Anna Vikman
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View article: Role of Mast-Cell-Derived RANKL in Ovariectomy-Induced Bone Loss in Mice
Role of Mast-Cell-Derived RANKL in Ovariectomy-Induced Bone Loss in Mice Open
Mast cells may contribute to osteoporosis development, because patients with age-related or post-menopausal osteoporosis exhibit more mast cells in the bone marrow, and mastocytosis patients frequently suffer from osteopenia. We previously…
View article: Osteoblast lineage <i>Sod2</i> deficiency leads to an osteoporosis-like phenotype in mice
Osteoblast lineage <i>Sod2</i> deficiency leads to an osteoporosis-like phenotype in mice Open
Osteoporosis is a systemic metabolic skeletal disease characterized by low bone mass and strength associated with fragility fractures. Oxidative stress, which results from elevated intracellular reactive oxygen species (ROS) and arises in …
View article: Deletion of nicotinic acetylcholine receptor alpha9 in mice resulted in altered bone structure
Deletion of nicotinic acetylcholine receptor alpha9 in mice resulted in altered bone structure Open
Alterations in bone strength and structure were found in knockout (KO) mouse strains with deletion of several acetylcholine receptors. Interestingly, the expression of the nicotinic acetylcholine receptors (nAChR) subunit α10 was down-regu…
View article: Reduced Terminal Complement Complex Formation in Mice Manifests in Low Bone Mass and Impaired Fracture Healing
Reduced Terminal Complement Complex Formation in Mice Manifests in Low Bone Mass and Impaired Fracture Healing Open
The terminal complement complex (TCC) is formed on activation of the complement system, a crucial arm of innate immunity. TCC formation on cell membranes results in a transmembrane pore leading to cell lysis. In addition, sublytic TCC conc…
View article: C5aR1 interacts with <scp>TLR</scp>2 in osteoblasts and stimulates the osteoclast‐inducing chemokine <scp>CXCL</scp>10
C5aR1 interacts with <span>TLR</span>2 in osteoblasts and stimulates the osteoclast‐inducing chemokine <span>CXCL</span>10 Open
The anaphylatoxin C5a is generated upon activation of the complement system, a crucial arm of innate immunity. C5a mediates proinflammatory actions via the C5a receptor C5aR1 and thereby promotes host defence, but also modulates tissue hom…