TY - JOUR
T1 - Role of macrophages in inflammatory lymphangiogenesis
T2 - Enhanced production of vascular endothelial growth factor C and D through NF-κB activation
AU - Watari, Kosuke
AU - Nakao, Shintaro
AU - Fotovati, Abbas
AU - Basaki, Yuji
AU - Hosoi, Fumihito
AU - Bereczky, Biborka
AU - Higuchi, Ryuichi
AU - Miyamoto, Tomofumi
AU - Kuwano, Michihiko
AU - Ono, Mayumi
N1 - Funding Information:
Acknowledgment of research support: This research was supported by a grant-in-aid for Scientific Research for Priorify areas, Cancer, from the Ministry of Education Culture, Sports, Science and Technology of Japan (M.O.), and by the 3rd Term Comprehensive Control Research for Cancer from the Ministry of Health, Labor and Welfare, Japan (M.K.). This study was also supported in part by the Formation of Innovation Center for Fusion of Advanced Technologies, Kyushu University, Japan (M.O., M.K.).
PY - 2008/12/19
Y1 - 2008/12/19
N2 - The close association of inflammation, angiogenesis and cancer progression is now highlighted, and in this study we especially focused on a close association of inflammation and lymphangiogenesis. We found that proinflammatory cytokine, interleukin-1β (IL-1β), could induce lymphangiogenesis in mouse cornea through enhanced production of potent lymphangiogenic factors, VEGF-A, VEGF-C and VEGF-D. IL-1β-induced lymphangiogenesis, but not angiogenesis, was inhibited by administration of a selective anti-VEGF receptor-3 (VEGFR-3) neutralizing antibody. And in mouse cornea we observed recruitment of monocyte/macrophages and neutrophils by IL-1β implanted cornea. Depletion of macrophages by a bisphosphonate encapsulated in liposomes inhibited this IL-1β-induced lymphangiogenesis and also up-regulation of VEGF-A, VEGF-C, and VEGF-D. Furthermore, IL-1β-induced lymphangiogenesis and angiogenesis were suppressed by NF-κB inhibition with marked suppression of VEGF-A, VEGF-C, and VEGF-D expression.
AB - The close association of inflammation, angiogenesis and cancer progression is now highlighted, and in this study we especially focused on a close association of inflammation and lymphangiogenesis. We found that proinflammatory cytokine, interleukin-1β (IL-1β), could induce lymphangiogenesis in mouse cornea through enhanced production of potent lymphangiogenic factors, VEGF-A, VEGF-C and VEGF-D. IL-1β-induced lymphangiogenesis, but not angiogenesis, was inhibited by administration of a selective anti-VEGF receptor-3 (VEGFR-3) neutralizing antibody. And in mouse cornea we observed recruitment of monocyte/macrophages and neutrophils by IL-1β implanted cornea. Depletion of macrophages by a bisphosphonate encapsulated in liposomes inhibited this IL-1β-induced lymphangiogenesis and also up-regulation of VEGF-A, VEGF-C, and VEGF-D. Furthermore, IL-1β-induced lymphangiogenesis and angiogenesis were suppressed by NF-κB inhibition with marked suppression of VEGF-A, VEGF-C, and VEGF-D expression.
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U2 - 10.1016/j.bbrc.2008.10.077
DO - 10.1016/j.bbrc.2008.10.077
M3 - Article
C2 - 18951870
AN - SCOPUS:56049087039
VL - 377
SP - 826
EP - 831
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -
