The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Suzanne Ostrand-rosenberg - One of the best experts on this subject based on the ideXlab platform.
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High-Mobility Group box protein 1 promotes the survival of myeloid-derived suppressor cells by inducing autophagy.
Journal of Leukocyte Biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived suppressor cells are immune-suppressive cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived suppressor cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule High-Mobility Group box protein 1 drives myeloid-derived suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As High-Mobility Group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if High-Mobility Group box protein 1 regulates myeloid-derived suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived suppressor cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived suppressor cells. Inhibition of High-Mobility Group box protein 1 similarly increased the level of apoptotic myeloid-derived suppressor cells and reduced myeloid-derived suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived suppressor cells, High-Mobility Group box protein 1 sustains myeloid-derived suppressor cell viability. Circulating myeloid-derived suppressor cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived suppressor cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived suppressor cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, High-Mobility Group box protein 1 contributes to tumor progression by increasing myeloid-derived suppressor cell viability by driving them into a proautophagic state.
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High‐mobility Group box protein 1 promotes the survival of myeloid‐derived suppressor cells by inducing autophagy
Journal of leukocyte biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived suppressor cells are immune-suppressive cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived suppressor cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule High-Mobility Group box protein 1 drives myeloid-derived suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As High-Mobility Group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if High-Mobility Group box protein 1 regulates myeloid-derived suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived suppressor cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived suppressor cells. Inhibition of High-Mobility Group box protein 1 similarly increased the level of apoptotic myeloid-derived suppressor cells and reduced myeloid-derived suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived suppressor cells, High-Mobility Group box protein 1 sustains myeloid-derived suppressor cell viability. Circulating myeloid-derived suppressor cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived suppressor cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived suppressor cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, High-Mobility Group box protein 1 contributes to tumor progression by increasing myeloid-derived suppressor cell viability by driving them into a proautophagic state.
Ikuro Maruyama - One of the best experts on this subject based on the ideXlab platform.
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hemoperfusion with a high mobility Group box 1 adsorption column can prevent the occurrence of hepatic ischemia reperfusion injury in rats
Critical Care Medicine, 2010Co-Authors: Tetsu Yamamoto, Akira Yamanoi, Ikuro Maruyama, Tsuneo TanakaAbstract:Objective. High-Mobility Group box 1, a ubiquitous nonhistone chromosomal protein, is passively released from necrotic cells and actively secreted by inflammatory cells. Extracellular High-Mobility Group box 1 has recently been recognized to be a mediator of hepatic ischemia-reperfusion injury; however, the kinetics of High-Mobility Group box 1 during hepatic ischemia-reperfusion and the role of High-Mobility Group box 1 in ischemia-reperfusion injury still remain poorly understood. This study was designed to assess the localization and the kinetics of High-Mobility Group box 1 during hepatic ischemia-reperfusion injury and the effects of High-Mobility Group box 1 adsorption column in hepatic ischemia-reperfusion injury. Design: A prospective, randomized animal study. Setting. University medical center research laboratory. Subjects: Male Sprague-Dawley rats. Investigation: The animals underwent 70% partial hepatic ischemia for 60 or 90 mins and were then reperfused. To investigate the High-Mobility Group box 1 levels in the serum and in the liver, the animals were killed at predetermined periods. As a lethal model, global hepatic ischemia-reperfusion was induced by portal triad cross-clamping for 30 mins. Hemoperfusion therapy using a cellulofine sulfate bead column (High-Mobility Group box 1 adsorption column) was performed during global hepatic ischemia. Measurements and Main Results; During 60 mins of 70% hepatic ischemia, nuclear High-Mobility Group box 1 was translocated to the cytoplasm in hepatocytes; however, serum High-Mobility Group box lwas not increased. Immediately after reperfusion, the serum High-Mobility Group box 1 was significantly increased (p < .05). High-Mobility Group box 1 mediated ischemia-reperfusion injury in not only liver but also the remote organ, lung. Removal of excess High-Mobility Group box 1 in blood using an adsorption column significantly improved animal survival (p < .03) and liver and lung injuries. Conclusions: High-Mobility Group box 1 plays an important role in the systemic as well as local pathogenesis of hepatic ischemia-reperfusion injury. The removal of excessive High-Mobility Group box 1 with adsorption column was beneficial and promising option in ischemia-related liver injuries.
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High-Mobility Group box 1 protein in endophthalmitis.
Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2008Co-Authors: Noboru Arimura, Yuya Kii, Teruto Hashiguchi, Taiji Sakamoto, Ikuro MaruyamaAbstract:Background High-Mobility Group box 1 protein (HMGB1) is recently described as a late mediator of lethal endotoxemia with proinflammatory cytokine-like properties. The purpose of this study was to determine whether HMGB1 is involved in endophthalmitis.
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High Mobility Group Box Chromosomal Protein 1 in Patients with Renal Diseases
Nephron. Clinical practice, 2008Co-Authors: Fumihiko Sato, Shoichi Maruyama, Hiroki Hayashi, Izumi Sakamoto, Shingo Yamada, Tomonori Uchimura, Yoshiki Morita, Yasuhiko Ito, Yukio Yuzawa, Ikuro MaruyamaAbstract:Background/Aim: The high mobility Group box chromosomal protein 1 (HMGB1), a nuclear DNA-binding protein, has recently been recognized as a new proinflammatory cytokine. The purpose
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tumor necrosis factor alpha stimulates gingival epithelial cells to release high mobility Group box 1
Journal of Periodontal Research, 2007Co-Authors: Yoko Morimoto, Teruto Hashiguchi, Koichi Kawahara, Salunya Tancharoen, Kiyoshi Kikuchi, Takashi Matsuyama, Yuichi Izumi, Ikuro MaruyamaAbstract:BACKGROUND AND OBJECTIVE: High-Mobility-Group box 1 functions as a late-phase inflammatory mediator. It can be released extracellularly by macrophages and necrotic cells through lipopolysaccharide and tumor necrosis factor-alpha. The objective of this study was to clarify the source of High-Mobility-Group box 1 in chronic periodontitis tissues and tumor necrosis factor-alpha-stimulated gingival epithelial cells, and subsequently elucidate its inducible inflammatory pathway. MATERIAL AND METHODS: Chronic periodontitis and healthy gingival sections were stained for High-Mobility-Group box 1 by immunohistochemistry and immunofluorescence. The amounts of High-Mobility-Group box 1 released into the gingival crevicular fluid and supernatants from gingival epithelial cells stimulated by tumor necrosis factor-alpha were examined by western blot. The phosphorylation of mitogen-activated protein kinases (MAPKs) in gingival epithelial cells was also examined. RESULTS: High-Mobility-Group box 1 was detected in the cytoplasm and nucleus of gingival epithelial cells with periodontitis. Western blotting revealed a significant increase in High-Mobility-Group box 1 expression in the gingival crevicular fluid from periodontitis patients. High-Mobility-Group box 1 production in gingival epithelial cells was increased following stimulation with tumor necrosis factor-alpha. The molecular dialogue between tumor necrosis factor-alpha and gingival epithelial cells involved modulation of the activities of p38MAPK, Jun N-terminal kinase and p44/42. Interestingly, only phosphorylation of p38MAPK contributed to more than half of the signaling initiated by tumor necrosis factor-alpha-elicited High-Mobility-Group box 1 release. CONCLUSION: High-Mobility-Group box 1 is continuously released from the gingival epithelial cells modulated by tumor necrosis factor-alpha. These findings imply that High-Mobility-Group box 1 expression and possibly p38MAPK constitute important features in periodontitis.
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high mobility Group box 1 protein interacts with multiple toll like receptors
American Journal of Physiology-cell Physiology, 2006Co-Authors: Jong Sung Park, Ikuro Maruyama, Shingo Yamada, Fabia Gambonirobertson, Daiva Svetkauskaite, Jaeyeol Kim, Derek Strassheim, Jangwon Sohn, Anirban Banerjee, Akitoshi IshizakaAbstract:High mobility Group box 1 (HMGB1), originally described as a DNA-binding protein, can also be released extracellularly and functions as a late mediator of inflammatory responses. Although recent re...
Katherine H. Parker - One of the best experts on this subject based on the ideXlab platform.
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High-Mobility Group box protein 1 promotes the survival of myeloid-derived suppressor cells by inducing autophagy.
Journal of Leukocyte Biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived suppressor cells are immune-suppressive cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived suppressor cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule High-Mobility Group box protein 1 drives myeloid-derived suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As High-Mobility Group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if High-Mobility Group box protein 1 regulates myeloid-derived suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived suppressor cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived suppressor cells. Inhibition of High-Mobility Group box protein 1 similarly increased the level of apoptotic myeloid-derived suppressor cells and reduced myeloid-derived suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived suppressor cells, High-Mobility Group box protein 1 sustains myeloid-derived suppressor cell viability. Circulating myeloid-derived suppressor cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived suppressor cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived suppressor cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, High-Mobility Group box protein 1 contributes to tumor progression by increasing myeloid-derived suppressor cell viability by driving them into a proautophagic state.
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High‐mobility Group box protein 1 promotes the survival of myeloid‐derived suppressor cells by inducing autophagy
Journal of leukocyte biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived suppressor cells are immune-suppressive cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived suppressor cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule High-Mobility Group box protein 1 drives myeloid-derived suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As High-Mobility Group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if High-Mobility Group box protein 1 regulates myeloid-derived suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived suppressor cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived suppressor cells. Inhibition of High-Mobility Group box protein 1 similarly increased the level of apoptotic myeloid-derived suppressor cells and reduced myeloid-derived suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived suppressor cells, High-Mobility Group box protein 1 sustains myeloid-derived suppressor cell viability. Circulating myeloid-derived suppressor cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived suppressor cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived suppressor cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, High-Mobility Group box protein 1 contributes to tumor progression by increasing myeloid-derived suppressor cell viability by driving them into a proautophagic state.
Tian-biao Zhou - One of the best experts on this subject based on the ideXlab platform.
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Role of high mobility Group box 1 and its signaling pathways in renal diseases
Journal of receptor and signal transduction research, 2014Co-Authors: Tian-biao ZhouAbstract:The high mobility Group box 1 (HMGB1) protein, a member of the high mobility Group nuclear protein family and an endogenous ligand for TLR2/4 and RAGE (receptor for advanced glycation end products), is one of the most evolutionarily conserved proteins and it has recently emerged as an extracellular signaling factor with key roles in cell differentiation, proliferation and disease pathogenesis. The present data indicate that HMGB1 is one of most important proinflammatory cytokines, and plays an important role in renal diseases. The literatures were searched extensively and this review was performed to sum up the role of HMGB1 in renal diseases.
Lucas A. Horn - One of the best experts on this subject based on the ideXlab platform.
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High-Mobility Group box protein 1 promotes the survival of myeloid-derived suppressor cells by inducing autophagy.
Journal of Leukocyte Biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived suppressor cells are immune-suppressive cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived suppressor cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule High-Mobility Group box protein 1 drives myeloid-derived suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As High-Mobility Group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if High-Mobility Group box protein 1 regulates myeloid-derived suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived suppressor cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived suppressor cells. Inhibition of High-Mobility Group box protein 1 similarly increased the level of apoptotic myeloid-derived suppressor cells and reduced myeloid-derived suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived suppressor cells, High-Mobility Group box protein 1 sustains myeloid-derived suppressor cell viability. Circulating myeloid-derived suppressor cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived suppressor cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived suppressor cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, High-Mobility Group box protein 1 contributes to tumor progression by increasing myeloid-derived suppressor cell viability by driving them into a proautophagic state.
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High‐mobility Group box protein 1 promotes the survival of myeloid‐derived suppressor cells by inducing autophagy
Journal of leukocyte biology, 2016Co-Authors: Katherine H. Parker, Lucas A. Horn, Suzanne Ostrand-rosenbergAbstract:Myeloid-derived suppressor cells are immune-suppressive cells that are elevated in most individuals with cancer, where their accumulation and suppressive activity are driven by inflammation. As myeloid-derived suppressor cells inhibit anti-tumor immunity and promote tumor progression, we are determining how their viability is regulated. Previous studies have established that the damage-associated molecular pattern molecule High-Mobility Group box protein 1 drives myeloid-derived suppressor cell accumulation and suppressive potency and is ubiquitously present in the tumor microenvironment. As High-Mobility Group box protein 1 also facilitates tumor cell survival by inducing autophagy, we sought to determine if High-Mobility Group box protein 1 regulates myeloid-derived suppressor cell survival through induction of autophagy. Inhibition of autophagy increased the quantity of apoptotic myeloid-derived suppressor cells, demonstrating that autophagy extends the survival and increases the viability of myeloid-derived suppressor cells. Inhibition of High-Mobility Group box protein 1 similarly increased the level of apoptotic myeloid-derived suppressor cells and reduced myeloid-derived suppressor cell autophagy, demonstrating that in addition to inducing the accumulation of myeloid-derived suppressor cells, High-Mobility Group box protein 1 sustains myeloid-derived suppressor cell viability. Circulating myeloid-derived suppressor cells have a default autophagic phenotype, and tumor-infiltrating myeloid-derived suppressor cells are more autophagic, consistent with the concept that inflammatory and hypoxic conditions within the microenvironment of solid tumors contribute to tumor progression by enhancing immune-suppressive myeloid-derived suppressor cells. Overall, these results demonstrate that in addition to previously recognized protumor effects, High-Mobility Group box protein 1 contributes to tumor progression by increasing myeloid-derived suppressor cell viability by driving them into a proautophagic state.