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Related Concept Videos

Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
The Bone Matrix01:18

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Bone contains a relatively small number of cells entrenched in a matrix of collagen fibers that provide an adherent surface for inorganic salt crystals. Both components of the matrix, organic and inorganic, contribute to the unusual properties of bone. Without collagen, bones would be brittle and shatter easily. Without mineral crystals, bones would flex and provide little support. This can be observed by an experiment: when the minerals of a bone are dissolved by soaking the bone in acid or...
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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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A Fluorescent Intravital Imaging Approach to Study Load-Induced Calcium Signaling Dynamics in Mouse Osteocytes
05:03

A Fluorescent Intravital Imaging Approach to Study Load-Induced Calcium Signaling Dynamics in Mouse Osteocytes

Published on: February 24, 2023

Fluid Flow Induced Calcium Response in Bone Cell Network.

Bo Huo1, Xin L Lu, Clark T Hung

  • 1Bone Bioengineering Laboratory, Department of Biomedical Engineering, Columbia University, 351 Engineering Terrace, 1210 Amsterdam Avenue, Mail Code 8904, New York, NY 10027, USA.

Cellular and Molecular Bioengineering
|September 21, 2010
PubMed
Summary
This summary is machine-generated.

Fluid flow triggers calcium signaling in patterned bone cells. Blocking gap junctions, ATP, or calcium stores reduced signaling, revealing key pathways in bone mechanotransduction.

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Area of Science:

  • Biotechnology
  • Cell Biology
  • Biomedical Engineering

Background:

  • Previous work established patterned bone cell networks using microcontact printing and self-assembled monolayers.
  • Intercellular communication via gap junctions is crucial for network function.

Purpose of the Study:

  • To investigate calcium response and signaling pathways in patterned bone cell networks under steady fluid flow.
  • To identify key molecular mediators of fluid flow-induced calcium signaling in bone cells.

Main Methods:

  • Patterned bone cell networks on glass slides were treated with pharmacological agents targeting specific signaling pathways.
  • Calcium transients were recorded and quantitatively evaluated using network parameters.
  • Inhibition of gap junctions (18α-GA), ATP (suramin), and intracellular calcium stores (thapsigargin) were tested.

Main Results:

  • 18α-GA, suramin, and thapsigargin significantly reduced multiple calcium peaks observed in untreated cells.
  • Disruption of COX-2/PGE(2) or NOS/nitric oxide pathways also decreased responsive peaks.
  • Cells treated with 18α-GA maintained high intracellular calcium after the initial peak.
  • Absence of external calcium abolished calcium transients during fluid flow.

Conclusions:

  • Gap junctions, ATP, intracellular calcium stores, COX-2/PGE(2), and NOS/nitric oxide pathways are critical for flow-mediated calcium signaling in patterned bone cell networks.
  • Fluid flow initiates calcium transients in bone cells, dependent on extracellular and intracellular calcium.
  • This study elucidates the complex signaling network involved in bone cell mechanotransduction.