Full Text Journal Articles by
Author Michael V L Bennett

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IL-4/STAT6 signaling facilitates innate hematoma resolution and neurological recovery after hemorrhagic stroke in mice.

Jing Xu, Zhouqing Chen, Fang Yu, Huan Liu, Cheng Ma, Di Xie, Xiaoming Hu, Rehana K Leak, Sherry H Y Chou, R Anne Stetler, Yejie Shi, Jun Chen, Michael V L Bennett, Gang Chen,

Intracerebral hemorrhage (ICH) is a devastating form of stroke affecting millions of people worldwide. Parenchymal hematoma triggers a series of reactions leading to primary and secondary brain injuries and permanent neurological deficits. Microglia and macrophages carry out hematoma clearance, thereby facilitating functional recovery after ICH. Here, we elucidate a pivotal ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2020, 117(51):32679-32690]

Cited: 6 times

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Protease-independent action of tissue plasminogen activator in brain plasticity and neurological recovery after ischemic stroke.

Hongjian Pu, Yejie Shi, Lili Zhang, Zhengyu Lu, Qing Ye, Rehana K Leak, Fei Xu, Shubei Ma, Hongfeng Mu, Zhishuo Wei, Na Xu, Yuguo Xia, Xiaoming Hu, T Kevin Hitchens, Michael V L Bennett, Jun Chen,

Emerging evidence suggests that tissue plasminogen activator (tPA), currently the only FDA-approved medication for ischemic stroke, exerts important biological actions on the CNS besides its well-known thrombolytic effect. In this study, we investigated the role of tPA on primary neurons in culture and on brain recovery and plasticity after ischemic ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2019, 116(18):9115-9124]

Cited: 5 times

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Introduction to Connexins and Pannexins in the Healthy and Diseased Nervous System with Thanks to Felikas Bukauskas.

David C Spray, Vytautas K Verselis, Michael V L Bennett,

Neurosci Lett (Neuroscience letters)
[2019, 695:1-3]

Cited: 0 times

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Tissue plasminogen activator promotes white matter integrity and functional recovery in a murine model of traumatic brain injury.

Yuguo Xia, Hongjian Pu, Rehana K Leak, Yejie Shi, Hongfeng Mu, Xiaoming Hu, Zhengyu Lu, Lesley M Foley, T Kevin Hitchens, C Edward Dixon, Michael V L Bennett, Jun Chen,

Recombinant tissue plasminogen activator (tPA) is a Food and Drug Administration-approved thrombolytic treatment for ischemic stroke. tPA is also naturally expressed in glial and neuronal cells of the brain, where it promotes axon outgrowth and synaptic plasticity. However, there are conflicting reports of harmful versus neuroprotective effects of tPA in ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2018, 115(39):E9230-E9238]

Cited: 17 times

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Activation of autophagy rescues synaptic and cognitive deficits in fragile X mice.

Jingqi Yan, Morgan W Porch, Brenda Court-Vazquez, Michael V L Bennett, R Suzanne Zukin,

Fragile X syndrome (FXS) is the most frequent form of heritable intellectual disability and autism. Fragile X (<i>Fmr1</i>-KO) mice exhibit aberrant dendritic spine structure, synaptic plasticity, and cognition. Autophagy is a catabolic process of programmed degradation and recycling of proteins and cellular components via the lysosomal pathway. However, a role ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2018, 115(41):E9707-E9716]

Cited: 26 times

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Oxidative stress and DNA damage after cerebral ischemia: Potential therapeutic targets to repair the genome and improve stroke recovery.

Peiying Li, R Anne Stetler, Rehana K Leak, Yejie Shi, Yan Li, Weifeng Yu, Michael V L Bennett, Jun Chen,

The past two decades have witnessed remarkable advances in oxidative stress research, particularly in the context of ischemic brain injury. Oxidative stress in ischemic tissues compromises the integrity of the genome, resulting in DNA lesions, cell death in neurons, glial cells, and vascular cells, and impairments in neurological recovery after ... Read more >>

Neuropharmacology (Neuropharmacology)
[2018, 134(Pt B):208-217]

Cited: 57 times

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Blood-brain barrier dysfunction and recovery after ischemic stroke.

Xiaoyan Jiang, Anuska V Andjelkovic, Ling Zhu, Tuo Yang, Michael V L Bennett, Jun Chen, Richard F Keep, Yejie Shi,

The blood-brain barrier (BBB) plays a vital role in regulating the trafficking of fluid, solutes and cells at the blood-brain interface and maintaining the homeostatic microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the BBB can be disrupted, followed by the extravasation of blood components into the ... Read more >>

Prog Neurobiol (Progress in neurobiology)
[2018, 163-164:144-171]

Cited: 132 times

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HIV-Associated Cardiovascular Disease: Role of Connexin 43.

Lisa Prevedel, Camilla Morocho, Michael V L Bennett, Eliseo A Eugenin,

Chronic HIV infection due to effective antiretroviral treatment has resulted in a broad range of clinical complications, including accelerated heart disease. Individuals with HIV infection have a 1.5 to 2 times higher incidence of cardiovascular diseases than their uninfected counterparts; however, the underlying mechanisms are poorly understood. To explore the ... Read more >>

Am J Pathol (The American journal of pathology)
[2017, 187(9):1960-1970]

Cited: 4 times

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Endothelium-targeted overexpression of heat shock protein 27 ameliorates blood-brain barrier disruption after ischemic brain injury.

Yejie Shi, Xiaoyan Jiang, Lili Zhang, Hongjian Pu, Xiaoming Hu, Wenting Zhang, Wei Cai, Yanqin Gao, Rehana K Leak, Richard F Keep, Michael V L Bennett, Jun Chen,

The damage borne by the endothelial cells (ECs) forming the blood-brain barrier (BBB) during ischemic stroke and other neurological conditions disrupts the structure and function of the neurovascular unit and contributes to poor patient outcomes. We recently reported that structural aberrations in brain microvascular ECs-namely, uncontrolled actin polymerization and subsequent ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2017, 114(7):E1243-E1252]

Cited: 46 times

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An Acute Mouse Spinal Cord Slice Preparation for Studying Glial Activation ex vivo.

Juan Mauricio Garré, Guang Yang, Feliksas F Bukauskas, Michael V L Bennett,

Pathological conditions such as amyotrophic lateral sclerosis, spinal cord injury and chronic pain are characterized by activation of astrocytes and microglia in spinal cord and have been modeled in rodents. <i>In vivo</i> imaging at cellular level in these animal models is limited due to the spinal cord's highly myelinated funiculi. ... Read more >>

Bio Protoc (Bio-protocol)
[2017, 7(2):]

Cited: 1 time

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Elevated ERK/p90 ribosomal S6 kinase activity underlies audiogenic seizure susceptibility in fragile X mice.

Kirsty Sawicka, Alexander Pyronneau, Miranda Chao, Michael V L Bennett, R Suzanne Zukin,

Fragile X syndrome (FXS) is the most common heritable cause of intellectual disability and a leading genetic form of autism. The Fmr1 KO mouse, a model of FXS, exhibits elevated translation in the hippocampus and the cortex. ERK (extracellular signal-regulated kinase) and mTOR (mechanistic target of rapamycin) signaling regulate protein ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2016, 113(41):E6290-E6297]

Cited: 27 times

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APE1/Ref-1 facilitates recovery of gray and white matter and neurological function after mild stroke injury.

R Anne Stetler, Yanqin Gao, Rehana K Leak, Zhongfang Weng, Yejie Shi, Lili Zhang, Hongjian Pu, Feng Zhang, Xiaoming Hu, Sulaiman Hassan, Carolyn Ferguson, Gregg E Homanics, Guodong Cao, Michael V L Bennett, Jun Chen,

A major hallmark of oxidative DNA damage after stroke is the induction of apurinic/apyrimidinic (AP) sites and strand breaks. To mitigate cell loss after oxidative DNA damage, ischemic cells rapidly engage the base excision-repair proteins, such as the AP site-repairing enzyme AP endonuclease-1 (APE1), also named redox effector factor-1 (Ref-1). ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2016, 113(25):E3558-67]

Cited: 19 times

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FGF-1 Triggers Pannexin-1 Hemichannel Opening in Spinal Astrocytes of Rodents and Promotes Inflammatory Responses in Acute Spinal Cord Slices.

Juan Mauricio Garré, Guang Yang, Feliksas F Bukauskas, Michael V L Bennett,

<h4>Unlabelled</h4>We show here that the growth factor FGF-1 is proinflammatory in the spinal cord and explore the inflammatory mechanisms. FGF-1 applied to rat spinal astrocytes in culture initiates calcium signaling and induces secretion of ATP that within minutes increases membrane permeability to ethidium (Etd(+)) and Ca(2+) by activating P2X7 receptors ... Read more >>

J Neurosci (The Journal of neuroscience : the official journal of the Society for Neuroscience)
[2016, 36(17):4785-4801]

Cited: 33 times

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Ion Channels in Inflammatory Processes: What Is Known and What Is Next?

Mauricio A Retamal, Michael V L Bennett, Pablo Pelegrin, Ricardo Fernandez,

Mediators Inflamm (Mediators of inflammation)
[2016, 2016:6245731]

Cited: 1 time

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Estradiol pretreatment ameliorates impaired synaptic plasticity at synapses of insulted CA1 neurons after transient global ischemia.

Koichi Takeuchi, Yupeng Yang, Yukihiro Takayasu, Michael Gertner, Jee-Yeon Hwang, Kelly Aromolaran, Michael V L Bennett, R Suzanne Zukin,

Global ischemia in humans or induced experimentally in animals causes selective and delayed neuronal death in pyramidal neurons of the hippocampal CA1. The ovarian hormone estradiol administered before or immediately after insult affords histological protection in experimental models of focal and global ischemia and ameliorates the cognitive deficits associated with ... Read more >>

Brain Res (Brain research)
[2015, 1621:222-230]

Cited: 8 times

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Fast structural responses of gap junction membrane domains to AB5 toxins.

Irina V Majoul, Liang Gao, Eric Betzig, Daria Onichtchouk, Eugenia Butkevich, Yuri Kozlov, Feliksas Bukauskas, Michael V L Bennett, Jennifer Lippincott-Schwartz, Rainer Duden,

Gap junctions (GJs) represent connexin-rich membrane domains that connect interiors of adjoining cells in mammalian tissues. How fast GJs can respond to bacterial pathogens has not been known previously. Using Bessel beam plane illumination and confocal spinning disk microscopy, we found fast (~500 ms) formation of connexin-depleted regions (CDRs) inside ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2013, 110(44):E4125-33]

Cited: 5 times

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The ATP required for potentiation of skeletal muscle contraction is released via pannexin hemichannels.

Manuel A Riquelme, Luis A Cea, José L Vega, Mauricio P Boric, Hannah Monyer, Michael V L Bennett, Marina Frank, Klaus Willecke, Juan C Sáez,

During repetitive stimulation of skeletal muscle, extracellular ATP levels raise, activating purinergic receptors, increasing Ca2+ influx, and enhancing contractile force, a response called potentiation. We found that ATP appears to be released through pannexin1 hemichannels (Panx1 HCs). Immunocytochemical analyses and function were consistent with pannexin1 localization to T-tubules intercalated with ... Read more >>

Neuropharmacology (Neuropharmacology)
[2013, 75:594-603]

Cited: 52 times

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Dysregulation of synaptic plasticity precedes appearance of morphological defects in a Pten conditional knockout mouse model of autism.

Koichi Takeuchi, Michael J Gertner, Jing Zhou, Luis F Parada, Michael V L Bennett, R Suzanne Zukin,

The phosphoinositide signaling system is a crucial regulator of neural development, cell survival, and plasticity. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) negatively regulates phosphatidylinositol 3-kinase signaling and downstream targets. Nse-Cre Pten conditional knockout mice, in which Pten is ablated in granule cells of the dentate gyrus and ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2013, 110(12):4738-4743]

Cited: 62 times

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Intracellular magnesium-dependent modulation of gap junction channels formed by neuronal connexin36.

Nicolás Palacios-Prado, Gregory Hoge, Alina Marandykina, Lina Rimkute, Sandrine Chapuis, Nerijus Paulauskas, Vytenis A Skeberdis, John O'Brien, Alberto E Pereda, Michael V L Bennett, Feliksas F Bukauskas,

Gap junction (GJ) channels composed of Connexin36 (Cx36) are widely expressed in the mammalian CNS and form electrical synapses between neurons. Here we describe a novel modulatory mechanism of Cx36 GJ channels dependent on intracellular free magnesium ([Mg(2+)]i). We examined junctional conductance (gj) and its dependence on transjunctional voltage (Vj) ... Read more >>

J Neurosci (The Journal of neuroscience : the official journal of the Society for Neuroscience)
[2013, 33(11):4741-4753]

Cited: 28 times

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Connexin and pannexin hemichannels in inflammatory responses of glia and neurons.

Michael V L Bennett, Juan M Garré, Juan A Orellana, Felix F Bukauskas, Maiken Nedergaard, Juan C Sáez,

Mammals express ∼20 different connexins, the main gap junction forming proteins in mammals, and 3 pannexins, homologs of innexins, the main gap junction forming proteins in invertebrates. In both classes of gap junction, each channel is formed by two hemichannels, one contributed by each of the coupled cells. There is ... Read more >>

Brain Res (Brain research)
[2012, 1487:3-15]

Cited: 114 times

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Stomatin inhibits pannexin-1-mediated whole-cell currents by interacting with its carboxyl terminal.

Haiying Zhan, Craig S Moore, Bojun Chen, Xin Zhou, Xin-Ming Ma, Kumiko Ijichi, Michael V L Bennett, Xue-Jun Li, Stephen J Crocker, Zhao-Wen Wang,

The pannexin-1 (Panx1) channel (often referred to as the Panx1 hemichannel) is a large-conductance channel in the plasma membrane of many mammalian cells. While opening of the channel is potentially detrimental to the cell, little is known about how it is regulated under physiological conditions. Here we show that stomatin ... Read more >>

PLoS One (PloS one)
[2012, 7(6):e39489]

Cited: 15 times

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The role of gap junction channels during physiologic and pathologic conditions of the human central nervous system.

Eliseo A Eugenin, Daniel Basilio, Juan C Sáez, Juan A Orellana, Cedric S Raine, Feliksas Bukauskas, Michael V L Bennett, Joan W Berman,

Gap junctions (GJs) are expressed in most cell types of the nervous system, including neuronal stem cells, neurons, astrocytes, oligodendrocytes, cells of the blood brain barrier (endothelial cells and astrocytes) and under inflammatory conditions in microglia/macrophages. GJs connect cells by the docking of two hemichannels, one from each cell with ... Read more >>

J Neuroimmune Pharmacol (Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology)
[2012, 7(3):499-518]

Cited: 73 times

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Repressor element-1 silencing transcription factor (REST)-dependent epigenetic remodeling is critical to ischemia-induced neuronal death.

Kyung-Min Noh, Jee-Yeon Hwang, Antonia Follenzi, Rodoniki Athanasiadou, Takahiro Miyawaki, John M Greally, Michael V L Bennett, R Suzanne Zukin,

Dysregulation of the transcriptional repressor element-1 silencing transcription factor (REST)/neuron-restrictive silencer factor is important in a broad range of diseases, including cancer, diabetes, and heart disease. The role of REST-dependent epigenetic modifications in neurodegeneration is less clear. Here, we show that neuronal insults trigger activation of REST and CoREST in ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2012, 109(16):E962-71]

Cited: 104 times

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Critical role of connexin 43 in secondary expansion of traumatic spinal cord injury.

Chunlan Huang, Xiaoning Han, Xi Li, Eric Lam, Weiguo Peng, Nanhong Lou, Arnulfo Torres, Meixiang Yang, Juan Mauricio Garre, Guo-Feng Tian, Michael V L Bennett, Maiken Nedergaard, Takahiro Takano,

Spinal cord injury (SCI) is often complicated by secondary injury as a result of the innate inflammatory response to tissue trauma and swelling. Previous studies have shown that excessive ATP release from peritraumatic regions contributes to the inflammatory response to SCI by activation of low-affinity P2X7 receptors. Because connexin hemichannels ... Read more >>

J Neurosci (The Journal of neuroscience : the official journal of the Society for Neuroscience)
[2012, 32(10):3333-3338]

Cited: 72 times

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Ischemia-induced calpain activation causes eukaryotic (translation) initiation factor 4G1 (eIF4GI) degradation, protein synthesis inhibition, and neuronal death.

Peter S Vosler, Yanqin Gao, Christopher S Brennan, Akiko Yanagiya, Yu Gan, Guodong Cao, Feng Zhang, Simon J Morley, Nahum Sonenberg, Michael V L Bennett, Jun Chen,

Persistent protein synthesis inhibition (PSI) is a robust predictor of eventual neuronal death following cerebral ischemia. We thus tested the hypothesis that persistent PSI inhibition and neuronal death are causally linked. Neuronal viability strongly correlated with both protein synthesis and levels of eukaryotic (translation) initiation factor 4G1 (eIF4G1). We determined ... Read more >>

Proc Natl Acad Sci U S A (Proceedings of the National Academy of Sciences of the United States of America)
[2011, 108(44):18102-18107]

Cited: 16 times

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