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Engineering Cell Migration to Chemic...

Mosabbir, Abdullah Al.

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Engineering Cell Migration to Chemical and Physical Stimuli using Ca2+ Based Signalling.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Engineering Cell Migration to Chemical and Physical Stimuli using Ca2+ Based Signalling./
作者:	Mosabbir, Abdullah Al.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:	140 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-04, Section: B.
Contained By:	Dissertations Abstracts International81-04B.
標題:	Cellular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10975152
ISBN:	9781687937278

Engineering Cell Migration to Chemical and Physical Stimuli using Ca2+ Based Signalling.
Mosabbir, Abdullah Al.

Engineering Cell Migration to Chemical and Physical Stimuli using Ca2+ Based Signalling. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 140 p.

Source: Dissertations Abstracts International, Volume: 81-04, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2019.

This item must not be sold to any third party vendors.

A major challenge of cell-based therapies is the appropriate and effective localization of cells to target sites. Engineering cell migration to a specific target site can offer a promising solution to this problem. Previously, a chimeric protein known as CaRQ was developed to modulate cell migration based on intracellular Ca2+ transients. CaRQ confers versatility in rewiring cell migration to chemical and physical stimuli, by combining CaRQ with receptors that generate Ca2+ transients. Through in vitro cell-based experiments, this thesis demonstrates the versatility of CaRQ in engineering cell migration in response to chemical (i.e. cytokines) and physical (i.e. magnetic fields) stimuli.First, migration towards vascular endothelial growth factor (VEGF) was engineered by a system composed of CaRQ and the VEGF receptor 2 (VEGFR2). VEGF binds to VEGFR2 and generates an intracellular Ca2+ transient. Stable cells expressing VEGFR2 and CaRQ displayed migratory blebbing, migration across porous membranes, directed migration, as well as wound healing in response to VEGF and VEGFR2 antibodies.Second, migration towards granulocyte-macrophage colony-stimulating factor (GM-CSF) was engineered by a system composed of CaRQ and a chimeric receptor (henceforth GMRchi). GMRchi is composed of the VEGFR2 cytoplasmic domain and GM-CSFreceptor extracellular domain. Since the GM-CSF receptor alone cannot generate Ca2+transients, the chimeric receptor was engineered, demonstrating that migration is not limited to the repertoire of naturally occurring receptors. Stable cells expressing GMRchiand CaRQ displayed migratory blebbing, migration across porous membranes, directed migration, as well as wound healing in response to GM-CSF.Third, cell migration towards physical stimuli (specifically magnetic fields) was engineered by a system composed of CaRQ and a magnetic-sensitive gene circuit (henceforth the TF circuit). The TF circuit is composed of a chimeric TRPV1 receptor and ferritin. It was observed that a magnetic field induced migration when the TF circuit was paired with CaRQ. Taken together, this thesis demonstrates the utility of CaRQ in engineering cell migration to different stimuli in vitro, thus taking a step forward in engineering a versatile system tolocalize cells for cell-based therapy. It remains to be seen if these genetically-encoded systems will have efficacy in vivo.

ISBN: 9781687937278Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Genetic engineering

Engineering Cell Migration to Chemical and Physical Stimuli using Ca2+ Based Signalling.
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520 $a A major challenge of cell-based therapies is the appropriate and effective localization of cells to target sites. Engineering cell migration to a specific target site can offer a promising solution to this problem. Previously, a chimeric protein known as CaRQ was developed to modulate cell migration based on intracellular Ca2+ transients. CaRQ confers versatility in rewiring cell migration to chemical and physical stimuli, by combining CaRQ with receptors that generate Ca2+ transients. Through in vitro cell-based experiments, this thesis demonstrates the versatility of CaRQ in engineering cell migration in response to chemical (i.e. cytokines) and physical (i.e. magnetic fields) stimuli.First, migration towards vascular endothelial growth factor (VEGF) was engineered by a system composed of CaRQ and the VEGF receptor 2 (VEGFR2). VEGF binds to VEGFR2 and generates an intracellular Ca2+ transient. Stable cells expressing VEGFR2 and CaRQ displayed migratory blebbing, migration across porous membranes, directed migration, as well as wound healing in response to VEGF and VEGFR2 antibodies.Second, migration towards granulocyte-macrophage colony-stimulating factor (GM-CSF) was engineered by a system composed of CaRQ and a chimeric receptor (henceforth GMRchi). GMRchi is composed of the VEGFR2 cytoplasmic domain and GM-CSFreceptor extracellular domain. Since the GM-CSF receptor alone cannot generate Ca2+transients, the chimeric receptor was engineered, demonstrating that migration is not limited to the repertoire of naturally occurring receptors. Stable cells expressing GMRchiand CaRQ displayed migratory blebbing, migration across porous membranes, directed migration, as well as wound healing in response to GM-CSF.Third, cell migration towards physical stimuli (specifically magnetic fields) was engineered by a system composed of CaRQ and a magnetic-sensitive gene circuit (henceforth the TF circuit). The TF circuit is composed of a chimeric TRPV1 receptor and ferritin. It was observed that a magnetic field induced migration when the TF circuit was paired with CaRQ. Taken together, this thesis demonstrates the utility of CaRQ in engineering cell migration to different stimuli in vitro, thus taking a step forward in engineering a versatile system tolocalize cells for cell-based therapy. It remains to be seen if these genetically-encoded systems will have efficacy in vivo.
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