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Related Concept Videos

Tension Response at Adherens Junctions01:26

Tension Response at Adherens Junctions

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The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
α-Catenin as a Mechanosensory Protein
The α-catenin of adherens junctions is an allosteric protein with three VH (vinculin...
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Cell-matrix's Response to Mechanical Forces01:13

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In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue. 
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Intracellular Signaling Affects Focal Adhesions01:17

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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Cell Motility through Blebbing01:16

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Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
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Actin Filament Depolymerization01:19

Actin Filament Depolymerization

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Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Live Cell Imaging during Mechanical Stretch
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Tensile Overload Injures Human Alveolar Epithelial Cells through YAP/F-Actin/MAPK Signaling.

Shan He1, Ruihan Liu1, Qing Luo1

  • 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400030, China.

Biomedicines
|July 29, 2023
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Tensile overload injures lung cells by disrupting the actin cytoskeleton and activating the YAP/MAPK pathway. Targeting this axis may offer new treatments for lung injuries.

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ERK1/2F-actinJNKapoptosishuman alveolar epithelial cellstensile overload

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Area of Science:

  • Cell Biology
  • Mechanobiology
  • Pulmonary Medicine

Background:

  • Explosion shockwaves cause mechanical forces leading to lung injuries.
  • The precise mechanisms of tensile overload-induced lung injury remain largely unknown.

Purpose of the Study:

  • To elucidate the cellular mechanisms underlying tensile overload-induced lung injury.
  • To identify potential therapeutic targets for lung tissue repair.

Main Methods:

  • Flow cytometry assessed apoptosis and 5-ethynyl-2'-deoxyuridine (EdU) detected proliferation in human alveolar epithelial cells (BEAS-2B) under tensile overload.
  • Immunofluorescence and Western blot analyzed the actin cytoskeleton, mitogen-activated protein kinase (MAPK) pathway proteins, and Yes-associated protein (YAP).

Main Results:

  • Tensile overload decreased BEAS-2B cell proliferation and increased apoptosis.
  • This injury involved actin cytoskeleton depolymerization, activation of JNK and ERK1/2 (MAPK pathway), and YAP upregulation.
  • Jasplakinolide treatment, JNK/ERK inhibition, and YAP inhibition mitigated apoptosis.

Conclusions:

  • The YAP/F-actin/MAPK signaling axis is crucial in tensile-induced BEAS-2B cell injury.
  • This pathway presents novel therapeutic strategies for treating and repairing lung injuries.