Advances in the Regulation of Osteoclasts and Osteoclast Functions

Abstract

Osteoclasts are derived from mononuclear hematopoietic myeloid lineage cells, which are formed in the bone marrow and are attracted to the bloodstream by factors, including sphingsine-1 phosphate. These circulating precursors are attracted to bone surfaces undergoing resorption by chemokines and other factors expressed at these sites, where they fuse to form multinucleated boneresorbing cells. All aspects of osteoclast formation and functions are regulated by macrophagecolony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL), cytokines essential for osteoclast formation and expressed by a variety of cell types, including osteoblast lineage cells. Since the discovery of RANKL in the mid1990s, mouse genetic and molecular studies have revealed numerous signaling pathways activated by RANKL and M-CSF. More recent studies indicate that osteoclasts and their precursors regulate immune responses and osteoblast formation and functions by means of direct cell-cell contact through ligands and receptors, such as ephrins and Ephs, and semaphorins and plexins, and through expression of clastokines. There is also growing recognition that osteoclasts are immune cells with roles in immune responses beyond mediating the bone destruction that can accompany them. This article reviews recent advances in the understanding of the molecular mechanisms regulating osteoclast formation and functions and their interactions with other cells in normal and pathologic states.

Osteoprotegerin exposure at different stages of osteoclastogenesis differentially affects osteoclast formation and function

“…Protons are produced by CA II from carbon dioxide and water in the cytoplasm, and are secreted into the extracellular space by V-ATPases (Tanabe et al 2004). Osteoclasts degrade bone by the polarized secretion of proteolytic enzymes (e.g., cathepsin K) and acids, which hydrolyze and solubilize the organic and inorganic components of bone, respectively (Boyce 2013). MMP-9 released from the ruffled border is highly expressed at early stages of osteoclast development and in mature osteoclasts, and helps regulate the osteoclast migration required for bone resorption (Engsig et al 2000;Reponen et al 1994).…”

LncRNA-AK131850 Sponges MiR-93-5p in Newborn and Mature Osteoclasts to Enhance the Secretion of Vascular Endothelial Growth Factor a Promoting Vasculogenesis of Endothelial Progenitor Cells

“…OCs are specialized multinucleated cells derived from hematopoietic stem cells or monocytes/macrophage progenitor cells [15]. There are three different stages during osteoclastogenesis: preosteoclast (Pre-OC), newborn osteoclast (N-OC) and mature osteoclast (M-OC) [16-18]. EPCs are a population of cells that are found circulating in the bone marrow and peripheral blood, which have the ability to differentiate into mature EC and then participate in vasculogenesis.…”

Вміст Вітаміну D І стан Кісткового Метаболізму При Синдромі Тиреотоксикозу (Огляд Літератури)

“…При цьому тривалість циклу становить майже половину від фізіологічного часу (3-4 місяці). Диспропорційні зміни остеокластів й остеобластів призводять до переважан-ня фази активації й резорбції, що супроводжується втратою кісткової маси тканини на 9,6 % при кожному ремоделюючому циклі [9]. При гіпотиреозі, навпаки, пролонгується процес ремоделювання, зменшується кістковий обмін і на 17 % зростає кісткова маса внаслі-док 700-денного циклу [10].…”