New Avenues in the LRP5-mediated Bone Mass Acquisition
Korean Journal of Bone Metabolism
; : 1-9, 2012.
Article
in Ko
| WPRIM
| ID: wpr-130880
Responsible library:
WPRO
ABSTRACT
Lipoprotein receptor-related protein (LRP5) signaling is well correlated with the bone mass in both human and mice. Loss-of-function mutations of LRP5 result in osteopenia or osteoporosis. In contrast, gain-of-function mutations show high bone mass phenotype. To elucidate the molecular mechanism of the LRP5-mediated bone mass acquisition, several groups have genetically dissected the Wingless and Int-1 (Wnt)beta-catenin signaling pathway using osteoblast-lineage specific Cre mice. Key players for LRP5-mediated bone mass acquisition turn out to be different molecules with respect to the expressing tissue and action mode of these molecules. One is serotonin, a tryptophan metabolite that originates from duodenum, which acts as a negative regulator for bone formation. LRP5 suppresses serotonin biosynthesis by inhibiting the expression of tryptophan hydroxylase 1 in the gut. The other is sclerostin, an osteocyte-producing antagonist for LRP5 signaling. Here is a summary of recent findings about these two molecules, providing a chance to speculate new avenues in the LRP5-mediated bone mass acquisition.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Osteogenesis
/
Osteoporosis
/
Phenotype
/
Skin Diseases
/
Tryptophan
/
Tryptophan Hydroxylase
/
Bone Diseases, Metabolic
/
Serotonin
/
Mitral Valve Prolapse
/
Duodenum
Limits:
Animals
/
Humans
Language:
Ko
Journal:
Korean Journal of Bone Metabolism
Year:
2012
Type:
Article