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Absence of angiotensin II type 1 receptor in bone marrow–derived cells is detrimental in the evolution of renal fibrosis
Masashi Nishida, … , Hiroaki Yoshida, Iekuni Ichikawa
Masashi Nishida, … , Hiroaki Yoshida, Iekuni Ichikawa
Published December 15, 2002
Citation Information: J Clin Invest. 2002;110(12):1859-1868. https://doi.org/10.1172/JCI15045.
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Article

Absence of angiotensin II type 1 receptor in bone marrow–derived cells is detrimental in the evolution of renal fibrosis

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Abstract

Research Article

Authors

Masashi Nishida, Hidehiko Fujinaka, Taiji Matsusaka, James Price, Valentina Kon, Agnes B. Fogo, Jeffrey M. Davidson, MacRae F. Linton, Sergio Fazio, Toshio Homma, Hiroaki Yoshida, Iekuni Ichikawa

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Figure 7

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Migrating activity and oxidative burst of Agtr1–/– and Agtr1+/+ macropha...
Migrating activity and oxidative burst of Agtr1–/– and Agtr1+/+ macrophages. (a) Migrating activity of isolated peritoneal macrophages was determined by using chemotaxis chambers. In the left panel, Agtr1–/– or Agtr1+/+ macrophages were incubated with either vehicle (black bars) or 0.1 μg/ml MCP-1(white bars). In the right panel, Agtr1+/+ macrophages were exposed to vehicle (white bar), 1 × 10–6 M angiotensin II alone (gray bar), or 0.1 μg/ml MCP-1 and 1 × 10–6 M angiotensin II (black bar). Migrated cells were counted and are shown as the number of migrated cells per field. *P < 0.05 for vehicle versus MCP-1. (b) Macrophages of the Agtr1–/– (black bar) or the Agtr1+/+ (white bar) genotype were examined for Fcγ receptor–mediated oxidative burst. Oxidative burst was detected as fluorescence emitted by macrophages and is indicated in arbitrary units. Ang II, angiotensin II; MCP-1, monocyte chemotactic protein-1.

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