scholarly journals Invasion of phagocytic Galectin 3 expressing macrophages in the diabetic brain disrupts vascular repair

2021 ◽  
Vol 7 (34) ◽  
pp. eabg2712
Author(s):  
Eslam M. F. Mehina ◽  
Stephanie Taylor ◽  
Roobina Boghozian ◽  
Emily White ◽  
Sun Eui Choi ◽  
...  
Keyword(s):  
Time Lapse ◽  
Diabetic Mice ◽  
Vascular Repair ◽  
Cerebral Microvessels ◽  
Cellular Events ◽  
Galectin 3 ◽  
At Risk Populations ◽  
Time Lapse Imaging ◽  
Imaging Gene Expression

The cellular events that dictate the repair of damaged vessels in the brain, especially in those with vascular risk factors such as diabetes, is poorly understood. Here, we dissected the role of resident microglia and infiltrative macrophages in determining the repair of ruptured cerebral microvessels. Using in vivo time-lapse imaging, gene expression analysis, and immunohistochemistry, we identified a unique population of phagocytic Galectin 3 (Gal3) expressing macrophages, distinct from resident microglia, which infiltrated and aggregated at the site of injury in diabetic mice and were associated with the elimination of microvessels. Depletion of these infiltrative macrophages in diabetic mice attenuated phagocytic activity and prevented the loss of blood vessels after injury. These findings highlight a previously unknown role for infiltrative Gal3 expressing macrophages in promoting vessel elimination after brain injury and provide impetus for future studies to determine whether depleting these cells can facilitate vascular repair in at risk populations.

Topical Review: Neuronal Migration in Cortical Development

2004 ◽  
Vol 19 (3) ◽  
pp. 274-279
Author(s):  
Shigeaki Kanatani ◽  
Hidenori Tabata ◽  
Kazunori Nakajima
Keyword(s):  
Neuronal Migration ◽  
Radial Glia ◽  
Asymmetric Cell Division ◽  
Time Lapse ◽  
Radial Glial Cells ◽  
Daughter Cells ◽  
Radial Glial ◽  
Time Lapse Imaging ◽  
Mitotic Behavior

Cortical formation in the developing brain is a highly complicated process involving neuronal production (through symmetric or asymmetric cell division) interaction of radial glia with neuronal migration, and multiple modes of neuronal migration. It has been convincingly demonstrated by numerous studies that radial glial cells are neural stem cells. However, the processes by which neurons arise from radial glia and migrate to their final destinations in vivo are not yet fully understood. Recent studies using time-lapse imaging of neuronal migration are giving investigators an increasingly more detailed understanding of the mitotic behavior of radial glia and the migrating behavior of their daughter cells. In this review, we describe recent progress in elucidating neuronal migration in brain formation and how neuronal migration is disturbed by mutations in genes that control this process. ( J Child Neurol 2005;20:274—279).

scholarly journals Individual neuronal subtypes control initial myelin sheath growth and stabilization

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Heather N. Nelson ◽  
Anthony J. Treichel ◽  
Erin N. Eggum ◽  
Madeline R. Martell ◽  
Amanda J. Kaiser ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Myelin Sheath ◽  
Time Lapse ◽  
Marked Individual ◽  
Larval Zebrafish ◽  
Sheath Formation ◽  
Time Lapse Imaging

Abstract Background In the developing central nervous system, pre-myelinating oligodendrocytes sample candidate nerve axons by extending and retracting process extensions. Some contacts stabilize, leading to the initiation of axon wrapping, nascent myelin sheath formation, concentric wrapping and sheath elongation, and sheath stabilization or pruning by oligodendrocytes. Although axonal signals influence the overall process of myelination, the precise oligodendrocyte behaviors that require signaling from axons are not completely understood. In this study, we investigated whether oligodendrocyte behaviors during the early events of myelination are mediated by an oligodendrocyte-intrinsic myelination program or are over-ridden by axonal factors. Methods To address this, we utilized in vivo time-lapse imaging in embryonic and larval zebrafish spinal cord during the initial hours and days of axon wrapping and myelination. Transgenic reporter lines marked individual axon subtypes or oligodendrocyte membranes. Results In the larval zebrafish spinal cord, individual axon subtypes supported distinct nascent sheath growth rates and stabilization frequencies. Oligodendrocytes ensheathed individual axon subtypes at different rates during a two-day period after initial axon wrapping. When descending reticulospinal axons were ablated, local spinal axons supported a constant ensheathment rate despite the increased ratio of oligodendrocytes to target axons. Conclusion We conclude that properties of individual axon subtypes instruct oligodendrocyte behaviors during initial stages of myelination by differentially controlling nascent sheath growth and stabilization.

scholarly journals NETosis proceeds by cytoskeleton and endomembrane disassembly and PAD4-mediated chromatin decondensation and nuclear envelope rupture

2020 ◽  
Vol 117 (13) ◽  
pp. 7326-7337 ◽  
Author(s):  
Hawa Racine Thiam ◽  
Siu Ling Wong ◽  
Rong Qiu ◽  
Mark Kittisopikul ◽  
Amir Vahabikashi ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Nuclear Envelope ◽  
Time Lapse ◽  
Extracellular Dna ◽  
Sterile Inflammation ◽  
Human Neutrophils ◽  
Chromatin Decondensation ◽  
Membrane Rupture ◽  
Cellular Events

Neutrophil extracellular traps (NETs) are web-like DNA structures decorated with histones and cytotoxic proteins that are released by activated neutrophils to trap and neutralize pathogens during the innate immune response, but also form in and exacerbate sterile inflammation. Peptidylarginine deiminase 4 (PAD4) citrullinates histones and is required for NET formation (NETosis) in mouse neutrophils. While the in vivo impact of NETs is accumulating, the cellular events driving NETosis and the role of PAD4 in these events are unclear. We performed high-resolution time-lapse microscopy of mouse and human neutrophils and differentiated HL-60 neutrophil-like cells (dHL-60) labeled with fluorescent markers of organelles and stimulated with bacterial toxins or Candida albicans to induce NETosis. Upon stimulation, cells exhibited rapid disassembly of the actin cytoskeleton, followed by shedding of plasma membrane microvesicles, disassembly and remodeling of the microtubule and vimentin cytoskeletons, ER vesiculation, chromatin decondensation and nuclear rounding, progressive plasma membrane and nuclear envelope (NE) permeabilization, nuclear lamin meshwork and then NE rupture to release DNA into the cytoplasm, and finally plasma membrane rupture and discharge of extracellular DNA. Inhibition of actin disassembly blocked NET release. Mouse and dHL-60 cells bearing genetic alteration of PAD4 showed that chromatin decondensation, lamin meshwork and NE rupture and extracellular DNA release required the enzymatic and nuclear localization activities of PAD4. Thus, NETosis proceeds by a stepwise sequence of cellular events culminating in the PAD4-mediated expulsion of DNA.

In Vivo Time-Lapse Imaging of Neuronal Development inXenopus

2013 ◽  
Vol 2013 (9) ◽  
pp. pdb.top077156 ◽  
Author(s):  
Edward S. Ruthazer ◽  
Anne Schohl ◽  
Neil Schwartz ◽  
Aydin Tavakoli ◽  
Marc Tremblay ◽  
...  
Keyword(s):  
Neuronal Development ◽  
Time Lapse ◽  
Time Lapse Imaging

scholarly journals Sindbis Virus-Induced Neuronal Death Is both Necrotic and Apoptotic and Is Ameliorated byN-Methyl-d-Aspartate Receptor Antagonists

2001 ◽  
Vol 75 (15) ◽  
pp. 7114-7121 ◽  
Author(s):  
Jennifer L. Nargi-Aizenman ◽  
Diane E. Griffin
Keyword(s):  
Cell Death ◽  
Cortical Neurons ◽  
Sindbis Virus ◽  
Apoptotic Cell ◽  
Time Lapse ◽  
Apoptotic Cell Death ◽  
Time Lapse Imaging ◽  
Alphavirus Infection

ABSTRACT Virus infection of neurons leads to different outcomes ranging from latent and noncytolytic infection to cell death. Viruses kill neurons directly by inducing either apoptosis or necrosis or indirectly as a result of the host immune response. Sindbis virus (SV) is an alphavirus that induces apoptotic cell death both in vitro and in vivo. However, apoptotic changes are not always evident in neurons induced to die by alphavirus infection. Time lapse imaging revealed that SV-infected primary cortical neurons exhibited both apoptotic and necrotic morphological features and that uninfected neurons in the cultures also died. Antagonists of the N-methyl-d-aspartate (NMDA) subtype of glutamate receptors protected neurons from SV-induced death without affecting virus replication or SV-induced apoptotic cell death. These results provide evidence that SV infection activates neurotoxic pathways that result in aberrant NMDA receptor stimulation and damage to infected and uninfected neurons.

scholarly journals In vivo Postnatal Electroporation and Time-lapse Imaging of Neuroblast Migration in Mouse Acute Brain Slices

10.3791/50905 ◽  
2013 ◽  
Author(s):  
Martina Sonego ◽  
Ya Zhou ◽  
Madeleine Julie Oudin ◽  
Patrick Doherty ◽  
Giovanna Lalli
Keyword(s):  
Brain Slices ◽  
Time Lapse ◽  
Neuroblast Migration ◽  
Time Lapse Imaging

In vivo time-lapse imaging of mitochondria in healthy and diseased peripheral myelin sheath

Mitochondrion ◽  
2015 ◽  
Vol 23 ◽  
pp. 32-41 ◽  
Author(s):  
Sergio Gonzalez ◽  
Ruani Fernando ◽  
Jade Berthelot ◽  
Claire Perrin-Tricaud ◽  
Emmanuelle Sarzi ◽  
...  
Keyword(s):  
Myelin Sheath ◽  
Time Lapse ◽  
Time Lapse Imaging

scholarly journals Long-term in vivo time-lapse imaging of synapse development and plasticity in the cerebellum

2014 ◽  
Vol 111 (1) ◽  
pp. 208-216 ◽  
Author(s):  
Naoko Nishiyama ◽  
Jeremy Colonna ◽  
Elise Shen ◽  
Jennifer Carrillo ◽  
Hiroshi Nishiyama
Keyword(s):  
In Vivo Imaging ◽  
Time Window ◽  
Time Lapse ◽  
Mammalian Brain ◽  
Cerebellar Neurons ◽  
Brain Functions ◽  
Time Lapse Imaging ◽  
Synaptic Circuitry

Synapses are continuously formed and eliminated throughout life in the mammalian brain, and emerging evidence suggests that this structural plasticity underlies experience-dependent changes of brain functions such as learning and long-term memory formation. However, it is generally difficult to understand how the rewiring of synaptic circuitry observed in vivo eventually relates to changes in animal's behavior. This is because afferent/efferent connections and local synaptic circuitries are very complicated in most brain regions, hence it is largely unclear how sensorimotor information is conveyed, integrated, and processed through a brain region that is imaged. The cerebellar cortex provides a particularly useful model to challenge this problem because of its simple and well-defined synaptic circuitry. However, owing to the technical difficulty of chronic in vivo imaging in the cerebellum, it remains unclear how cerebellar neurons dynamically change their structures over a long period of time. Here, we showed that the commonly used method for neocortical in vivo imaging was not ideal for long-term imaging of cerebellar neurons, but simple optimization of the procedure significantly improved the success rate and the maximum time window of chronic imaging. The optimized method can be used in both neonatal and adult mice and allows time-lapse imaging of cerebellar neurons for more than 5 mo in ∼80% of animals. This method allows vital observation of dynamic cellular processes such as developmental refinement of synaptic circuitry as well as long-term changes of neuronal structures in adult cerebellum under longitudinal behavioral manipulations.

scholarly journals Cytoplasmic dynamics of myosin IIA and IIB: spatial ‘sorting’ of isoforms in locomoting cells

1998 ◽  
Vol 111 (15) ◽  
pp. 2085-2095 ◽  
Author(s):  
J. Kolega
Keyword(s):  
Cultured Cells ◽  
Myosin Ii ◽  
Cell Movement ◽  
Leading Edge ◽  
Time Lapse ◽  
Living Cells ◽  
Immunofluorescence Staining ◽  
Spatial Sorting ◽  
Time Lapse Imaging

Different isoforms of non-muscle myosin II have different distributions in vivo, even within individual cells. In order to understand how these different distributions arise, the distribution and dynamics of non-muscle myosins IIA and myosin IIB were examined in cultured cells using immunofluorescence staining and time-lapse imaging of fluorescent analogs. Cultured bovine aortic endothelia contained both myosins IIA and IIB. Both isoforms distributed along stress fibers, in linear or punctate aggregates within lamellipodia, and diffusely around the nucleus. However, the A isoform was preferentially located toward the leading edge of migrating cells when compared with myosin IIB by double immunofluorescence staining. Conversely, the B isoform was enriched in structures at the cells' trailing edges. When fluorescent analogs of the two isoforms were co-injected into living cells, the injected myosins distributed with the same disparate localizations as endogenous myosins IIA and IIB. This indicated that the ability of the myosins to ‘sort’ within the cytoplasm is intrinsic to the proteins themselves, and not a result of localized synthesis or degradation. Furthermore, time-lapse imaging of injected analogs in living cells revealed differences in the rates at which the two isoforms rearranged during cell movement. The A isoform appeared in newly formed structures more rapidly than the B isoform, and was also lost more rapidly when structures disassembled. These observations suggest that the different localizations of myosins IIA and IIB reflect different rates at which the isoforms transit through assembly, movement and disassembly within the cell. The relative proportions of different myosin II isoforms within a particular cell type may determine the lifetimes of various myosin II-based structures in that cell.

Sign in / Sign up

Export Citation Format

Share Document