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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone...
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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
09:37

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Published on: March 15, 2018

A TRPC1 protein-dependent pathway regulates osteoclast formation and function.

E-Ching Ong1, Vasyl Nesin, Courtney L Long

  • 1Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73014, USA.

The Journal of Biological Chemistry
|June 18, 2013
PubMed
Summary
This summary is machine-generated.

The inhibitor of MyoD family, I-mfa, and the transient receptor potential canonical 1 (TRPC1) channel regulate bone health by controlling osteoclast formation. Their antagonistic roles fine-tune calcium signaling crucial for skeletal development.

Keywords:
BoneCalcium Intracellular ReleaseCalcium SignalingI-mfaOrai1OsteoclastTRP ChannelsTRPC1

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Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow
11:11

Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow

Published on: May 19, 2019

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Calcium (Ca2+) signaling is vital for maintaining bone homeostasis and skeletal development.
  • Osteoclastogenesis, the process of forming bone-resorbing cells, is a key target for regulating bone mass.

Purpose of the Study:

  • To investigate the antagonistic roles of the transient receptor potential canonical 1 (TRPC1) channel and the inhibitor of MyoD family, I-mfa, in osteoclastogenesis.
  • To identify novel TRPC1 splice variants involved in calcium signaling and bone regulation.

Main Methods:

  • Utilized I-mfa null mice and double mutant (Trpc1/I-mfa) mice to study osteoclast numbers, bone surface, and resorption.
  • Performed in vitro differentiation of pre-osteoclasts and measured whole-cell currents.
  • Identified and characterized a novel TRPC1 splice variant (TRPC1ε) using heterologous expression in HEK293 cells.

Main Results:

  • I-mfa deficiency led to osteopenia with increased osteoclast numbers and activity, which were normalized in double mutant mice.
  • TRPC1ε was identified as a novel splice variant that amplifies Ca2+ release-activated Ca2+ (CRAC) channel activity by interacting with Orai1.
  • I-mfa interacts with the TRPC1ε-Orai1 complex, suppressing CRAC channel activity, suggesting a cell-autonomous role in regulating osteoclastogenesis.

Conclusions:

  • TRPC1 and I-mfa function antagonistically to regulate osteoclastogenesis and bone homeostasis.
  • TRPC1ε amplifies CRAC channel activity, while I-mfa suppresses it, providing a mechanism for fine-tuning calcium signaling in osteoclasts.
  • This interplay is crucial for regulating the dynamic range of CRAC channel activity and controlling osteoclast formation for skeletal health.