymphangiogenesis: Enhanced production of vascular endothelial growth factor C and D through NF-κB activation

Watari, Kosuke; Nakao, Shintaro; Fotovati, Abbas; Basaki, Yuji; Hosoi, Fumihito; Bereczky, Biborka; Higuchi, Ryota; Miyamoto, Tomofumi; Kuwano, Michihiko; Ono, Masahiro

doi:10.1016/j.bbrc.2008.10.077

Cited by 96 publications

(102 citation statements)

References 24 publications

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“…Both of these molecules are secreted by inflammatory cells as activated macrophages and induce the recruitment of some immune cells expressing the corresponding VEGFR, in addition to their (lymph)angiogenic role [42][43][44]. This bridge between angiogenesis, lymphangiogenesis, which are respectively the growth of new blood and lymphatic vessels from pre-existing ones, and inflammation underline the importance of vascular remodelling in psoriasis and the potential therapeutic perspectives by inhibiting these processes.…”

Section: Discussionmentioning

confidence: 99%

Histological and transcriptional study of angiogenesis and lymphangiogenesis in uninvolved skin, acute pinpoint lesions and established psoriasis plaques: An approach of vascular development chronology in psoriasis

Henno

Blacher

Lambert

et al. 2010

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 99%

Histological and transcriptional study of angiogenesis and lymphangiogenesis in uninvolved skin, acute pinpoint lesions and established psoriasis plaques: An approach of vascular development chronology in psoriasis

Henno

Blacher

Lambert

et al. 2010

Journal of Dermatological Science

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“…Tissue necrosis factor α, as well as newly recruited macrophages and granulocytes, can enhance the local expression of VEGF-C within inflamed tissue to promote lymphangiogenesis [103]. Another pro-inflammatory cytokine, interleukin (IL)-1β, promotes lymphangiogenesis by stimulating VEGF-A, VEGF-C, and VEGF-D [104]. In addition to the inflamed tissue, lymphangiogenesis also occurs in the LN draining this tissue [14,16,51].…”

Section: Chronic Inflammationmentioning

confidence: 99%

“…Blocking lymphangiogenesis using anti-VEGFR-3 antibodies promote the acceptance of grafted tissue [104], although it is difficult to generalize this to other tissues that are normally not alymphatic like the cornea. For bone implants, lymphangiogenesis at the bone-implant interface can promote host destruction of the tissue as well as the formation of distal granulomas, neoplasia and lymphoma [15].…”

Section: Chronic Graft Rejectionmentioning

confidence: 99%

Role of Lymphatic Vessels in Tumor Immunity: Passive Conduits or Active Participants?

Lund

Swartz

2010

J Mammary Gland Biol Neoplasia

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Research in lymphatic biology and cancer immunology may soon intersect as emerging evidence implicates the lymphatics in the progression of chronic inflammation and autoimmunity as well as in tumor metastasis and immune escape. Like the blood vasculature, the lymphatic system comprises a highly dynamic conduit system that regulates fluid homeostasis, antigen transport and immune cell trafficking, which all play important roles in the progression and resolution of inflammation, autoimmune diseases, and cancer. This review presents emerging evidence that lymphatic vessels are active modulators of immunity, perhaps fine-tuning the response to adjust the balance between peripheral tolerance and immunity. This suggests that the tumor-associated lymphatic vessels and draining lymph node may be important in tumor immunity which in turn governs metastasis.

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“…Over expression of Her-2/neu causes VEGF-C production via NF-kB activation cascade in epithelial ovarian carcinoma (Hsieh et al, 2004). The pro-inflammatory cytokine, interleukin-1β (IL-1β), was found to induce inflammatory lymphangiogenesis via enhanced production of VEGF-C expression through NF-kB activation (Watari et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

5-Aminoisoquinolinone Reduces the Expression of Vascular Endothelial Growth Factor-C via the Nuclear Factor-kappa B Signaling Pathway in CT26 Cells

Fauzee²,

Wang³

2012

Asian Pacific Journal of Cancer Prevention

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Asian Pacific J Cancer Prev, 13, 991-994 IntroductionCancer metastatic dissemination plays a pivotal role in the progression of malignant tumors. Therefore, the principal goal for the treatment of malignant tumors is to prevent tumor proliferation, invasion and metastasis. Tumor lymphangiogenesis is a key factor for the spread of carcinomatous cells and therefore, usually affects the prognosis of patients. Various evidences from recent advances have demonstrated that tumor-induced lymphangiogenesis is an important mechanism promoting lymphatic metastasis (Karpanen et al., 2001;Mandriota et al., 2001;Skobe et al., 2001).PARP-1 is a monomeric, chromatin-bound enzyme, which is abundantly present in eukaryocytes (except yeast) and is activated by DNA single-strand breaks (Isabelle et al., 2010). PARP-1 uses ADP-ribose units from its substrate NAD + to build a polyanionic poly (ADPribose) polymer onto Glu residues on its acceptor proteins including histones, transcription factors and mainly PARP-1 itself and then recruit the repair apparatus to repair the DNA breaks (Diefenbach and Bürkle, 2005; Woo and Threadgill, 2005). 5-AIQ, a highly water soluble inhibitor, is known to inhibit the activation of PARP-1. Inhibition of PARP-1 activation has been found to prevent angiogenesis

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Role of macrophages in inflammatory lymphangiogenesis: Enhanced production of vascular endothelial growth factor C and D through NF-κB activation

Cited by 96 publications

References 24 publications

Histological and transcriptional study of angiogenesis and lymphangiogenesis in uninvolved skin, acute pinpoint lesions and established psoriasis plaques: An approach of vascular development chronology in psoriasis

Histological and transcriptional study of angiogenesis and lymphangiogenesis in uninvolved skin, acute pinpoint lesions and established psoriasis plaques: An approach of vascular development chronology in psoriasis

Role of Lymphatic Vessels in Tumor Immunity: Passive Conduits or Active Participants?

5-Aminoisoquinolinone Reduces the Expression of Vascular Endothelial Growth Factor-C via the Nuclear Factor-kappa B Signaling Pathway in CT26 Cells

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