TY  - JOUR
A1  - Liedert, Astrid
A1  - Nemitz, Claudia
A1  - Haffner-Luntzer, Melanie
A1  - Schick, Fabian
A1  - Jakob, Franz
A1  - Ignatius, Anita
T1  - Effects of estrogen receptor and Wnt signaling activation on mechanically induced bone formation in a mouse model of postmenopausal bone loss
JF  - International Journal of Molecular Sciences
N2  - In the adult skeleton, bone remodeling is required to replace damaged bone and functionally adapt bone mass and structure according to the mechanical requirements. It is regulated by multiple endocrine and paracrine factors, including hormones and growth factors, which interact in a coordinated manner. Because the response of bone to mechanical signals is dependent on functional estrogen receptor (ER) and Wnt/β-catenin signaling and is impaired in postmenopausal osteoporosis by estrogen deficiency, it is of paramount importance to elucidate the underlying mechanisms as a basis for the development of new strategies in the treatment of osteoporosis. The present study aimed to investigate the effectiveness of the activation of the ligand-dependent ER and the Wnt/β-catenin signal transduction pathways on mechanically induced bone formation using ovariectomized mice as a model of postmenopausal bone loss. We demonstrated that both pathways interact in the regulation of bone mass adaption in response to mechanical loading and that the activation of Wnt/β-catenin signaling considerably increased mechanically induced bone formation, whereas the effects of estrogen treatment strictly depended on the estrogen status in the mice.
KW  - bone remodeling
KW  - mechanotransduction
KW  - ER signaling
KW  - Wnt/β-catenin signaling
KW  - ovariectomy
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-285487
SN  - 1422-0067
VL  - 21
IS  - 21
ER  - 
TY  - JOUR
A1  - Herrmann, Marietta
A1  - Engelke, Klaus
A1  - Ebert, Regina
A1  - Müller-Deubert, Sigrid
A1  - Rudert, Maximilian
A1  - Ziouti, Fani
A1  - Jundt, Franziska
A1  - Felsenberg, Dieter
A1  - Jakob, Franz
T1  - Interactions between muscle and bone — Where physics meets biology
JF  - Biomolecules
N2  - Muscle and bone interact via physical forces and secreted osteokines and myokines. Physical forces are generated through gravity, locomotion, exercise, and external devices. Cells sense mechanical strain via adhesion molecules and translate it into biochemical responses, modulating the basic mechanisms of cellular biology such as lineage commitment, tissue formation, and maturation. This may result in the initiation of bone formation, muscle hypertrophy, and the enhanced production of extracellular matrix constituents, adhesion molecules, and cytoskeletal elements. Bone and muscle mass, resistance to strain, and the stiffness of matrix, cells, and tissues are enhanced, influencing fracture resistance and muscle power. This propagates a dynamic and continuous reciprocity of physicochemical interaction. Secreted growth and differentiation factors are important effectors of mutual interaction. The acute effects of exercise induce the secretion of exosomes with cargo molecules that are capable of mediating the endocrine effects between muscle, bone, and the organism. Long-term changes induce adaptations of the respective tissue secretome that maintain adequate homeostatic conditions. Lessons from unloading, microgravity, and disuse teach us that gratuitous tissue is removed or reorganized while immobility and inflammation trigger muscle and bone marrow fatty infiltration and propagate degenerative diseases such as sarcopenia and osteoporosis. Ongoing research will certainly find new therapeutic targets for prevention and treatment.
KW  - muscle
KW  - bone
KW  - mechanosensing
KW  - mechanotransduction
KW  - myokines
KW  - osteokines adaptation
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-203399
SN  - 2218-273X
VL  - 10
IS  - 3
ER  -