| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Jingyang Huang, Baoyi Liu, Chenghui Yang, Haili Chen, Dzivor Eunice, Zhongrui Yua. Acute hyperglycemia worsens ischemic stroke-induced brain damage via high mobility group box-1 in rats. Brain research. vol 1535. 2014-05-08. PMID:24012767. |
in conclusion, enhanced early extracellular release of hmgb1 might represent an important mechanism for worsened ischemic damage, particularly early bbb disruption, during hyperglycemic stroke. |
2014-05-08 |
2023-08-12 |
rat |
| Jingyang Huang, Baoyi Liu, Chenghui Yang, Haili Chen, Dzivor Eunice, Zhongrui Yua. Acute hyperglycemia worsens ischemic stroke-induced brain damage via high mobility group box-1 in rats. Brain research. vol 1535. 2014-05-08. PMID:24012767. |
an hmgb1 inhibitor glycyrrhizin is a potential therapeutic option for hyperglycemic stroke. |
2014-05-08 |
2023-08-12 |
rat |
| Kiyoshi Kikuchi, Salunya Tancharoen, Takashi Ito, Yoko Morimoto-Yamashita, Naoki Miura, Ko-ichi Kawahara, Ikuro Maruyama, Yoshinaka Murai, Eiichiro Tanak. Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke. International journal of molecular sciences. vol 14. issue 9. 2014-04-07. PMID:24065095. |
extracellular hmgb1 causes multiple organ failure and contributes to the pathogenesis of hypertension, hyperlipidemia, diabetes mellitus, atherosclerosis, thrombosis, and stroke. |
2014-04-07 |
2023-08-12 |
Not clear |
| Min He, Bin Zhang, Xinbing Wei, Ziying Wang, Baoxia Fan, Pengchao Du, Yan Zhang, Wencheng Jian, Lin Chen, Linlin Wang, Hao Fang, Xiang Li, Ping-An Wang, Fan Y. HDAC4/5-HMGB1 signalling mediated by NADPH oxidase activity contributes to cerebral ischaemia/reperfusion injury. Journal of cellular and molecular medicine. vol 17. issue 4. 2013-11-22. PMID:23480850. |
our results for the first time provide evidence that nadph oxidase-mediated hdac4 and hdac5 expression contributes to cerebral ischaemia injury via hmgb1 signalling pathway, suggesting that it is important to elucidate the role of individual hdacs within the brain, and the development of hdac inhibitors with improved specificity is required to develop effective therapeutic strategies to treat stroke. |
2013-11-22 |
2023-08-12 |
Not clear |
| Kazuhide Hayakawa, Loc-Duyen D Pham, Ken Arai, Eng H L. High-mobility group box 1: an amplifier of stem and progenitor cell activity after stroke. Acta neurochirurgica. Supplement. vol 118. 2013-08-13. PMID:23564100. |
but during the brain remodeling phase of stroke recovery, hmgb1 can mediate beneficial plasticity and enhance stem and progenitor cell recruitment, proliferation, and differentiation within damaged brain. |
2013-08-13 |
2023-08-12 |
Not clear |
| Kazuhide Hayakawa, Loc-Duyen D Pham, Ken Arai, Eng H L. High-mobility group box 1: an amplifier of stem and progenitor cell activity after stroke. Acta neurochirurgica. Supplement. vol 118. 2013-08-13. PMID:23564100. |
these emerging findings support the hypothesis that hmgb1 might be an important molecule for regulating stem and progenitor cell therapies in stroke patients. |
2013-08-13 |
2023-08-12 |
Not clear |
| A W S de Souza, J Westra, P C Limburg, M Bijl, C G M Kallenber. HMGB1 in vascular diseases: Its role in vascular inflammation and atherosclerosis. Autoimmunity reviews. vol 11. issue 12. 2013-02-06. PMID:22495229. |
patients with acute coronary syndromes or stroke present significantly higher serum levels of hmgb1 than healthy controls and levels are associated with disease severity and mortality. |
2013-02-06 |
2023-08-12 |
Not clear |
| Il-Doo Kim, Joo-Hyun Shin, Hye-Kyung Lee, Yin-Chuan Jin, Ja-Kyeong Le. Intranasal delivery of HMGB1-binding heptamer peptide confers a robust neuroprotection in the postischemic brain. Neuroscience letters. vol 525. issue 2. 2012-12-10. PMID:22877697. |
in the present study, we investigated the therapeutic efficacy of intranasally delivered hmgb1 binding heptamer peptide (hbhp; hmskpvq), which was selected using a phage display approach, in the same stroke animal model. |
2012-12-10 |
2023-08-12 |
rat |
| Kazuhide Hayakawa, Loc-Duyen D Pham, Zvonimir S Katusic, Ken Arai, Eng H L. Astrocytic high-mobility group box 1 promotes endothelial progenitor cell-mediated neurovascular remodeling during stroke recovery. Proceedings of the National Academy of Sciences of the United States of America. vol 109. issue 19. 2012-08-13. PMID:22529378. |
here, we show that reactive astrocytes can release a damage-associated molecular-pattern molecule called high-mobility-group-box-1 (hmgb1) that promotes endothelial progenitor cell (epc)-mediated neurovascular remodeling during stroke recovery. |
2012-08-13 |
2023-08-12 |
mouse |
| Kazuhide Hayakawa, Loc-Duyen D Pham, Zvonimir S Katusic, Ken Arai, Eng H L. Astrocytic high-mobility group box 1 promotes endothelial progenitor cell-mediated neurovascular remodeling during stroke recovery. Proceedings of the National Academy of Sciences of the United States of America. vol 109. issue 19. 2012-08-13. PMID:22529378. |
taken together, these molecular and in vivo findings support a previously undescribed mechanism of crosstalk between reactive astrocytes and epcs wherein hmgb1 promotes neurovascular remodeling and functional recovery after stroke and brain injury. |
2012-08-13 |
2023-08-12 |
mouse |
| Andréy Mazarati, Mattia Maroso, Valentina Iori, Annamaria Vezzani, Mirjana Carl. High-mobility group box-1 impairs memory in mice through both toll-like receptor 4 and Receptor for Advanced Glycation End Products. Experimental neurology. vol 232. issue 2. 2011-12-20. PMID:21884699. |
this mechanism may contribute to memory deficits under various neurological and psychiatric conditions associated with the increased hmgb1 levels, such as epilepsy, alzheimer's disease and stroke. |
2011-12-20 |
2023-08-12 |
mouse |
| Yu Zhou, Kun-Lin Xiong, Sen Lin, Qi Zhong, Feng-Lin Lu, Hong Liang, Jing-Cheng Li, Jing-Zhou Wang, Qing-Wu Yan. Elevation of high-mobility group protein box-1 in serum correlates with severity of acute intracerebral hemorrhage. Mediators of inflammation. vol 2010. 2011-01-28. PMID:20936104. |
the purpose of this study was to examine the correlation between changes in serum levels of hmgb1 following acute ich and the severity of stroke as well as the underlying mechanism. |
2011-01-28 |
2023-08-12 |
mouse |
| Kazuhide Hayakawa, Jianhua Qiu, Eng H L. Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke. Annals of the New York Academy of Sciences. vol 1207. 2010-11-09. PMID:20955426. |
biphasic actions of hmgb1 signaling in inflammation and recovery after stroke. |
2010-11-09 |
2023-08-12 |
Not clear |
| Kazuhide Hayakawa, Ken Arai, Eng H L. Role of ERK map kinase and CRM1 in IL-1beta-stimulated release of HMGB1 from cortical astrocytes. Glia. vol 58. issue 8. 2010-07-12. PMID:20222144. |
however, we previously showed that reactive astrocytes may also contribute to stroke recovery, partly via the release of a nuclear protein called high-mobility group box 1 (hmgb1). |
2010-07-12 |
2023-08-12 |
rat |
| Antje Vogelgesang, Verena E L May, Uwe Grunwald, Maren Bakkeboe, Soenke Langner, Henry Wallaschofski, Christof Kessler, Barbara M Bröker, Alexander Dresse. Functional status of peripheral blood T-cells in ischemic stroke patients. PloS one. vol 5. issue 1. 2010-05-20. PMID:20090932. |
also, in sera of stroke patients hmgb1 concentrations were increased (p = 0.0002). |
2010-05-20 |
2023-08-12 |
Not clear |
| Antje Vogelgesang, Verena E L May, Uwe Grunwald, Maren Bakkeboe, Soenke Langner, Henry Wallaschofski, Christof Kessler, Barbara M Bröker, Alexander Dresse. Functional status of peripheral blood T-cells in ischemic stroke patients. PloS one. vol 5. issue 1. 2010-05-20. PMID:20090932. |
the data demonstrate that surviving t cells in stroke patients remain fully functional and are primed towards a th1 response, in addition we provide evidence that catecholamine mediated inhibition of ctla-4 expression and serum hmgb1 release are possible mediators in stroke induced activation of t cells. |
2010-05-20 |
2023-08-12 |
Not clear |
| Sajjad Muhammad, Waleed Barakat, Stoyan Stoyanov, Sasidhar Murikinati, Huan Yang, Kevin J Tracey, Martin Bendszus, Grazisa Rossetti, Peter P Nawroth, Angelika Bierhaus, Markus Schwaninge. The HMGB1 receptor RAGE mediates ischemic brain damage. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 28. issue 46. 2009-01-26. PMID:19005067. |
the rage ligand high mobility group box 1 (hmgb1) was elevated in serum of stroke patients and was released from ischemic brain tissue in a mouse model of cerebral ischemia. |
2009-01-26 |
2023-08-12 |
mouse |
| Wei Li, Jianhua Li, Mala Ashok, Rongqian Wu, Dazhi Chen, Lihong Yang, Huan Yang, Kevin J Tracey, Ping Wang, Andrew E Sama, Haichao Wan. A cardiovascular drug rescues mice from lethal sepsis by selectively attenuating a late-acting proinflammatory mediator, high mobility group box 1. Journal of immunology (Baltimore, Md. : 1950). vol 178. issue 6. 2007-05-22. PMID:17339485. |
the therapeutic effects were partly attributable to attenuation of systemic accumulation of hmgb1 (but not tnf and no) and improvement of cardiovascular physiologic parameters (e.g., decrease in total peripheral vascular resistance and increase in cardiac stroke volume) in septic animals. |
2007-05-22 |
2023-08-12 |
mouse |