scholarly journals The Role of Ca2+-NFATc1 Signaling and Its Modulation on Osteoclastogenesis

2020 ◽  
Vol 21 (10) ◽  
pp. 3646
Author(s):  
Jung Yun Kang ◽  
Namju Kang ◽  
Yu-Mi Yang ◽  
Jeong Hee Hong ◽  
Dong Min Shin
Keyword(s):  
Bone Loss ◽  
Calcium Signaling ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Osteoclast Differentiation ◽  
Receptor Potential ◽  
Cytosolic Calcium ◽  
Transient Receptor Potential Channels ◽  
Potential Channels ◽  
Transient Receptor

The increasing of intracellular calcium concentration is a fundamental process for mediating osteoclastogenesis, which is involved in osteoclastic bone resorption. Cytosolic calcium binds to calmodulin and subsequently activates calcineurin, leading to NFATc1 activation, a master transcription factor required for osteoclast differentiation. Targeting the various activation processes in osteoclastogenesis provides various therapeutic strategies for bone loss. Diverse compounds that modulate calcium signaling have been applied to regulate osteoclast differentiation and, subsequently, attenuate bone loss. Thus, in this review, we summarized the modulation of the NFATc1 pathway through various compounds that regulate calcium signaling and the calcium influx machinery. Furthermore, we addressed the involvement of transient receptor potential channels in osteoclastogenesis.

scholarly journals Receptor-Operated Osteoclast Calcium Sensing*

Endocrinology ◽  
2001 ◽  
Vol 142 (5) ◽  
pp. 1968-1974 ◽  
Author(s):  
Brian D. Bennett ◽  
Ulises Alvarez ◽  
Keith A. Hruska
Keyword(s):  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Independent Manner ◽  
Calcium Sensing ◽  
Store Depletion ◽  
Potential Channels ◽  
Transient Receptor ◽  
Channel Type

Abstract Osteoclasts “sense” elevated extracellular calcium, which leads to cytoskeletal changes that may be linked to phospholipase C (PLC) activation and the associated rise in intracellular calcium ([Ca2+]i). Since PLC is linked to transient receptor potential channels (trp), we hypothesized that receptor activated calcium influx due to this channel type would be activated by osteoclasts sensing [Ca2+]e. We found that high [Ca2+]e induced similar intracellular Ca2+ rises in chicken osteoclasts with or without intracellular Ca2+ store depletion by either TPEN or thapsigargin, thus defining store-insensitive Ca2+ influx. This store-insensitive calcium sensing component was blocked by the PLC antagonist U73122. Also, the calcium channel inhibitor SKF 96365, a blocker of store-independent trp-like channels, was effective in inhibiting calcium sensing in the presence of thapsigargin. Thus, a store-independent component of calcium sensing was associated with ion channels linked to PLC. Since receptor activated transient receptor potential (trp) family cation channels open in a PLC-dependent and store-independent manner, we suggest that receptor operated channels are activated in osteoclasts stimulated by high extracellular Ca2+.

scholarly journals Effects of Ginger and its Pungent Constituents on Transient Receptor Potential Channels

2017 ◽  
Vol 112 (3) ◽  
pp. 250a
Author(s):  
Young-Soo Kim ◽  
Chan Sik Hong ◽  
Sang Weon Lee ◽  
Joo Hyun Nam ◽  
Byung Joo Kim
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Potential Channels ◽  
Transient Receptor

What Evolutionary Evidence Implies About the Identity of the Mechanoelectrical Couplers in Vascular Smooth Muscle Cells

Physiology ◽  
2021 ◽  
Vol 36 (5) ◽  
pp. 292-306
Author(s):  
Heather A. Drummond
Keyword(s):  
Transient Receptor Potential ◽  
Molecular Model ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Potential Channels ◽  
Transient Receptor ◽  
Paradigm Shifting ◽  
G Protein Coupled ◽  
Evolutionary Role

Loss of pressure-induced vasoconstriction increases susceptibility to renal and cerebral vascular injury. Favored paradigms underlying initiation of the response include transient receptor potential channels coupled to G protein-coupled receptors or integrins as transducers. Degenerin channels may also mediate the response. This review addresses the 1) evolutionary role of these molecules in mechanosensing, 2) limitations to identifying mechanosensitive molecules, and 3) paradigm shifting molecular model for a VSMC mechanosensor.

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