In vivo imaging of myocardial cell death using a peptide probe and assessment of long-term heart function

2013 ◽  
Vol 172 (1) ◽  
pp. 367-373 ◽  
Author(s):  
Bodhraj Acharya ◽  
Kai Wang ◽  
In-San Kim ◽  
WoongChol Kang ◽  
Chanil Moon ◽  
...  
Keyword(s):  
Cell Death ◽  
In Vivo Imaging ◽  
Heart Function ◽  
Myocardial Cell ◽  
Peptide Probe

Long-Term In Vivo Imaging of Individual Microglial Cells

2019 ◽  
pp. 177-189
Author(s):  
Angelos A. Skodras ◽  
Jasmin K. Hefendehl ◽  
Jonas J. Neher
Keyword(s):  
In Vivo Imaging ◽  
Microglial Cells

scholarly journals Formation of Mallory Body-like Inclusions and Cell Death Induced by Deregulated Expression of Keratin 18

2002 ◽  
Vol 13 (10) ◽  
pp. 3441-3451 ◽  
Author(s):  
Ikuo Nakamichi ◽  
Shigetsugu Hatakeyama ◽  
Keiichi I. Nakayama
Keyword(s):  
Cell Death ◽  
Important Determinant ◽  
Cellular Model ◽  
Microtubule Network ◽  
Cytoplasmic Inclusions ◽  
Mallory Bodies ◽  
Keratin 18 ◽  
Intracellular Aggregates

Mallory bodies (MBs) are cytoplasmic inclusions that contain keratin 8 (K8) and K18 and are present in hepatocytes of individuals with alcoholic liver disease, nonalcoholic steatohepatitis, or benign or malignant hepatocellular neoplasia. Mice fed long term with griseofulvin are an animal model of MB formation. However, the lack of a cellular model has impeded understanding of the molecular mechanism of this process. Culture of HepG2 cells with griseofulvin has now been shown to induce both the formation of intracellular aggregates containing K18 as well as an increase in the abundance of K18 mRNA. Overexpression of K18 in HepG2, HeLa, or COS-7 cells also induced the formation of intracellular aggregates that stained with antibodies to ubiquitin and with rhodamine B (characteristics of MBs formed in vivo), eventually leading to cell death. The MB-like aggregates were deposited around centrosomes and disrupted the microtubular array. Coexpression of K8 with K18 restored the normal fibrous pattern of keratin distribution and reduced the toxicity of K18. In contrast, an NH2-terminal deletion mutant of K8 promoted the formation of intracellular aggregates even in the absence of K18 overexpression. Deregulated expression of K18, or an imbalance between K8 and K18, may thus be an important determinant of MB formation, which compromises the function of centrosomes and the microtubule network and leads to cell death.

Long-term in vivo imaging of experience-dependent synaptic plasticity in adult cortex

Nature ◽  
2002 ◽  
Vol 420 (6917) ◽  
pp. 788-794 ◽  
Author(s):  
Joshua T. Trachtenberg ◽  
Brian E. Chen ◽  
Graham W. Knott ◽  
Guoping Feng ◽  
Joshua R. Sanes ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
In Vivo Imaging

In vivo imaging of nuclear-cytoplasmic deformation and partition during cancer cell death due to immune rejection

2012 ◽  
Vol 113 (2) ◽  
pp. 465-472 ◽  
Author(s):  
Yasuyuki Amoh ◽  
Yuko Hamada ◽  
Kensei Katsuoka ◽  
Robert M. Hoffman
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
In Vivo Imaging ◽  
Immune Rejection ◽  
Cancer Cell Death

scholarly journals Efficacy, long-term toxicity, and mechanistic studies of gold nanorods photothermal therapy of cancer in xenograft mice

2017 ◽  
Vol 114 (15) ◽  
pp. E3110-E3118 ◽  
Author(s):  
Moustafa R. K. Ali ◽  
Mohammad Aminur Rahman ◽  
Yue Wu ◽  
Tiegang Han ◽  
Xianghong Peng ◽  
...  
Keyword(s):  
Cell Death ◽  
Mechanism Of Action ◽  
Gold Nanorods ◽  
Photothermal Therapy ◽  
Near Infrared ◽  
Infrared Light ◽  
Mouse Tumor ◽  
Maximal Induction

Gold nanorods (AuNRs)-assisted plasmonic photothermal therapy (AuNRs-PPTT) is a promising strategy for combating cancer in which AuNRs absorb near-infrared light and convert it into heat, causing cell death mainly by apoptosis and/or necrosis. Developing a valid PPTT that induces cancer cell apoptosis and avoids necrosis in vivo and exploring its molecular mechanism of action is of great importance. Furthermore, assessment of the long-term fate of the AuNRs after treatment is critical for clinical use. We first optimized the size, surface modification [rifampicin (RF) conjugation], and concentration (2.5 nM) of AuNRs and the PPTT laser power (2 W/cm2) to achieve maximal induction of apoptosis. Second, we studied the potential mechanism of action of AuNRs-PPTT using quantitative proteomic analysis in mouse tumor tissues. Several death pathways were identified, mainly involving apoptosis and cell death by releasing neutrophil extracellular traps (NETs) (NETosis), which were more obvious upon PPTT using RF-conjugated AuNRs (AuNRs@RF) than with polyethylene glycol thiol-conjugated AuNRs. Cytochrome c and p53-related apoptosis mechanisms were identified as contributing to the enhanced effect of PPTT with AuNRs@RF. Furthermore, Pin1 and IL18-related signaling contributed to the observed perturbation of the NETosis pathway by PPTT with AuNRs@RF. Third, we report a 15-month toxicity study that showed no long-term toxicity of AuNRs in vivo. Together, these data demonstrate that our AuNRs-PPTT platform is effective and safe for cancer therapy in mouse models. These findings provide a strong framework for the translation of PPTT to the clinic.

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 Long-term in vivo imaging of translated RNAs for gene therapy

Gene Therapy ◽  
2014 ◽  
Vol 21 (4) ◽  
pp. 434-439 ◽  
Author(s):  
K Pinel ◽  
J Lacoste ◽  
G Plane ◽  
M Ventura ◽  
F Couillaud
Keyword(s):  
Gene Therapy ◽  
In Vivo Imaging

Programmed cell death with a necrotic-like phenotype

2013 ◽  
Vol 4 (3) ◽  
pp. 259-275 ◽  
Author(s):  
Michael J. Morgan ◽  
Zheng-gang Liu
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mammalian Development ◽  
Programmed Necrosis ◽  
Physiological Processes ◽  
Molecular Events ◽  
Regulated Necrosis

AbstractProgrammed cell death is the process by which an individual cell in a multicellular organism commits cellular ‘suicide’ to provide a long-term benefit to the organism. Thus, programmed cell death is important for physiological processes such as development, cellular homeostasis, and immunity. Importantly, in this process, the cell is not eliminated in response to random events but in response to an intricate and genetically defined set of internal cellular molecular events or ‘program’. Although the apoptotic process is generally very well understood, programmed cell death that occurs with a necrotic-like phenotype has been much less studied, and it is only within the past few years that the necrotic program has begun to be elucidated. Originally, programmed necrosis was somewhat dismissed as a nonphysiological phenomenon that occurs in vitro. Recent in vivo studies, however, suggest that regulated necrosis is an authentic classification of cell death that is important in mammalian development and other physiological processes, and programmed necrosis is now considered a significant therapeutic target in major pathological processes as well. Although the RIP1-RIP3-dependent necrosome complex is recognized as being essential for the execution of many instances of programmed necrosis, other downstream and related necrotic molecules and pathways are now being characterized. One of the current challenges is understanding how and under what conditions these pathways are linked together.

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