Grant: Operating Grant
McGill University
$758,575.00
Transglutaminases and cell-matrix interactions during osteoblast differentiation
EF 2011-12
Résumé
Osteoporosis is characterized by bone loss, bone fragility and increased prevalence of fractures. It is a disease hindering the lives of close 2 million Canadians. Osteoporosis and related fractures results in loss of mobility, increased pain and dramatically compromised quality of life. The cost of treating osteoporosis related fractures and immobility is close to 2 billion dollars each year and it is predicted that these numbers will keep increasing as Canadian population ages. The causes for osteoporosis can be linked to genetics, nutrition, medication, and it can occur at any time during life. Achieving high bone mass at younger age protects from bone loss occurring later in life. Bones are composed of cells and substance between cells called the extracellular matrix which is mostly collagen and mineral. Collagen is produced by resident cells, and in bones it undergoes a stabilization process that is required for proper bone cell function. We have discovered that transglutaminase-enzymes, TG2 and Factor XIIIA, are responsible for this matrix stabilization. Mice lacking these enzymes develop osteporosis and have low bone mass. In this proposal we plan to further explore how these two enzymes jointly promote bone cell activity. Our specific aims are: 1) to complete our analysis of the bones lacking these two enzymes; 2) to study the role of TG2 in bone cell attachment to bone; 3) to study a newly discovered form of FXIIIA on bone cell surface; 4) to study how matrix stabilization occurs in detail and molecular level and how it can lead to better functioning bone cells. From this work we hope to understand how also human bone tissue is made and assembled and how bone cell activity could be given a boost via therapeutics in osteoporosis to maintain optimal bone formation activity thoughout life.
Programme
Operating Grant
Bénéficiaire
Emplacement
Quebec, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
238029
Name
Kaartinen Mari T
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Musculoskeletal Health and Arthritis
Theme2
Biomedical
Prcname2
Clinical Investigation - B: Arthritis, Bone, Skin and Cartilage
Projecttitle
Transglutaminases and cell-matrix interactions during osteoblast differentiation
Programtype2
Operating Grants
Orgnameinp2
McGill University
Cihramount2
$758,575
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Biochemistry; Bone; Cell Biology; Cell Culture; Collagen; Extracellular Matrix
Abstract
Osteoporosis is characterized by bone loss, bone fragility and increased prevalence of fractures. It is a disease hindering the lives of close 2 million Canadians. Osteoporosis and related fractures results in loss of mobility, increased pain and dramatically compromised quality of life. The cost of treating osteoporosis related fractures and immobility is close to 2 billion dollars each year and it is predicted that these numbers will keep increasing as Canadian population ages. The causes for osteoporosis can be linked to genetics, nutrition, medication, and it can occur at any time during life. Achieving high bone mass at younger age protects from bone loss occurring later in life. Bones are composed of cells and substance between cells called the extracellular matrix which is mostly collagen and mineral. Collagen is produced by resident cells, and in bones it undergoes a stabilization process that is required for proper bone cell function. We have discovered that transglutaminase-enzymes, TG2 and Factor XIIIA, are responsible for this matrix stabilization. Mice lacking these enzymes develop osteporosis and have low bone mass. In this proposal we plan to further explore how these two enzymes jointly promote bone cell activity. Our specific aims are: 1) to complete our analysis of the bones lacking these two enzymes; 2) to study the role of TG2 in bone cell attachment to bone; 3) to study a newly discovered form of FXIIIA on bone cell surface; 4) to study how matrix stabilization occurs in detail and molecular level and how it can lead to better functioning bone cells. From this work we hope to understand how also human bone tissue is made and assembled and how bone cell activity could be given a boost via therapeutics in osteoporosis to maintain optimal bone formation activity thoughout life.
Competitiondate
201109
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Kaartinen, Mari T
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $758,575~ $0~