MMP-2 inhibition reduces renal macrophage infiltration with increased fibrosis in UUO

Nishida, Masashi; Okumura, Yasuko; Ozawa, Seiichiro; Shiraishi, Isao; Itoi, Toshiyuki; Hamaoka, Kenji

doi:10.1016/j.bbrc.2006.12.165

Cited by 46 publications

(34 citation statements)

References 15 publications

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“…Their data suggest that angiotensin II affects the quantity and phagocytic activity of M⌽ through Agtr1 (64). The inverse correlation between interstitial M⌽ number and interstitial fibrosis at late stage (day 14) of UUO was confirmed by using cyclophosphamide-mediated M⌽ depletion and matrix metalloproteinase (MMP)-2 inhibitor studies (65,66). These findings are consistent with those from the different groups.…”

Section: Pathogenic and Protective Role Of M⌽ In Acute Kidney Diseasesupporting

confidence: 60%

Pathogenic and protective role of macrophages in kidney disease

Cao

Wang

Harris

2013

American Journal of Physiology-Renal Physiology

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Macrophages (MΦ) are located throughout kidney tissue, where they play important roles in homeostasis, surveillance, tolerance, and cytoprotection. MΦ are highly heterogeneous cells and exhibit distinct phenotypic and functional characteristics depending on their microenvironment and the disease type and stage. Recent studies have identified a dual role for MΦ in several murine models of kidney disease. In this review, we discuss the pathogenic and protective roles of the various MΦ subsets in experimental and human kidney diseases and summarize current progress toward the therapeutic use of MΦ in kidney diseases.

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Section: Pathogenic and Protective Role Of M⌽ In Acute Kidney Diseasesupporting

confidence: 60%

Pathogenic and protective role of macrophages in kidney disease

Cao

Wang

Harris

2013

American Journal of Physiology-Renal Physiology

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“…Surprisingly, immunofluorescence and immunohistochemistry results revealed a marked increase in the accumulation of Col 1 and α-SMA+ myofibroblasts in the kidneys of the 5-week BDL-watertreated group, as determined by real-time PCR. It has been reported that TGF-β1/Smad signaling is a key mediator of renal tubular interstitial fibrosis (Nishida et al, 2007;Okano et al, 2010;Choi et al, 2011;Falke et al, 2012;Huen et al, 2013). Consistent with these reports, renal fibrosis was also observed in this study.…”

Section: Discussionsupporting

confidence: 92%

Xiayuxue decoction reduces renal injury by promoting macrophage apoptosis in hepatic cirrhotic rats

et al. 2015

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ABSTRACT. Renal pathological changes in cirrhotic rat have not been extensively reported. The aim of this study was to investigate whether Xiayuxue decoction (XYXD) could attenuate renal injury induced by bile duct ligation (BDL), with special focus on the mechanisms promoting renal macrophage apoptosis. The rats were treated with BDL for 5 weeks and administered 0.36 g/kg XYXD intragastrically from day 1 of initiating BDL. Renal tissue was monitored by hematoxylin-eosin and Sirius red staining. Macrophage infiltration and proinflammatory cytokines such as tumor necrosis factor and chemokine ligand 2 were detected by quantitative polymerase chain reaction. Macrophage apoptosis was detected by double immunofluorescence staining. Blood urea nitrogen, creatinine, and glomerulus diameter increased significantly after a 5-week BDL treatment in XYXD (BDL-XYXD) rats. CD68 and pro-inflammatory cytokine (2015) mRNA increased in the kidneys of control (BDL-water) rats. Fluorescence microscopy analysis showed that XYXD promoted apoptosis in renal CD68+ macrophages. Collogen1 (Col 1), pro-fibrogenic cytokines, and α-smooth muscle actin in kidneys of BDL-water rats increased significantly compared to the sham group. XYXD inhibited Col 1 and pro-fibrotic factors in BDL-XYXD rats. Our results demonstrated that XYXD significantly reduced renal injury by, at least in part, promoting macrophage apoptosis in rats with damaged renal histopathology due to BDL-induced cirrhosis.

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“…Also, MMP-2 has been found to be highly expressed in fibrotic liver myofibroblasts (293), which incidentally has been proven to constitute a noteworthy predisposition to developing hepatic cell carcinoma (86). Nonetheless, a downregulation of MMP-2 has been reported during in vitro myofibroblastic differentia- tion of rat embryonic fibroblasts (141), while its inhibition has been shown to accelerate murine renal fibrosis (268).…”

Section: Mmpsmentioning

confidence: 99%

The wound healing, chronic fibrosis, and cancer progression triad

Rybinski

Franco‐Barraza

Cukierman

2014

Physiological Genomics

215

175

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For decades tumors have been recognized as “wounds that do not heal.” Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct signaling pathways, also fuel chronic fibrosis and tumor progression. Hence, here we review the relationship between fibrosis and cancer through the lens of wound healing.

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MMP-2 inhibition reduces renal macrophage infiltration with increased fibrosis in UUO

Cited by 46 publications

References 15 publications

Pathogenic and protective role of macrophages in kidney disease

Pathogenic and protective role of macrophages in kidney disease

Xiayuxue decoction reduces renal injury by promoting macrophage apoptosis in hepatic cirrhotic rats

The wound healing, chronic fibrosis, and cancer progression triad

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