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| 1 | Platelet aggregation but not activation and degranulation during the acute post-ischemic reperfusion phase in livers with no underlying disease显示文摘Background:Platelets and P-selectin(CD62P)play an unequivocal role in the pathology of hepatic ischemia/reperfusion(I/R)injury.Inhibition or knock-out of P-selectin or immunodepletion of platelets results in amelioration of post-ischemic inflammation,reduced hepatocellular damage,and improved survival.However,P-selectin expression on platelets and endothelial cells,which concurs with platelet activation,has never been clearly demonstrated in I/R-subjected livers.Aims:To determine whether platelets become activated and degranulate in the acute phase of liver I/R and whether the platelets interact with neutrophils.Methods:Hepatic I/R was induced in male C57BL/6J mice(N=12)using 37.5-min ischemia time.Platelets,endothelial cells,and neutrophils were fluorescently labeled by systemic administration of non-blocking antibodies.Cell kinetics were monitored by intravital spinning disk confocal microscopy during 90 min of reperfusion.Image analysis and quantification was performed with dedicated software.Results:Platelets adhered to sinusoids more extensively in post-ischemic livers compared to livers not subjected to I/R and formed aggregates,which occurred directly after ischemia.Platelets and endothelial cells did not express P-selectin in post-ischemic livers.There was no interaction between platelets and neutrophils.Conclusions:Platelets aggregate but do not become activated and do not degranulate in post-ischemic livers.There is no platelet-neutrophil interplay during the early reperfusion phase in a moderate model of hepatic I/R injury.The mechanisms underlying the biological effects of platelets and P-selectin in this setting warrant further investigation.Relevance for patients:I/R in surgical liver patients may compromise outcome due to post-ischemic oxidative stress and sterile inflammation.Both processes are mediated in part by platelets.Understanding platelet function during I/R is key to developing effective interventions for I/R injury and improving clinical outcomes. | Rowan F.van Golen Katarzyna M.Stevens Pina Colarusso Hartmut Jaeschke Michal Heger | 2015 | Journal of Clinical & Translational Research2015，1，2： | 2 |
| 2 | Post-hepatectomy liver regeneration in the context of bile acid homeostasis and the gut-liver signaling axis显示文摘Background:Liver regeneration following partial hepatectomy(PHx)is a complicated process involving multiple organs and several types of signaling networks.The bile acid-activated metabolic pathways occupy an auxiliary yet important chapter in the entire biochemical story.PHx is characterized by rapid but transient bile acid overload in the liver,which constitutes the first wave of proliferative signaling in the remnant hepatocytes.Bile acids trigger hepatocyte proliferation through activation of several nuclear receptors.Following biliary passage into the intestines,enterocytes reabsorb the bile acids,which results in the activation of farnesoid X receptor(FXR),the consequent excretion of fibroblast growth factor(FGF)19/FGF15,and its release into the enterohepatic circulation.FGF19/FGF15 subsequently binds to its cognate receptor,fibroblast growth factor receptor 4(FGFR4)complexed withβ-klotho,on the hepatocyte membrane,which initiates the second wave of proliferative signaling.Because some bile acids are toxic,the remnant hepatocytes must resolve the potentially detrimental state of bile acid excess.Therefore,the hepatocytes orchestrate a bile acid detoxification and elimination response as a protective mechanism in concurrence with the proliferative signaling.The response in part results in the excretion of(biotransformed)bile acids into the canalicular system,causing the bile acids to end up in the intestines.Relevance for patients:Recently,FXR agonists have been shown to promote regeneration via the gut-liver axis.This type of pharmacological intervention may prove beneficial for patients with hepatobiliary tumors undergoing PHx.In light of these developments,the review provides an in-depth account of the pathways that underlie post-PHx liver regeneration in the context of bile acid homeostasis in the liver and the gut-liver signaling axis. | Lianne de Haan Sarah Jvan der Lely Anne-Loes K.Warps Quincy Hofsink Pim B.Olthof Mark J.de Keijzer Daniel A.Lionarons Lionel Mendes-Dias Bote G.Bruinsma Korkut Uygun Hartmut Jaeschke Geoffrey C.Farrell Narci Teoh Rowan Fvan Golen Tiangang Li Michal Heger | 2018 | Journal of Clinical & Translational Research2018，4，1： | 2 |
| 3 | Flashover Breakdown of an Insulator in Vacuum by a Voltage Impulse in the Presence of a Magnetic Field显示文摘 | Kapertanakos C A | 1977 | J Appl Phys1977，48，： | 1 |
| 4 | SLOOP promotes pancreatic cancer growth, smwival, and invasion 显示文摘 | Arumugam T Simeone DM Van Golen K | 2005 | Clin Canc er Res2005，11，15： | 1 |
| 5 | Reversion of RhoC GT- Pase induced inflammatory breast cancer phenotype by treatment with a farnesyl transferase inhibitor显示文摘 | Van Golen KL Bao L DiVito MM | 2002 | Mol Cancer Ther2002，1，8： | 1 |
| 6 | Farnesyl transferase inhibitor treatment of breast cancer cells leads to altered RhoA and RhoC GTPase activity and induces adormant phenotype显示文摘 | Chatterjee M van Golen KL | | 0，，： | 1 |
| 7 | Multiple signaling pathways are activated during insulin-like growth factor-Ⅰ (IGF-Ⅰ) stimulated breast cancer cell migration显示文摘 | Zhang X Lin M van Golen KL | 2005 | Breast Cancer Res Treat2005，93，2： | 1 |
| 8 | RhoC GTPase, a novel transforming oncogene for human mammary epithelial cells that partially recapitulates the inflammatory breast cancer phenotype 显示文摘 | Van Golen KL Wu ZF Qiao XT | 2000 | Cancer Res2000，60，： | 1 |
| 9 | Characterization of RhoC expression in benign and malignant breast disease:a potential new marker for small breast carcinomas with metastatic ability 显示文摘 | Kleer CG van Golen KL Zhang Y | 2002 | Am J Pathol2002，160，： | 1 |
| 10 | Persistent E -cadherin expression in inflammatory breast cancer 显示文摘 | Kleer CG Van Golen KL Braun T | 2001 | Mod Pathol2001，14，5： | 1 |
| 11 | Type I collagen receptor α2β1 signaling promotes the growth of human prostate cancer cells within the bone显示文摘 | Hall CL Dai JL van Golen KL | 2006 | Cancer Res2006，66，： | 1 |
| 12 | Pc:rsistent Ecadherin expression in inflammatory breast cancer显示文摘 | Kleer CG Van Golen KL Braun T | | 0，，05： | 1 |
| 13 | Insulin-like growth factor-1 regulates glucose-induced mitochondrial depolari- zation and apoptosis in human neuroblastoma 显示文摘 | Leinninger G M Russell J W van Golen C M | 2004 | Cell Death Differ2004，11，8： | 1 |
| 14 | Persistent E-cadherin expression in inflammatory breast cancer 显示文摘 | Kleer CG van Golen KL Braun T | 2001 | Mod Pathol2001，14，5： | 1 |
| 15 | Cofilin activity during insulin-like growth factor I-stimulated neuroblastoma cell motility显示文摘 | G. Meyer B. Kim C. Golen E. L. Feldman | 2005 | CMLS Cellular and Molecular Life Sciences2005，，4： | 1 |
| 16 | Characterization of RhoC expression in benign and malignant breast disease: a potential new marker for small breast carcinomas with metastatic ahility显示文摘 | Kleer CG Van Golen KL Zhang Y | 2002 | Am J Pathol2002，16，2： | 1 |
| 17 | Cofilin activity during insulin-like growth factor-1 stimulated neuroblastoma cell motility 显示文摘 | Myer G KimB van Golen C | 2005 | Cell Mol Life Sci2005，62，4： | 1 |
| 18 | Angiogene-sis,lymphangiogenesis,growth pattern,and tumor emboli in in-flammatory breast cancer:a review of the current knowledge显示文摘 | Vermeulen P B van Golen K L Dirix L Y | | 0，，： | 1 |
| 19 | Structural identification,neuronal synthesis,and role in male copulation of myomodulin-A of Lymnaea:a study involving direct peptide profiling of nervous tissue by mass spectrometry显示文摘 | Li K W van Golen F A van Minnen J | 1994 | Molecular Brain Research1994，25，34： | 1 |
| 20 | Mitogen activated protein kinase pathway is involved in RhoC GTPase induced motility, invasion and angiogenesis in inflammatory breast cancer显示文摘 | Bao LW Pan Q | 2002 | Clin Exp Metastasis2002，19，4： | 1 |
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