Grant: Project Grant
University of Toronto
$1,071,000.00
Regulation of satellite stem cell fate by LINC complex proteins
FY 2022-23
Summary
More than 50,000 Canadians live with a neuromuscular disease (NMD), and the economic burden for families and the health care system, is significant. NMD progressively reduces skeletal muscle strength, which impacts independence and can shorten lifespan. Despite this, there are no cures for NMDs. Emery-Dreifuss muscular dystrophy (EDMD) is a type of NMD caused by mutations in genes that encode for proteins associated with the nuclear envelope, which is a membrane that encloses the genetic material in every cell of the body, protecting it from damage. Mutations in nuclear envelope proteins can make muscle fibres more susceptible to damage by a normal muscle contraction, and this is thought to cause muscle weakness in EDMD. Nuclear envelope proteins are also found in muscle stem cells, which repair the damaged fibres throughout life in healthy muscle, so EDMD mutations may also affect the ability of muscle stem cells to repair skeletal muscle. However, this is currently unknown. The goal of this research project is to determine if and how EDMD-associated nuclear envelope proteins influence muscle stem cell repair. First (Aim 1), we shall assess when and where each of four EDMD-associated proteins is found in muscle stem cells and their progeny. Next (Aim 2), we will remove these proteins, to study how the loss influences the ability of the stem cells to repair muscle tissue. We will then (Aim 3) identify strategies to restore the ability of muscle stem cells to repair muscle, even when EDMD-associated proteins are disabled. Finally (Aim 4), we will leverage humanized EDMD culture assays to establish pre-clinical evidence that the biology discovered herein is conserved across species. Together, this research will identify if a stem cell defect contributes to EDMD disease progression, and aspires to establish a potential drug treatment strategy to treat patients.
Department
Program
Project Grant
Recipient
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
468525
Name
Gilbert Penney M
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Musculoskeletal Health and Arthritis
Theme2
Biomedical
Prcname2
Cell Biology - Disease
Projecttitle
Regulation of satellite stem cell fate by LINC complex proteins
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$1,071,000
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Emery Dreifuss Muscular Dystrophy; Linc Complex; Satellite Cells; Skeletal Muscle
Abstract
More than 50,000 Canadians live with a neuromuscular disease (NMD), and the economic burden for families and the health care system, is significant. NMD progressively reduces skeletal muscle strength, which impacts independence and can shorten lifespan. Despite this, there are no cures for NMDs. Emery-Dreifuss muscular dystrophy (EDMD) is a type of NMD caused by mutations in genes that encode for proteins associated with the nuclear envelope, which is a membrane that encloses the genetic material in every cell of the body, protecting it from damage. Mutations in nuclear envelope proteins can make muscle fibres more susceptible to damage by a normal muscle contraction, and this is thought to cause muscle weakness in EDMD. Nuclear envelope proteins are also found in muscle stem cells, which repair the damaged fibres throughout life in healthy muscle, so EDMD mutations may also affect the ability of muscle stem cells to repair skeletal muscle. However, this is currently unknown. The goal of this research project is to determine if and how EDMD-associated nuclear envelope proteins influence muscle stem cell repair. First (Aim 1), we shall assess when and where each of four EDMD-associated proteins is found in muscle stem cells and their progeny. Next (Aim 2), we will remove these proteins, to study how the loss influences the ability of the stem cells to repair muscle tissue. We will then (Aim 3) identify strategies to restore the ability of muscle stem cells to repair muscle, even when EDMD-associated proteins are disabled. Finally (Aim 4), we will leverage humanized EDMD culture assays to establish pre-clinical evidence that the biology discovered herein is conserved across species. Together, this research will identify if a stem cell defect contributes to EDMD disease progression, and aspires to establish a potential drug treatment strategy to treat patients.
Competitiondate
202209
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Gilbert, Penney M
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,071,000~ $0~