Abstract
Extracellular acidification occurs under physiologic and pathologic conditions, such as exercise, ischemia, and inflammation. It has been shown that acidosis has various adverse effects on bone. In recent years there has been increasing evidence which indicates that ovarian cancer G protein-coupled receptor 1 (OGR1) is a pH-sensing receptor and mediates a variety of extracellular acidification-induced actions on bone cells and other cell types. Recent studies have shown that OGR1 is involved in the regulation of osteoclast differentiation, survival, and function, as well as osteoblast differentiation and bone formation. Moreover, OGR1 also regulates acid-induced apoptosis of endplate chondrocytes in intervertebral discs. These observations demonstrate the importance of OGR1 in skeletal development and metabolism. Here, we provide an overview of OGR1 regulation ofosteoclasts, osteoblasts, and chondrocytes, and the molecular actions of OGR1 induced by extracellular acidification in the maintenance of bone health.
Highlights
Bone and cartilage are the two primary components that form the skeleton in vertebrates [1].These two tissues consist of three specific cell types scattered within the extracellular matrix (ECM): Bone-forming osteoblasts, bone-resorbing osteoclasts in bone, and cartilage-forming chondrocytes in cartilage [2]
The transcripts of proton-sensing G protein-coupled receptors (GPCRs), ovarian cancer G protein-coupled receptor 1 (OGR1), are widely distributed and expressed on bone cells that are involved in the regulation of osteoclast differentiation, survival, and function, osteoblast differentiation and bone formation, as well as apoptosis of endplate chondrocytes in intervertebral discs [13,15,16]
Interesting results were noted when cultures of rat lumbar endplate chondrocytes were exposed to acidosis; the mRNA levels of OGR1 increased in response to acidosis, whereas the mRNA levels of the other receptors were unchanged
Summary
Bone and cartilage are the two primary components that form the skeleton in vertebrates [1]. It has been shown that transient receptor potential V1 (TRPV1) is a calcium-permeable channel which is modulated or activated by extracellular protons [11]. Another family of molecular acid sensors is the acid-sensing ion channels (ASICs), which encode at least six different ASIC subunits, including ASIC1a, ASIC1b, ASIC2a, ASIC2b, ASIC3, and ASIC4 [12]. The transcripts of proton-sensing GPCRs, ovarian cancer G protein-coupled receptor 1 (OGR1), are widely distributed and expressed on bone cells that are involved in the regulation of osteoclast differentiation, survival, and function, osteoblast differentiation and bone formation, as well as apoptosis of endplate chondrocytes in intervertebral discs [13,15,16]. It has been showed that in bone cells metabolic acidosis increased [Ca2+]i from intracellular stores through activation of OGR1
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