Grant: Operating Grant
University of Toronto
$569,575.00
A calreticulin-cytomechanical switch in osteoblast-adipocyte fate choice in an ES cell model
FY 2009-10
Summary
Work from several laboratories has demonstrated that cell shape, cytoskeletal tension and substratum elasticity direct differentiation in many cell types including embryonic stem cells. Calreticulin, a Ca-binding protein either by its role in intracellular Ca homeostasis or as a helper protein, modulates signalling pathways that control cell lineage specification and tissue formation. The growth substratum also influences the formation of tissues by affecting the cell adhesion and shape, which are modulated by calreticulin. Thus, both cell shape and signalling pathways are affected by calreticulin expression level. Consequently, we postulate that the cell fate choice is controlled by the combinatorial action of calreticulin level of expression and biomechanics of the substratum.
While the role of calreticulin in adipogenesis and cardiomyogenesis from ES cells has been established, its role in skeletogenesis is not yet clear. In the present proposal, we thus wish to first elucidate the role of calreticulin in differentiation of embryonic stem cells towards skeletal tissue. Next, we will elucidate the role of substratum biomechanics in directing differentiation of embryonic stem cells in the presence or absence of calreticulin.
These experiments will allow us to delineate the role of calreticulin in cell differentiation from embryonic stem cells and will address the emerging question of the impact of the biomechanics of the environment on cell fate. The results may have important implications for tissue engineering and regenerative medicine.
Department
Program
Operating Grant
Recipient
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
201119
Name
Opas Michal J
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Musculoskeletal Health and Arthritis
Theme2
Biomedical
Prcname2
Cell Biology & Mechanisms of Disease
Projecttitle
A calreticulin-cytomechanical switch in osteoblast-adipocyte fate choice in an ES cell model
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$569,575
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Ca Binding Proteins; Chondro/Osteogenesis; Development; Es Cells
Abstract
Work from several laboratories has demonstrated that cell shape, cytoskeletal tension and substratum elasticity direct differentiation in many cell types including embryonic stem cells. Calreticulin, a Ca-binding protein either by its role in intracellular Ca homeostasis or as a helper protein, modulates signalling pathways that control cell lineage specification and tissue formation. The growth substratum also influences the formation of tissues by affecting the cell adhesion and shape, which are modulated by calreticulin. Thus, both cell shape and signalling pathways are affected by calreticulin expression level. Consequently, we postulate that the cell fate choice is controlled by the combinatorial action of calreticulin level of expression and biomechanics of the substratum.
While the role of calreticulin in adipogenesis and cardiomyogenesis from ES cells has been established, its role in skeletogenesis is not yet clear. In the present proposal, we thus wish to first elucidate the role of calreticulin in differentiation of embryonic stem cells towards skeletal tissue. Next, we will elucidate the role of substratum biomechanics in directing differentiation of embryonic stem cells in the presence or absence of calreticulin.
These experiments will allow us to delineate the role of calreticulin in cell differentiation from embryonic stem cells and will address the emerging question of the impact of the biomechanics of the environment on cell fate. The results may have important implications for tissue engineering and regenerative medicine.
Competitiondate
201003
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Opas, Michal J
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $569,575~ $0~