Kupffer Cell Inactivation Delays Repair in a Rat Model of Reversible Biliary Obstruction

Roggin, Kevin K.; Papa, Elaine; Kurkchubasche, Arlet G.; Tracy, Thomas F.

doi:10.1006/jsre.2000.5879

Cited by 28 publications

(25 citation statements)

References 21 publications

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“…While these classic inflammatory contributions are undoubtedly important, resident tissue macrophages that have acquired specific adaptations to their local microenvironment (41) also can participate during tissue repair. (42,43) This study revealed that both inflammatory macrophages and osteomacs, specialized resident bone macrophages, were located within bone injury sites during all major phases of stabilized fracture repair. Osteomacs were specifically associated with sites of intramembranous bone deposition, forming an organized canopy structure over matrix-producing and -mineralizing osteoblasts.…”

Section: Discussionmentioning

confidence: 91%

Osteal macrophages promote in vivo intramembranous bone healing in a mouse tibial injury model

Alexander

Chang

Maylin

et al. 2011

Journal of Bone and Mineral Research

406

393

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Bone-lining tissues contain a population of resident macrophages termed osteomacs that interact with osteoblasts in vivo and control mineralization in vitro. The role of osteomacs in bone repair was investigated using a mouse tibial bone injury model that heals primarily through intramembranous ossification and progresses through all major phases of stabilized fracture repair. Immunohistochemical studies revealed that at least two macrophage populations, F4/80matory macrophages, were present within the bone injury site and persisted throughout the healing time course. In vivo depletion of osteomacs/macrophages (either using the Mafia transgenic mouse model or clodronate liposome delivery) or osteoclasts (recombinant osteoprotegerin treatment) established that osteomacs were required for deposition of collagen type 1 þ (CT1 þ ) matrix and bone mineralization in the tibial injury model, as assessed by quantitative immunohistology and micro-computed tomography. Conversely, administration of the macrophage growth factor colony-stimulating factor 1 (CSF-1) increased the number of osteomacs/macrophages at the injury site significantly with a concurrent increase in new CT1 þ matrix deposition and enhanced mineralization. This study establishes osteomacs as participants in intramembranous bone healing and as targets for primary anabolic bone therapies. ß

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Section: Discussionmentioning

confidence: 91%

Osteal macrophages promote in vivo intramembranous bone healing in a mouse tibial injury model

Alexander

Chang

Maylin

et al. 2011

Journal of Bone and Mineral Research

406

393

View full text Add to dashboard Cite

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“…Destruction of Kupffer cells attenuated liver fibrosis caused by carbon tetrachloride (41). By contrast, in a rat model of reversible biliary obstruction, inactivation of Kupffer cells impaired collagen metabolism and inhibited the resolution of fibrosis (42). Kupffer cells release many mediators that activate stellate cells, including TNF-␣, TGF-␤, human growth factor, PDGF, and reactive oxygen species (2, 13).…”

Section: Discussionmentioning

confidence: 99%

Polyphenols fromCamellia sinenesisattenuate experimental cholestasis-induced liver fibrosis in rats

Zhong¹,

Froh²,

Lehnert³

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Accumulation of hydrophobic bile acids during cholestasis leads to generation of oxygen free radicals in the liver. Accordingly, this study investigated whether polyphenols from green tea Camellia sinenesis, which are potent free radical scavengers, decrease hepatic injury caused by experimental cholestasis. Rats were fed a standard chow or a diet containing 0.1% polyphenolic extracts from C. sinenesis starting 3 days before bile duct ligation. After bile duct ligation, serum alanine transaminase increased to 760 U/l after 1 day in rats fed a control diet. Focal necrosis and bile duct proliferation were also observed after 1–2 days, and fibrosis developed 2–3 wk after bile duct ligation. Additionally, procollagen-α1(I) mRNA increased 30-fold 3 wk after bile duct ligation, accompanied by increased expression of α-smooth muscle actin and transforming growth factor-β and the accumulation of 4-hydroxynenonal, an end product of lipid peroxidation. Polyphenol feeding blocked or blunted all of these bile duct ligation-dependent changes by 45–73%. Together, the results indicate that cholestasis due to bile duct ligation causes liver injury by mechanisms involving oxidative stress. Polyphenols from C. sinenesis scavenge oxygen radicals and prevent activation of stellate cells, thereby minimizing liver fibrosis.

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“…Destruction of Kupffer cells attenuated liver fibrosis caused by carbon tetrachloride [45] . By contrast, in a rat model of reversible biliary obstruction, inactivation of Kupffer cells impaired collagen metabolism and inhibited the resolution of fibrosis [46] . Kupffer cells release many mediators, like TNF-α, TGF-β, human growth factor, PDGF, and reactive oxygen species [47,48] that activate stellate cells leading to fibrosis.…”

Section: How Does Dietary Glycine Decrease Cholestasis-induced Liver mentioning

confidence: 93%

Dietary glycine blunts liver injury after bile duct ligation in rats

Froh¹,

Zhong²,

Walbrun³

et al. 2008

WJG

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Kupffer Cell Inactivation Delays Repair in a Rat Model of Reversible Biliary Obstruction

Cited by 28 publications

References 21 publications

Osteal macrophages promote in vivo intramembranous bone healing in a mouse tibial injury model

Osteal macrophages promote in vivo intramembranous bone healing in a mouse tibial injury model

Polyphenols fromCamellia sinenesisattenuate experimental cholestasis-induced liver fibrosis in rats

Dietary glycine blunts liver injury after bile duct ligation in rats

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