Matrix vesicles promote bone repair after a femoral bone defect in mice.

Matrix vesicles (MtVs) are one of the extracellular vesicles (EVs) secreted by osteoblasts. Although MtVs have a classically-defined function as an initiator of ossification and recent findings suggest a role for MtVs in the regulation of bone cell biology, the effects of MtVs on bone repair remain unclear. In the present study, we employed collagenase-released EVs (CREVs) containing abundant MtVs from mouse osteoblasts.

Tumor Necrosis Factor-α Blunts the Osteogenic Effects of Muscle Cell-Derived Extracellular Vesicles by Affecting Muscle Cells.

Extracellular vesicles (EVs) play crucial roles in physiological and pathophysiological processes. Although studies have described muscle-bone interactions via humoral factors, we reported that EVs from C2C12 muscle cells (Myo-EVs) suppress osteoclast formation. Current clinical evidence suggests that inflammation induces both sarcopenia and osteoporosis.

Effects of Growth Hormone on Muscle and Bone in Female Mice: Role of Follistatin.

The interactions between muscle and bone are noted in the clinical relationships between sarcopenia and osteoporosis. Myokines secreted from the skeletal muscles play roles in muscle-bone interactions related to various physiological and pathophysiological states. Although numerous evidence suggests that growth hormone (GH) influences both muscle and bone, the effects of GH on the muscle-bone interactions have remained unknown.

Extracellular vesicles secreted from mouse muscle cells improve delayed bone repair in diabetic mice.

Humoral factors that are secreted from skeletal muscles can regulate bone metabolism and contribute to muscle-bone relationships. Although extracellular vesicles (EVs) play important roles in physiological and pathophysiological processes, the roles of EVs that are secreted from skeletal muscles in bone repair have remained unclear. In the present study, we investigated the effects of the local administration of muscle cell-derived EVs on bone repair in control and streptozotocin-treated diabetic female mice.

Irisin improves delayed bone repair in diabetic female mice.

Introduction: Irisin is a proteolytic product of fibronectin type II domain-containing 5, which is related to the improvement in glucose metabolism. Numerous studies have suggested that irisin is a crucial myokine linking muscle to bone in physiological and pathophysiological states.

Materials And Methods: We examined the effects of local irisin administration with gelatin hydrogel sheets and intraperitoneal injection of irisin on the delayed femoral bone repair caused by streptozotocin (STZ)-induced diabetes in female mice.

Role of peripheral myelin protein 22 in chronic exercise-induced interactions of muscle and bone in mice.

Exercise is important for the prevention and treatment of sarcopenia and osteoporosis. Although the interactions between skeletal muscles and bone have recently been reported, the myokines linking muscle to bone during exercise remain unknown. We previously revealed that chronic exercise using treadmill running blunts ovariectomy-induced osteopenia in mice.

Role of Macrophages and Plasminogen Activator Inhibitor-1 in Delayed Bone Repair Induced by Glucocorticoids in Mice.

Glucocorticoids delay fracture healing and induce osteoporosis. However, the mechanisms by which glucocorticoids delay bone repair have yet to be clarified. Plasminogen activator inhibitor-1 (PAI-1) is the principal inhibitor of plasminogen activators and an adipocytokine that regulates metabolism.

Renal failure suppresses muscle irisin expression, and irisin blunts cortical bone loss in mice.

Background: Chronic renal failure induces bone mineral disorders and sarcopenia. Skeletal muscle affects other tissues, including bone, by releasing myokines. However, the effects of chronic renal failure on the interactions between muscle and bone remain unclear.

Role of tissue factor in delayed bone repair induced by diabetic state in mice.

Background: Tissue factor (TF) is the primary activator of the extrinsic coagulation protease cascade. Although TF plays roles in various pathological states, such as thrombosis, inflammatory diseases, cancer, and atherosclerosis, its involvement in bone metabolism remains unknown.

Materials And Methods: The present study examined the roles of TF in delayed bone repair induced by a diabetic state in mice using wild-type (WT) and low TF-expressing (LTF) male mice.

Role of plasminogen activator inhibitor-1 in muscle wasting induced by a diabetic state in female mice.

Muscle wasting is a complication in patients with diabetes and leads to a reduced quality of life. However, the detailed mechanisms of diabetes-induced muscle wasting remain unknown. Plasminogen activator inhibitor-1 (PAI-1), a serine protease inhibitor that suppresses plasminogen activator activity, is involved in the pathophysiology of various diseases, including diabetes.

Serpinb1a suppresses osteoclast formation.

Serpinb1a, a serine protease inhibitor family protein, has been implicated in immunoregulation and several metabolic disorders, such as diabetes and obesity; however, its roles in bone remain unknown. Therefore, we herein investigated the physiological functions of Serpinb1a in osteoclastic and osteoblastic differentiation using mouse cell lines. Serpinb1a overexpression markedly reduced the number of tartrate-resistant acid phosphatase (TRAP)- and calcitonin receptor-positive multinucleated cells increased by receptor activator nuclear factor κB ligand (RANKL) in mouse preosteoclastic RAW 264.

Effects of fluid flow shear stress to mouse muscle cells on the bone actions of muscle cell-derived extracellular vesicless.

The interactions between skeletal muscle and bone have been recently noted, and muscle-derived humoral factors related to bone metabolism play crucial roles in the muscle/bone relationships. We previously reported that extracellular vesicles from mouse muscle C2C12 cells (Myo-EVs) suppress osteoclast formation in mice. Although mechanical stress is included in extrinsic factors which are important for both muscle and bone, the detailed roles of mechanical stress in the muscle/bone interactions have still remained unknown.

[Controlling Cell Dynamics by Cell-surface Modification].

Although the concept of a drug delivery system (DDS) is usually applied to conventional drug therapy, it is also important for cell-based therapy. The surface manipulation of living cells represents a powerful tool for controlling cell behaviors in the body, such as enhancement of cell-cell interactions, targeted delivery of cells, and protection from immunological rejection. Functional groups, including amines, thiols, and carbonyls, offer excellent opportunities for chemical modification through the formation of covalent bonds with exogenous molecules.

Influence of Angptl1 on osteoclast formation and osteoblastic phenotype in mouse cells.

Background: Osteoblasts and osteoclasts play important roles during the bone remodeling in the physiological and pathophysiological states. Although angiopoietin family Angiopoietin like proteins (Angptls), including Angptl1, have been reported to be involved in inflammation, lipid metabolism and angiogenesis, the roles of Angptl1 in bone have not been reported so far.

Methods: We examined the effects of Angptl1 on the osteoblast and osteoclast phenotypes using mouse cells.

Role of irisin in effects of chronic exercise on muscle and bone in ovariectomized mice.

Introduction: Exercise is beneficial for the prevention and treatment of osteoporosis. Skeletal muscle affects other tissues via myokines, the release of which is regulated by acute exercise. However, the effects of chronic exercise on myokines linking muscle to bone have not been fully elucidated.

MicroRNA-196a-5p in Extracellular Vesicles Secreted from Myoblasts Suppresses Osteoclast-like Cell Formation in Mouse Cells.

Muscle/bone interaction has been recently noted. Extracellular vesicles (EVs) play a vital role in physiological and pathophysiological processes by transferring microRNA (miRNA) to distant tissues. We previously reported that EVs secreted from C2C12 myoblasts (Myo-EVs) suppress osteoclast differentiation.

Myonectin inhibits the differentiation of osteoblasts and osteoclasts in mouse cells.

Myonectin is a myokine, which is involved in the pathophysiology of diabetes and obesity, and various myokines are involved in the interactions between skeletal muscle and bone. However, roles of myonectin in bone have still remained unknown. We therefore examined the effects of myonectin on mouse osteoblast and osteoclast differentiation .

Roles of Olfactomedin 1 in Muscle and Bone Alterations Induced by Gravity Change in Mice.

Microgravity causes both muscle and bone loss. Although we previously revealed that gravity change influences muscle and bone through the vestibular system in mice, its detailed mechanism has not been elucidated. In this study, we investigated the roles of olfactomedin 1 (OLFM1), whose expression was upregulated during hypergravity in the soleus muscle, in mouse bone cells.

PAI-1 is involved in delayed bone repair induced by glucocorticoids in mice.

Glucocorticoid (GC) treatments induce osteoporosis and chronic GC treatments have been suggested to induce delayed bone repair; however, the mechanisms by which GC induces delayed bone repair remain unclear. We herein investigated the roles of plasminogen activator inhibitor-1 (PAI-1) in GC-induced effects on bone repair after femoral bone injury using female mice with a PAI-1 deficiency and their wild-type counterparts. Dexamethasone (Dex) increased plasma PAI-1 levels as well as PAI-1 mRNA levels in the adipose tissues and muscles of wild-type mice.

Extracellular vesicles secreted from mouse muscle cells suppress osteoclast formation: Roles of mitochondrial energy metabolism.

Recent reports have described the interactions of muscle and bone. Various muscle-derived humoral factors, known as myokines, affect bone. Although extracellular vesicles (EVs) play a vital role in physiological and pathophysiological processes by transferring their contents to distant tissues during bone metabolism, the roles of EVs in the muscle-bone interactions remain unknown.

Roles of the vestibular system in obesity and impaired glucose metabolism in high-fat diet-fed mice.

The vestibular system controls balance, posture, blood pressure, and gaze. However, the roles of the vestibular system in energy and glucose metabolism remain unknown. We herein examined the roles of the vestibular system in obesity and impaired glucose metabolism using mice with vestibular lesions (VL) fed a high-sucrose/high-fat diet (HSHFD).

Humoral factors secreted from adipose tissue-derived mesenchymal stem cells ameliorate atherosclerosis in Ldlr-/- mice.

Aims: Atherosclerosis is a chronic inflammatory disease of the vasculature. Mesenchymal stem cells (MSCs) exert immunomodulatory and immunosuppressive effects by secreting humoral factors; however, the intravascular MSC administration presents a risk of vascular occlusion. Here, we investigated both the effect of conditioned medium from cultured MSCs (MSC-CM) on atherosclerosis and the underlying mechanism.

Plasminogen activator inhibitor-1 deficiency suppresses osteoblastic differentiation of mesenchymal stem cells in mice.

Plasminogen activator inhibitor-1 (PAI-1) is known as an inhibitor of fibrinolytic system. Previous studies suggest that PAI-1 is involved in the pathogenesis of osteoporosis induced by ovariectomy, diabetes, and glucocorticoid excess in mice. However, the roles of PAI-1 in early-stage osteogenic differentiation have remained unknown.

Roles of plasminogen in the alterations in bone marrow hematopoietic stem cells during bone repair.

We previously revealed that stromal cell-derived factor-1 (SDF-1) is involved in the changes in the number of bone marrow stem cells during the bone repair process in mice. Moreover, we reported that plasminogen (Plg) deficiency delays bone repair and the accumulation of macrophages at the site of bone damage in mice. We investigated the roles of Plg in the changes in bone marrow stem cells during bone repair.