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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Microtubules tune mechanotransduction through NOX2 and TRPV4 to decrease sclerostin abundance in osteocytes.

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Osteocytes sense mechanical forces via a pathway involving microtubules and reactive oxygen species (ROS), reducing sclerostin to influence bone formation. This microtubule-dependent mechanism regulates cytoskeletal stiffness and osteocyte response to mechanical stress.

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Area of Science:

  • Bone biology
  • Cellular mechanotransduction
  • Skeletal adaptation

Background:

  • Osteocytes are key mechanosensors in bone, regulating bone formation by controlling sclerostin levels.
  • Understanding the molecular pathways linking mechanical stimuli to osteocyte response is crucial for bone health.

Purpose of the Study:

  • To define a novel microtubule-dependent pathway for osteocyte mechanotransduction.
  • To investigate the role of cytoskeletal dynamics and reactive oxygen species (ROS) in regulating sclerostin abundance.

Main Methods:

  • Utilized cultured osteocytes subjected to fluid shear stress.
  • Investigated the role of microtubules, detyrosination, NADPH oxidase 2 (NOX2), ROS, calcium (Ca2+) signaling (TRPV4), and CaMKII.
  • Assessed changes in sclerostin abundance and cytoskeletal stiffness.

Main Results:

  • Identified a pathway where fluid shear stress reduces sclerostin via ROS and Ca2+ signaling.
  • Demonstrated that detyrosination-stabilized microtubules dictate cytoskeletal stiffness and mechanoresponsiveness.
  • Showed that NOX2-derived ROS activate TRPV4 channels, leading to Ca2+ influx and CaMKII activation, ultimately decreasing sclerostin.

Conclusions:

  • Elucidated a microtubule-dependent mechanotransduction pathway in osteocytes involving ROS and Ca2+ signaling.
  • Highlighted the role of cytoskeletal detyrosination in modulating osteocyte mechanosensitivity.
  • Suggests potential therapeutic targets within this pathway for improving bone quality.