Functional Heterogeneity of the Kupffer Cell Population Is Involved in the Mechanism of Gadolinium Chloride in Rats Administered Endotoxin

Kono, Hiroshi; Fujii, Hideki; Asakawa, Masami; Yamamoto, Masayuki; Maki, Akira; Matsuda, Masanori; Rusyn, Ivan; Matsumoto, Yoshirô

doi:10.1006/jsre.2002.6434

Cited by 53 publications

(52 citation statements)

References 26 publications

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“…Similar results have previously been observed by other authors (Kohno et al 1997, Rizzardini et al 1998, Kono et al 2001. Furthermore, Kono et al (2002) have reported that although gadolinium administration prevented LPS-induced increase in TNF-gene expression in the liver, it did not modify the serum concentrations of TNF-. However, it has recently been reported that gadolinium treatment decreased superoxide generation, but conversely increased Kupffer cell TNF-production after LPS stimulation (Kinoshita et al 2005).…”

Section: Discussionsupporting

confidence: 91%

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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Gram-negative bacterial infection or treatment of animals with bacterial lipopolysaccharide (LPS) induces a catabolic state with proteolysis, liver injury and an inhibition of the insulin-like growth factor-I (IGF-I) system. The purpose of this work was to elucidate the role of Kupffer cells in LPS-induced inhibition of the IGF-I/IGF-binding protein-3 (IGFBP-3) system. Adult male Wistar rats were either pretreated with the Kupffer cell inhibitor gadolinium chloride (10 mg/kg, i.v., 24 h prior to LPS exposure) or saline vehicle. Rats received two i.p. injections of 1 mg/kg LPS (at 17:30 and 08:30 h the following day) and were killed 4 h after the second injection. LPS administration induced a significant decrease in body weight and in serum concentrations of IGF-I and IGFBP-3 (P<0·01), as well as in their gene expression in the liver. LPS-injected rats had increased serum concentrations of ACTH, corticosterone (P<0·05), tumour necrosis factor-(TNF-) and nitrites (P<0·01). Pretreatment of the animals with gadolinium chloride blocked the inhibitory effect of LPS on body weight, and on serum concentrations of IGF-I, IGFBP-3 and nitrites, as well as growth hormone receptor (GHR), IGF-I and IGFBP-3 gene expression in the liver. In contrast, gadolinium chloride administration did not modify the stimulatory effect of LPS on serum concentrations of ACTH, corticosterone and TNF-. These results suggest that Kupffer cells are important mediators in the inhibitory effect of LPS on GHR, IGF-I and IGFBP-3 gene expression in the liver, leading to a decrease in serum concentrations of IGF-I and IGFBP-3.

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Section: Discussionsupporting

confidence: 91%

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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“…12 MCT reproduced changes associated with hepatic veno-occlusive disease in rat liver and additionally depleted Kupffer cells capable of reacting with ED2 antibody, 13 which recognizes the CD163 scavenger receptor antigen. This is noteworthy because gadolinium chloride also depleted ED2-positive Kupffer cells, 14 and such Kupffer cell depletion promoted engraftment of transplanted cells in the liver, consistent with an inhibitory role of Kupffer cells in this process. 3 In larger doses, MCT caused hepatocyte apoptosis, 15 whereas in lower doses, it promoted genotoxic DNA adduct formation in hepatocytes.…”

mentioning

confidence: 60%

Monocrotaline promotes transplanted cell engraftment and advances liver repopulation in rats via liver conditioning

Joseph¹,

Kumaran²,

Berishvili³

et al. 2006

Hepatology

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Disruption of the hepatic endothelial barrier or Kupffer cell function facilitates transplanted cell engraftment in the liver. To determine whether these mechanisms could be activated simultaneously, we studied the effects of monocrotaline, a pyrollizidine alkaloid, with reported toxicity in liver sinusoidal endothelial cells and Kupffer cells. The effects of monocrotaline in Fischer 344 rats were examined by tissue morphology, serum hyaluronic acid levels, and liver tests (endothelial and hepatocyte injury) or incorporation of carbon and 99m Tc-sulfur colloid (Kupffer cell damage). To study changes in cell engraftment and liver repopulation, Fischer 344 rat hepatocytes were transplanted into syngeneic dipeptidyl peptidase IV-deficient rats followed by histological assays. We observed extensive endothelial injury without Kupffer cell or hepatocyte damage in monocrotaline-treated rats. Monocrotaline enhanced transplanted cell engraftment without changes in transplanted cell numbers or induction of proliferation in native hepatocytes over 3 months. In monocrotaline-treated rats, transplanted cells integrated into the liver parenchyma and survived in vascular spaces. To determine whether native hepatocytes suffered inapparent damage after monocrotaline, we introduced further liver injury with carbon tetrachloride subsequent to cell transplantation. Monocrotaline sensitized the liver to carbon tetrachlorideinduced necrosis, which advanced transplanted cell proliferation, leading to significant liver repopulation. During this process, we observed proliferation of bile duct cells and small epithelial cells, although transplanted hepatocytes did not appear to reconstitute bile ducts. The studies showed that perturbation of multiple liver cell compartments by monocrotaline promoted transplanted cell engraftment and proliferation. In conclusion, development of drugs with monocrotaline-like effects will help advance liver cell therapy. (HEPATOLOGY 2006;44:1411-1420

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“…GdCl 3 at this dose was previously determined to result in significant depletion of KCs. [58][59][60][61] Captopril treatment continued from the time of tumor induction to tissue collection at day 21.…”

Section: Methodsmentioning

confidence: 99%

The renin angiotensin system regulates Kupffer cells in colorectal liver metastases

Wen

Ager

Neo

et al. 2013

Cancer Biology & Therapy

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Functional Heterogeneity of the Kupffer Cell Population Is Involved in the Mechanism of Gadolinium Chloride in Rats Administered Endotoxin

Cited by 53 publications

References 26 publications

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Monocrotaline promotes transplanted cell engraftment and advances liver repopulation in rats via liver conditioning

The renin angiotensin system regulates Kupffer cells in colorectal liver metastases

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