• Title/Summary/Keyword: Kupffer cells

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Identification and Expression Patterns of kif3bz during the Zebrafish Embryonic Development

  • Lee, A-Ram;Rhee, Myung-Chull
    • Animal cells and systems
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    • v.13 no.4
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    • pp.411-418
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    • 2009
  • We are reporting the identification, expression patterns, and possible biological functions of zebrafish kif3b (kif3bz) encoding 475 amino acids. Kif3Bz contains the kinesin motor domain, catalytic domain, KISc domain, and one single coiled coil domain. Phylogenetic analysis indicates that kif3bz is a highly conserved gene among the tested vertebrates. First of all, both maternal and zygotic messages of kif3bz were evenly distributed in the blastomeres at 2-cell stage. Its ubiquitous expression throughout the blastomeres continued till 40% epiboly. However, kif3bz transcripts became restricted in Kupffer's vesicle at tailbud and 6-somite stages. At 13-somite stage, kif3bz expression pattern became specific to the telencephalon, diencephalon, trigeminal placode, and somites. Such expression patterns were further intensified in the telencephalon, diencephalons, hind brain, pronephric ducts, optic vesicles, and spinal cord neurons in the 23-somite stage embryos, and last till 24 hpf. We discussed possible functions of Kif3Bz related to the vertebrate embryonic development.

Ultrastructure of virus particles in the liver of piglets infected with porcine enterovirus serotype 3 (Enterovirus 감염 돼지의 간에서 virus의 형태학적 관찰)

  • Shin, Tae-kyun;Lee, Cha-soo;Huh, Min-do
    • Korean Journal of Veterinary Research
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    • v.32 no.2
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    • pp.207-210
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    • 1992
  • Oral infection of colostrum-deprived, neonatal piglets with porcine enterovirus serotype 3 can result in hepatic lesions with a short incubation period. In the thin section of the affected liver, crystalline arrays of virus particles characteristic of picornavirus were identified in the sinusoid endothelial cells and Kupffer cells. There were also cytoplasmic aggregates of electron- dense, virus-like particles in the hepatocytes. These findings suggest that porcine enterovirus serotype 3 has hepatotropism as well as neurotropism.

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Ultrastructural Changes Induced by Telluric Acid in the Rat Liver (Telluric Acid가 흰쥐 간조직의 미세구조에 미치는 영향)

  • Son, Serk-Joo;Jeong, Young-Gil;Cho, Seung-Muk;Baik, Tai-Kyung;Choi, Chang-Do;Choi, Wol-Bong
    • Applied Microscopy
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    • v.25 no.4
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    • pp.83-103
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    • 1995
  • This experiment was carried out to investigate the effects of telluric acid on the histological and fine structural changes in the rat liver. Fischer 344 rats($150{\sim}200gm$) were used in this study as control and experimental groups. Telluric acid(5 mg/100 gm of body weight) suspensed in olive oil was given intraperitoneally to the animals of the experimental group and only olive oil to those of the control group. At the intervals of 3, 6 and 12 hours, 1, 2, 3, 5, 10, 20, 30 and 60 days after administration, the animals were sacrificed, and livers were obtained from the rats. For light microscopic examination of the liver, sections($5{\mu}m$) were stained with hematoxylineosin(H-E). For electron microscopic examination of the liver, sections were stained with uranyl acetate and lead citrate, finally examined with Zeiss EM 109 electron microscopes. The results obtained were as follows. 1. In the control group, round nucleus. well developed mitochondria, Golgi apparatus, rough endoplasmic reticulum(RER) and numerous glycogen particles were observed in the cytoplasm of the hepatocyte. In the cytoplasmic membranes of the hepatocyte, sinusoidal surface had numerous microvilli and cellular surface is combinated adjacent hepatocyte with desmosomes. The RER cisterns were dilated and zymogen granules were fewer than those of the dark cells. Kupffer cells with irregular nuclear membrane were observed. Fat storing cell and collagenous fiber bundle were observed in the Disse space. 2. Kupffer cell, inflammatory cells in the connective tissue of hepatic triad and lysosome were increased in the 3, 6, and 12 hour experimental group comparing with that of the control group. 3. In the 1 day experimental group, infiltration of inflammatory cells in interlobular connective tissue, dilatation of sinusoidal capillary and increasing of Kupffer cell were observed. Atropic change of hepatocyte and aggregation of glycogen particles in the cytoplasm of hepatocyte were observed. In this group, desmosome near bile canaliculi and collagenous fiber bundle in the Disse space were increased comparing with that of the 12 hours experimental group. In the 2 days experimental group, desmosome, lysosome, peroxisome and collagenous fiber bundle were increased comparing with that of the 1 day experimental group. Furthermore, lamellated bodies were also seen in the cytoplasm of the hepatocyte. 4. In 3 and 5 days experimental groups, transformations of hepatic cell cord and degeneration of the hepatocyte were markedly inclosed comparing with the all experimental groups. And damaged RER and mitochondria. collagenous fiber bundle were also inclosed comparing with that of the 2 days experimental group. Autophagosome and fat storing cells with large lipid droplets were also observed comparing with that of the 2 days experimental group. Tight junction and desmosome between the hepatocytes were separated. These degenerating changes were severe through the all experimental groups. 5. In the 10 and 20 days experimental groups, arrangement of hepatic cell cords and cell organelles of hepatocytes were similar to those of the control group. However, aggregation of glycogen particles, dilatation of sinusoidal capillary and infiltration of inflammatory cells remained. 6. In the 30 days experimental group, the tissue findings were similar to those of the control grout. But lamellated bodies in some hepatocytes and lysosome were remained in the cytoplasms of the Kupffer cells. In the 60 days experimental group, these all changes were recovered as the control group. In conclusion, telluric acid would directly induce the degenerative and necrotic changes on the hepatic tissue. However, these changes were perfectly recoverd in the 60 days experimental group as the control group.

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Akap12beta supports asymmetric heart development via modulating the Kupffer's vesicle formation in zebrafish

  • Kim, Jeong-gyun;Kim, Hyun-Ho;Bae, Sung-Jin
    • BMB Reports
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    • v.52 no.8
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    • pp.526-531
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    • 2019
  • The vertebrate body plan is accomplished by left-right asymmetric organ development and the heart is a representative asymmetric internal organ which jogs to the left-side. Kupffer's vesicle (KV) is a spherical left-right organizer during zebrafish embryogenesis and is derived from a cluster of dorsal forerunner cells (DFCs). Cadherin1 is required for collective migration of a DFC cluster and failure of DFC collective migration by Cadherin1 decrement causes KV malformation which results in defective heart laterality. Recently, loss of function mutation of A-kinase anchoring protein 12 (AKAP12) is reported as a high-risk gene in congenital heart disease patients. In this study, we demonstrated the role of $akap12{\beta}$ in asymmetric heart development. The $akap12{\beta}$, one of the akap12 isoforms, was expressed in DFCs which give rise to KV and $akap12{\beta}$-deficient zebrafish embryos showed defective heart laterality due to the fragmentation of DFC clusters which resulted in KV malformation. DFC-specific loss of $akap12{\beta}$ also led to defective heart laterality as a consequence of the failure of collective migration by cadherin1 reduction. Exogenous $akap12{\beta}$ mRNA not only restored the defective heart laterality but also increased cadherin1 expression in $akap12{\beta}$ morphant zebrafish embryos. Taken together, these findings provide the first experimental evidence that $akap12{\beta}$ regulates heart laterality via cadherin1.

The role of hepatic macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis

  • Cha, Ji-Young;Kim, Da-Hyun;Chun, Kyung-Hee
    • Laboraroty Animal Research
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    • v.34 no.4
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    • pp.133-139
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    • 2018
  • Nonalcoholic steatohepatitis (NASH) is becoming common chronic liver disease because of the increasing global prevalence of obesity and consequently Nonalcoholic fatty liver disease (NAFLD). However, the mechanism for progression of NAFLD to NASH and then cirrhosis is not completely understood, yet. The triggering of these hepatic diseases is thought from hepatocyte injury caused by over-accumulated lipid toxicity. Injured hepatocytes release damage-associated molecular patterns (DAMPs), which can stimulate the Kupffer cells (KCs), liver-resident macrophages, to release pro-inflammatory cytokines and chemokines, and recruit monocyte-derived macrophages (MDMs). The increased activation of KCs and recruitment of MDMs accelerate the progression of NAFLD to NASH and cirrhosis. Therefore, characterization for activation of hepatic macrophages, both KCs and MDMs, is a baseline to figure out the progression of hepatic diseases. The purpose of this review is to discuss the current understanding of mechanisms of NAFLD and NASH, mainly focusing on characterization and function of hepatic macrophages and suggests the regulators of hepatic macrophages as the therapeutic target in hepatic diseases.

Histological and Histochemical Study on Toxicity of Ricin in the Rat Liver (흰쥐 간에 미치는 Ricin의 독성에 대한 조직학적 및 조직화학적 연구)

  • 조운복;최병태
    • Journal of Environmental Science International
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    • v.6 no.1
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    • pp.53-60
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    • 1997
  • The toxicity of purified ricln from Ricinus communis to rats was examined by histological and histochemical methods. Sprague-Dawley rats were injected intraperitoneally with 75$\mu\textrm{g}$/kg body weight of ricin and were sacrified at itntervals of 6, 24, 48 and 120 hours after injectoon. The major morphological changes, such as cloudy swelling, hydropic degeneration, necrosis, fatty change, blood congestion, increase of Kupffer cells in number and extension of sinusoids, were obvious in the liver of experimental group. These morphological changes of hepatic cells were mainly observed in both the periportal and midlobular region of hepatic lobule. The extension of sinusoids was obvious in the controlobular region. And glycogen dlstrlbution of hepatic cells tended to decrease in the same region showing morphlogical changes as compared with the control group.

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A Nuclear Medicine Study on the Effect of High Energy Gamma Irradiation on Rabbit Liver (고(高)에너지 방사선(放射線) 조사(照射)가 가토(家兎) 간장(肝臟)에 미치는 영향(影響)에 관(關)한 핵의학적(核醫學的) 연구(硏究))

  • Lee, Joon-Il;Min, Bong-Hee
    • Journal of radiological science and technology
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    • v.12 no.1
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    • pp.3-16
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    • 1989
  • In order to investigate the in vivo effect of $^{60}Co$ radiation on rabbit liver, the uptake ratio and regional excretory value in hepatocytes and Kupffer cells were estimated during acute and chronic hepatic injuries. The left lobe of liver was irradiated at 15 Gy or 30 Gy with a single dose and subsequent changes were analysed with a seial nuclear medicine imaging by using $^{99m}Tc-phytate,\;^{99m}Tc-DISIDA\;and\;^{99m}Tc-HSA$ and resulting data were computerized. The degree of hepatic damage, duration of the injury, and recovery pattern after the irradation were in agreement with the findings of other investigations. However, out values were more quantitative evacuation than those of other publications. Recovery of decreased uptake of $^{99m}Tc-phytate$ was delayed approximately $2{\sim}3$ days later than that of $^{99m}Tc-DISIDA$. In acute radiation induced injury, the results demonstrated that the recovery of Kupffer cells was delayed more than that of hepatocytes. This discrepancy was considered due to the differences in repair activities between these cell types. The decreased of regional excretory value in irradiated area was found to be dose-dependent but had no corelation with regional uptakes of DISIDA and phytate. The decreased of regional excretory value observed in non-irradiated region suggested that irradiated liver might induce an indirect effect.

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Involvement of Hepatic Innate Immunity in Alcoholic Liver Disease

  • Byun, Jin-Seok;Jeong, Won-Il
    • IMMUNE NETWORK
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    • v.10 no.6
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    • pp.181-187
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    • 2010
  • Excessive alcohol consumption is one of the critical causative factors leading to alcoholic liver disease (ALD). ALD is characterized by a wide spectrum of liver damage, ranging from simple uncomplicated liver steatosis (fatty liver) to steatohepatitis and liver fibrosis/cirrhosis. It has been believed that the obvious underlying cause for ALD is due to hepatocyte death induced by alcohol itself. However, recent sparkling studies have shown that diverse immune responses contribute to ALD because liver is enriched with numerous immune cells. Especially, a line of evidence has suggested that innate immune cells such as Kupffer cells and natural killer (NK)/NKT cells are significantly involved in the pathogenesis of ALD via production of pro-inflammatory cytokines and other mediators. Indeed, more interestingly, hepatic stellate cells (HSCs), known as a major cell inducing liver steatosis and fibrosis, can be killed by liver NK cells, which could be suppressed by chronic alcohol consumption. In this review, with the view of liver as predominant innate immune organ, we describe the pathogenesis of ALD in which what roles of innate immune cells are and how they are interacting with HSCs.

Ultrastructural Alterations of Rabbit Liver after Overdose of Nitrate (질산염과잉투여(窒酸鹽過剩投與)에 의(依)한 간장(肝臟)의 변화(變化)에 관한 전자현미경적연구(電子顯微鏡的硏究))

  • Kim, Soon Bok;Lee, Cha Soo
    • Korean Journal of Veterinary Research
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    • v.16 no.2
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    • pp.141-150
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    • 1976
  • In order to know the morphological changes of liver in nitrate poisoning, the ultrastructural studies were carried out on the rabbit liver after potassium nitrate was administered orally at lethal dose, in single treatment, as acute case and at two different levels. 1.0 and 0.5g/kg of body weight daily for 43 and 60 days as chronic case, respectively, The results were summarized as followings: 1. In the hepatic cells of acute case, mitochondria were swollen, disappearance of cristae and variable in shape. Dilatation of rough endoplasmic reticulum and vacuoles containing degenerated cell organells were observed. Glyogen particles were decreased in number. Degenerated Kupffer cells were often seen in acute case. 2. In the hepatic cells of chronic case, there were increase of smooth endoplasmic reticulum, marked enlargement of rough endcplasmic reticulum, detachment of membrane bound ribosome and some rough endoplasmic reticulum changed into smooth endoplasmic reticulum. Secondary lysosome, abundant glycogen paricles and myelin-figure structures were also observed in the cytoplasm of the hepatic cells. The endothelial cells were proliferated in the area of the necrotic cells.

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Detection of Metastases of Primary Hepatocellular Carcinoma with $^{99m}Tc-HIDA$ Scintigraphy ($^{99m}Tc-HIDA$를 이용(利用)한 원발성간세포암전이(原發性肝細胞癌轉移) 병소(病巢)의 진단(診斷))

  • Hong, Kee-Suk;Hong, Seong-Woon;Lee, Jhin-Oh;Kang, Tae-Woong;Huh, Dai-Suk
    • The Korean Journal of Nuclear Medicine
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    • v.17 no.1
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    • pp.85-87
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    • 1983
  • $^{99m}Tc-Sulfur$ Colloid is concentrated in Kupffer cells of the liver, whereas the new biliary agents such as $^{99m}Tc-HIDA$ are processed by hepatic parenchymal cells. The distant metastatic lesiors in skull and lung of the primary hepatocellular carcinoma in 38-year old Korean male were detected with $^{99m}Tc-HIDA$ scintigraphy. The chest PA, skull bone X-ray and radionuclide scintigraphic studies are illustrated. This observation suggests that $^{99m}Tc-HIDA$ scintigraphy is useful for detection of distant metastases of primary hepatocellular carcinoma.

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