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Eduardo Marbán - One of the best experts on this subject based on the ideXlab platform.

  • Targeting extracellular vesicles to Injured Tissue using membrane cloaking and surface display
    Journal of Nanobiotechnology, 2018
    Co-Authors: Travis J. Antes, Ryan C. Middleton, Kristin M. Luther, Takeshi Ijichi, Kiel A. Peck, Weixin Jane Liu, Jackie Valle, Antonio K. Echavez, Eduardo Marbán
    Abstract:

    Background Extracellular vesicles (EVs) and exosomes are nano-sized, membrane-bound vesicles shed by most eukaryotic cells studied to date. EVs play key signaling roles in cellular development, cancer metastasis, immune modulation and Tissue regeneration. Attempts to modify exosomes to increase their targeting efficiency to specific Tissue types are still in their infancy. Here we describe an EV membrane anchoring platform termed “cloaking” to directly embed Tissue-specific antibodies or homing peptides on EV membrane surfaces ex vivo for enhanced vesicle uptake in cells of interest. The cloaking system consists of three components: DMPE phospholipid membrane anchor, polyethylene glycol spacer and a conjugated streptavidin platform molecule, to which any biotinylated molecule can be coupled for EV decoration. Results We demonstrate the utility of membrane surface engineering and biodistribution tracking with this technology along with targeting EVs for enhanced uptake in cardiac fibroblasts, myoblasts and ischemic myocardium using combinations of fluorescent tags, Tissue-targeting antibodies and homing peptide surface cloaks. We compare cloaking to a complementary approach, surface display, in which parental cells are engineered to secrete EVs with fusion surface targeting proteins. Conclusions EV targeting can be enhanced both by cloaking and by surface display; the former entails chemical modification of preformed EVs, while the latter requires genetic modification of the parent cells. Reduction to practice of the cloaking approach, using several different EV surface modifications to target distinct cells and Tissues, supports the notion of cloaking as a platform technology.

  • targeting extracellular vesicles to Injured Tissue using membrane cloaking and surface display
    Journal of Nanobiotechnology, 2018
    Co-Authors: Travis J. Antes, Takeshi Ijichi, Weixin Jane Liu, Jackie Valle, Antonio K. Echavez, Ryan Middleton, Kristin Luther, Kiel Peck, Eduardo Marbán
    Abstract:

    Extracellular vesicles (EVs) and exosomes are nano-sized, membrane-bound vesicles shed by most eukaryotic cells studied to date. EVs play key signaling roles in cellular development, cancer metastasis, immune modulation and Tissue regeneration. Attempts to modify exosomes to increase their targeting efficiency to specific Tissue types are still in their infancy. Here we describe an EV membrane anchoring platform termed “cloaking” to directly embed Tissue-specific antibodies or homing peptides on EV membrane surfaces ex vivo for enhanced vesicle uptake in cells of interest. The cloaking system consists of three components: DMPE phospholipid membrane anchor, polyethylene glycol spacer and a conjugated streptavidin platform molecule, to which any biotinylated molecule can be coupled for EV decoration. We demonstrate the utility of membrane surface engineering and biodistribution tracking with this technology along with targeting EVs for enhanced uptake in cardiac fibroblasts, myoblasts and ischemic myocardium using combinations of fluorescent tags, Tissue-targeting antibodies and homing peptide surface cloaks. We compare cloaking to a complementary approach, surface display, in which parental cells are engineered to secrete EVs with fusion surface targeting proteins. EV targeting can be enhanced both by cloaking and by surface display; the former entails chemical modification of preformed EVs, while the latter requires genetic modification of the parent cells. Reduction to practice of the cloaking approach, using several different EV surface modifications to target distinct cells and Tissues, supports the notion of cloaking as a platform technology.

Travis J. Antes - One of the best experts on this subject based on the ideXlab platform.

  • Targeting extracellular vesicles to Injured Tissue using membrane cloaking and surface display
    Journal of Nanobiotechnology, 2018
    Co-Authors: Travis J. Antes, Ryan C. Middleton, Kristin M. Luther, Takeshi Ijichi, Kiel A. Peck, Weixin Jane Liu, Jackie Valle, Antonio K. Echavez, Eduardo Marbán
    Abstract:

    Background Extracellular vesicles (EVs) and exosomes are nano-sized, membrane-bound vesicles shed by most eukaryotic cells studied to date. EVs play key signaling roles in cellular development, cancer metastasis, immune modulation and Tissue regeneration. Attempts to modify exosomes to increase their targeting efficiency to specific Tissue types are still in their infancy. Here we describe an EV membrane anchoring platform termed “cloaking” to directly embed Tissue-specific antibodies or homing peptides on EV membrane surfaces ex vivo for enhanced vesicle uptake in cells of interest. The cloaking system consists of three components: DMPE phospholipid membrane anchor, polyethylene glycol spacer and a conjugated streptavidin platform molecule, to which any biotinylated molecule can be coupled for EV decoration. Results We demonstrate the utility of membrane surface engineering and biodistribution tracking with this technology along with targeting EVs for enhanced uptake in cardiac fibroblasts, myoblasts and ischemic myocardium using combinations of fluorescent tags, Tissue-targeting antibodies and homing peptide surface cloaks. We compare cloaking to a complementary approach, surface display, in which parental cells are engineered to secrete EVs with fusion surface targeting proteins. Conclusions EV targeting can be enhanced both by cloaking and by surface display; the former entails chemical modification of preformed EVs, while the latter requires genetic modification of the parent cells. Reduction to practice of the cloaking approach, using several different EV surface modifications to target distinct cells and Tissues, supports the notion of cloaking as a platform technology.

  • targeting extracellular vesicles to Injured Tissue using membrane cloaking and surface display
    Journal of Nanobiotechnology, 2018
    Co-Authors: Travis J. Antes, Takeshi Ijichi, Weixin Jane Liu, Jackie Valle, Antonio K. Echavez, Ryan Middleton, Kristin Luther, Kiel Peck, Eduardo Marbán
    Abstract:

    Extracellular vesicles (EVs) and exosomes are nano-sized, membrane-bound vesicles shed by most eukaryotic cells studied to date. EVs play key signaling roles in cellular development, cancer metastasis, immune modulation and Tissue regeneration. Attempts to modify exosomes to increase their targeting efficiency to specific Tissue types are still in their infancy. Here we describe an EV membrane anchoring platform termed “cloaking” to directly embed Tissue-specific antibodies or homing peptides on EV membrane surfaces ex vivo for enhanced vesicle uptake in cells of interest. The cloaking system consists of three components: DMPE phospholipid membrane anchor, polyethylene glycol spacer and a conjugated streptavidin platform molecule, to which any biotinylated molecule can be coupled for EV decoration. We demonstrate the utility of membrane surface engineering and biodistribution tracking with this technology along with targeting EVs for enhanced uptake in cardiac fibroblasts, myoblasts and ischemic myocardium using combinations of fluorescent tags, Tissue-targeting antibodies and homing peptide surface cloaks. We compare cloaking to a complementary approach, surface display, in which parental cells are engineered to secrete EVs with fusion surface targeting proteins. EV targeting can be enhanced both by cloaking and by surface display; the former entails chemical modification of preformed EVs, while the latter requires genetic modification of the parent cells. Reduction to practice of the cloaking approach, using several different EV surface modifications to target distinct cells and Tissues, supports the notion of cloaking as a platform technology.

Jens Lykkeandersen - One of the best experts on this subject based on the ideXlab platform.

  • post transcriptional regulation of satellite cell quiescence by ttp mediated mrna decay
    eLife, 2015
    Co-Authors: Melissa Hausburg, Jason D Doles, Sandra L Clement, Adam B Cadwallader, Monica N Hall, Perry J Blackshear, Jens Lykkeandersen
    Abstract:

    When muscles are damaged, they can repair themselves to some extent by making new muscle cells. These develop from groups of cells called satellite cells, which are found near the surface of muscle fibers. Once the muscle is Injured, the satellite cells are activated and can divide to form two cells with different properties. One remains a satellite cell, while the other forms a ‘myoblast’ that eventually fuses into a mature muscle fiber. Under normal conditions the satellite cells remain in a dormant state and do not divide, but it is not clear how they maintain this dormant state. To create a protein, the gene that encodes it is first ‘transcribed’ to produce a molecule called mRNA, which is then used as a template to build the protein. A protein called Tristetraprolin (TTP) can bind to mRNA molecules and cause them to break down or decay, and so TTP can prevent the mRNA from being used to make a protein. Hausburg, Doles et al. analyzed satellite cells from unInjured muscle and compared them with those from Injured Tissue. This revealed that when Injured, the satellite cells reduced the abundance of several mRNAs, including TTP. Further investigation found that in satellite cells from unInjured Tissue, TTP causes the decay of mRNA molecules that are used to produce a protein called MyoD. As MyoD helps the satellite cells to specialize, this decay therefore prevents the formation of myoblasts and keeps the satellite cells in a dormant state. In contrast, damage to the muscle Tissue activates a signaling pathway that ultimately inactivates TTP. This enables more of the MyoD protein to be made and the myoblast population to expand. When Hausburg, Doles et al. experimentally reduced the levels of TTP inside satellite cells, the cells developed into myoblasts even when the Tissue was unInjured. Thus, TTP is an important regulator that allows satellite cells to remain in a dormant state. In dormant adult stem cells, regulation of protein availability by RNA binding proteins, such as TTP, may co-ordinate rapid changes in metabolic state to promptly repair Injured Tissue. A major challenge will be to identify the group of proteins involved and determine the precise mechanisms involved in regulating their availability.

Ronald E Allen - One of the best experts on this subject based on the ideXlab platform.

  • skeletal muscle satellite cell migration to Injured Tissue measured with111in oxine and high resolution spect imaging
    Journal of Muscle Research and Cell Motility, 2013
    Co-Authors: Jennifer L Elster, Christopher R Rathbone, Zhonglin Liu, Xiasong Liu, Harrison H Barrett, R P Rhoads, Ronald E Allen
    Abstract:

    The delivery of adult skeletal muscle stem cells, called satellite cells, to several Injured muscles via the circulation would be useful, however, an improved understanding of cell fate and biodistribution following their delivery is important for this goal to be achieved. The objective of this study was to evaluate the ability of systemically delivered satellite cells to home to Injured skeletal muscle using single-photon emission computed tomography (SPECT) imaging of 111In-labeled satellite cells. Satellite cells labeled with 111In-oxine and green fluorescent protein (GFP) were injected intravenously after bupivicaine-induced injury to the tibialis anterior muscle. Animals were imaged with a high-resolution SPECT system called FastSPECT II for up to 7 days after transplantation. In vivo FastSPECT II imaging demonstrated a three to five-fold greater number of transplanted satellite cells in bupivicaine-Injured muscle as compared to un-Injured muscle after transplantation; a finding that was verified through autoradiograph analysis and quantification of GFP expression. Satellite cells also accumulated in other organs including the lung, liver, and spleen, as determined by biodistribution measurements. These data support the ability of satellite cells to home to Injured muscle and support the use of SPECT and autoradiograph imaging techniques to track systemically transplanted 111In labeled satellite cells in vivo, and suggest their homing may be improved by reducing their entrapment in filter organs.

Weixin Jane Liu - One of the best experts on this subject based on the ideXlab platform.

  • Targeting extracellular vesicles to Injured Tissue using membrane cloaking and surface display
    Journal of Nanobiotechnology, 2018
    Co-Authors: Travis J. Antes, Ryan C. Middleton, Kristin M. Luther, Takeshi Ijichi, Kiel A. Peck, Weixin Jane Liu, Jackie Valle, Antonio K. Echavez, Eduardo Marbán
    Abstract:

    Background Extracellular vesicles (EVs) and exosomes are nano-sized, membrane-bound vesicles shed by most eukaryotic cells studied to date. EVs play key signaling roles in cellular development, cancer metastasis, immune modulation and Tissue regeneration. Attempts to modify exosomes to increase their targeting efficiency to specific Tissue types are still in their infancy. Here we describe an EV membrane anchoring platform termed “cloaking” to directly embed Tissue-specific antibodies or homing peptides on EV membrane surfaces ex vivo for enhanced vesicle uptake in cells of interest. The cloaking system consists of three components: DMPE phospholipid membrane anchor, polyethylene glycol spacer and a conjugated streptavidin platform molecule, to which any biotinylated molecule can be coupled for EV decoration. Results We demonstrate the utility of membrane surface engineering and biodistribution tracking with this technology along with targeting EVs for enhanced uptake in cardiac fibroblasts, myoblasts and ischemic myocardium using combinations of fluorescent tags, Tissue-targeting antibodies and homing peptide surface cloaks. We compare cloaking to a complementary approach, surface display, in which parental cells are engineered to secrete EVs with fusion surface targeting proteins. Conclusions EV targeting can be enhanced both by cloaking and by surface display; the former entails chemical modification of preformed EVs, while the latter requires genetic modification of the parent cells. Reduction to practice of the cloaking approach, using several different EV surface modifications to target distinct cells and Tissues, supports the notion of cloaking as a platform technology.

  • targeting extracellular vesicles to Injured Tissue using membrane cloaking and surface display
    Journal of Nanobiotechnology, 2018
    Co-Authors: Travis J. Antes, Takeshi Ijichi, Weixin Jane Liu, Jackie Valle, Antonio K. Echavez, Ryan Middleton, Kristin Luther, Kiel Peck, Eduardo Marbán
    Abstract:

    Extracellular vesicles (EVs) and exosomes are nano-sized, membrane-bound vesicles shed by most eukaryotic cells studied to date. EVs play key signaling roles in cellular development, cancer metastasis, immune modulation and Tissue regeneration. Attempts to modify exosomes to increase their targeting efficiency to specific Tissue types are still in their infancy. Here we describe an EV membrane anchoring platform termed “cloaking” to directly embed Tissue-specific antibodies or homing peptides on EV membrane surfaces ex vivo for enhanced vesicle uptake in cells of interest. The cloaking system consists of three components: DMPE phospholipid membrane anchor, polyethylene glycol spacer and a conjugated streptavidin platform molecule, to which any biotinylated molecule can be coupled for EV decoration. We demonstrate the utility of membrane surface engineering and biodistribution tracking with this technology along with targeting EVs for enhanced uptake in cardiac fibroblasts, myoblasts and ischemic myocardium using combinations of fluorescent tags, Tissue-targeting antibodies and homing peptide surface cloaks. We compare cloaking to a complementary approach, surface display, in which parental cells are engineered to secrete EVs with fusion surface targeting proteins. EV targeting can be enhanced both by cloaking and by surface display; the former entails chemical modification of preformed EVs, while the latter requires genetic modification of the parent cells. Reduction to practice of the cloaking approach, using several different EV surface modifications to target distinct cells and Tissues, supports the notion of cloaking as a platform technology.