Follicle-Stimulating Hormone Does Not Impact RANKL-Induced Osteoclastogenesis

Follicle-stimulating hormone

Bioactive Follicle-Stimulating Hormone

Specific and sensitive in vitro bioassays suitable for measurement of follicle-stimulating hormone (FSH) in small quantities of serum and urine have recently been validated. Comparisons of bioassay (B-FSH) potencies with immunoassay (I-FSH) estimates and chromatofocusing patterns have facilitated new discoveries regarding the regulation of FSH biosynthesis, storage, secretion, serum concentrati...

TRPM7 Is Essential for RANKL-Induced Osteoclastogenesis

The transient receptor potential melastatin type 7 (TRPM7) channel is a widely expressed non-selective cation channel with fusion to the C-terminal alpha kinase domain and regarded as a key regulator of whole body Mg(2+) homeostasis in mammals. However, the roles of TRPM7 during osteoclastogenesis in RAW264.7 cells and bone marrow-derived monocyte/macrophage precursor cells (BMMs) are not clear...

Mapping the Follicle-Stimulating Hormone-Induced Signaling Networks

Follicle-stimulating hormone (FSH) is a central regulator of male and female reproductive function. Over the last decade, there has been a growing perception of the complexity associated with FSH-induced cellular signaling. It is now clear that the canonical Gs/cAMP/PKA pathway is not the sole mechanism that must be considered in FSH biological actions. In parallel, consistent with the emerging...

Proinflammatory M1 Macrophages Inhibit RANKL-Induced Osteoclastogenesis.

In response to a defined panel of stimuli, immature macrophages can be classified into two major phenotypes: proinflammatory (M1) and anti-inflammatory (M2). Although both phenotypes have been implicated in several chronic inflammatory diseases, their direct role in bone resorption remains unclear. The present study investigated the possible effects of M1 and M2 macrophages on RANKL-induced ost...