Platelet Dynamics in the Early Phase of Postischemic Liver In Vivo

Nakano, Yoritaka; Kondo, Tadashi; Matsuo, Ryota; Hashimoto, Ikuka; Kawasaki, Takuya; Kohno, Keisuke; Myronovych, Andriy; Tadano, Sosuke; Hisakura, Katsuji; Ikeda, Osamu; Watanabe, Motonobu; Murata, Soichiro; Fukunaga, Kiyoshi; Ohkohchi, Nobuhiro

doi:10.1016/j.jss.2007.09.016

Cited by 53 publications

(73 citation statements)

References 34 publications

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“…27 It has been reported that platelets accumulate in the liver under certain pathological conditions, such as ischemia/reperfusion, 28,29 cirrhosis, cholestasis, 16 viral hepatitis, 30 and the residual liver after hepatectomy. 6 Platelets and liver fibrosis Currently, liver fibrosis is known to be part of a dynamic process of continuous extracellular matrix (ECM) remodeling in the setting of chronic liver injury; this process leads to excessive accumulation of several extracellular proteins, proteoglycans, and carbohydrates.…”

Section: -22mentioning

confidence: 99%

“…62 Rats depleted of Kupffer cells were subjected to ischemia/reperfusion, which suppressed platelet adherence in sinusoids, and, as a consequence, there was attenuation of sinusoidal perfusion failure and endothelial damage. 29 Tamura et al 63 reported that platelets adhered to Kupffer cells at the early period of ischemia/reperfusion and that the platelets that adhered Kupffer cells were involved in apoptosis of hepatocytes and the mechanism of hepatic ischemia/reperfusion injury. Nakamura et al described different characteristics for platelets and Kupffer cells.…”

Section: 54mentioning

confidence: 99%

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Novel functions of platelets in the liver

Kurokawa

Zheng

Ohkohchi

2016

J of Gastro and Hepatol

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Platelets contain not only proteins needed for hemostasis but also many growth factors that are required for organ development, tissue regeneration, and repair. Thrombocytopenia, which is frequently observed in patients with chronic liver disease (CLD) and cirrhosis, is due to various causes, such as decreased thrombopoietin production and accelerated platelet destruction caused by hypersplenism; however, the relationship between thrombocytopenia and hepatic pathogenesis and the role of platelets in CLD are poorly understood. Thus, in this paper, the experimental evidence for platelets improving liver fibrosis and accelerating liver regeneration is summarized and addressed based on studies conducted in our laboratory and current progress reports from other investigators. Platelets improve liver fibrosis by inactivating hepatic stellate cells to decrease collagen production. The level of intracellular cAMP is increased by adenosine through its receptors on hepatic stellate cells, thereby resulting in inactivation of these cells. Adenosine is produced by degradation of adenine nucleotides, which are stored in abundance within the dense granules of platelets. The regenerative effect of platelets in the liver consists of three mechanisms: a direct effect on hepatocytes, a cooperative effect with liver sinusoidal endothelial cells, and a collaborative effect with Kupffer cells. Based on these experiments, a clinical trial suggested that the increase in platelets induced by platelet transfusion improved liver function in patients with CLD in a clinical setting.We highlight the current knowledge concerning the role of platelets in CLD and expect to open a novel avenue for application of these clinical therapies to treat liver disease.

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Section: -22mentioning

confidence: 99%

Section: 54mentioning

confidence: 99%

Novel functions of platelets in the liver

Kurokawa

Zheng

Ohkohchi

2016

J of Gastro and Hepatol

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“…Studies have indicated an important role for platelets both in the development of liver injury and also in hepatoprotection and liver regeneration [20][21][22][23][24][25][26][27][28][29]. Following different forms of liver injury, platelets are recruited to the liver, adhere to endothelial lining, and cause leukocyte accumulation, sinusoidal flow disturbances [20][21][22] and even apoptosis of sinusoidal endothelial cells [20]. Adherent platelets can also release serotonin, markedly impair sinusoidal microcirculation, and decrease O 2 tension [23].…”

Section: Discussionmentioning

confidence: 99%

Ethamsylate Protects Against the Carbon Tetrachloride-Induced Liver Damage in Rats

Abdel-Salam¹

2017

JDMDC

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Ethamsylate is a synthetic haemostatic drug used for controlling capillary bleeding. In this study, the effect of ethamsylate on liver injury induced by acute carbon tetrachloride (CCl 4 ) administration in rats was investigated. Ethamsylate (45, 90 or 180 mg/kg) was given once daily orally simultaneously with CCl 4 and continued for 1 week thereafter. The extent of liver damage was determined by measuring serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) as well as by liver histopathology. Ethamsylate given at the above doses conferred significant hepatic protection against the CCl 4 -induced hepatotoxicity. It reduced serum ALT activities by 44.8%-70.9%, AST by 46.1%-51.4%, and ALP by 30.7%-48.5%, respectively, compared to the CCl 4 control group. Ethamsylate given at 90 mg/kg to CCl 4 -treated rats resulted in the preservation of the normal architecture of the liver tissue and no lymphocytic infiltration. These data indicate a beneficial effect for ethamsylate in the CCl 4 model of hepatotoxicity. Keywords:

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“…We have investigated the roles of leukocytes, platelets, and KCs in hepatic IR injury using IVM (Nakano et al 2008(Nakano et al , 2009Pak et al 2010;Tamura et al 2012). We previously showed that KC-platelet interaction such as adhesion induced hepatic IR injury (Tamura et al 2012.…”

Section: Discussionmentioning

confidence: 99%

Interaction of Kupffer Cells and Platelets Determines the Severity of Ischemia-Reperfusion Injury in Steatosis

Ogawa

Kondo

Tamura

et al. 2014

Tohoku J. Exp. Med.

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Liver steatosis increases the risk of postoperative complications following major liver resection, since the steatotic liver is susceptible to ischemia-reperfusion (IR) injury. However, it is unclear how IR injury changes in relation to the degree of hepatic steatosis. Previously, we reported that interaction between Kupffer cells (KCs) and platelets induced hepatic IR injury. The aim of our present study was to evaluate the relationship between the degree of liver steatosis and IR injury by focusing on the interaction of KCs and platelets. Mild and moderate steatotic liver models were generated in Wistar rats by feeding a cholinedeficient diet for 2 and 4 weeks, respectively. The intensity of steatosis was defined based on the proportion of hepatocytes with fatty infiltration: normal (less than 5%), a mild steatosis (5-30%), and moderate steatosis (30-60%). All groups were subjected to 20 min of warm ischemia followed by 120 min of reperfusion. The number of adhesion of KCs to platelets in sinusoids was observed by intravital microscopy. IR injury was evaluated with serum alanine aminotransferase levels, histological findings, and sinusoidal perfusion. Compared to the normal liver, mild steatosis reduced the adhesion of KCs to platelets, inducing the attenuation of IR injury. In contrast, moderate steatosis increased the adhesion of KCs to platelets, aggravating IR injury relative to the normal liver. IR injury in the steatotic liver was not simply proportional to the degree of steatosis. Mild steatosis ameliorates IR injury compared to the normal liver, whereas moderate steatosis increases IR injury.

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Platelet Dynamics in the Early Phase of Postischemic Liver In Vivo

Cited by 53 publications

References 34 publications

Novel functions of platelets in the liver

Novel functions of platelets in the liver

Ethamsylate Protects Against the Carbon Tetrachloride-Induced Liver Damage in Rats

Interaction of Kupffer Cells and Platelets Determines the Severity of Ischemia-Reperfusion Injury in Steatosis

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