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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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Adherens Junctions01:24

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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
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Cell Adhesion Molecules - Types and Functions01:20

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Cell adhesion molecules (CAMs) are pivotal to multicellularity and the coordinated functioning of tissues and organ systems. They enable physical interactions between cells and provide mechanical strength to tissues. They also function as receptors for signal transmission across the plasma membrane. The CAMs are broadly classified into four families - integrins, cadherins, selectins, and immunoglobulin-like CAMs (IgCAMs).
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Anchoring Junctions01:03

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Anchoring junctions are multiprotein complexes that help cells connect to other cells and the extracellular matrix. Anchoring junctions are present on the lateral and basal surfaces of cells, providing strong and flexible connections. Focal adhesions are often formed due to cell interactions with the ECM substrata, which initiate signal transduction via kinase cascades and other mechanisms. Together, they provide stability and tissue integrity. There are three types of anchoring junctions:...
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Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
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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.
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Exploring the evolving function of soluble intercellular adhesion molecule-1 in junction dynamics during

Xiang Xiao1,2, Yating Han1,3, Qin Li4

  • 1Center for Reproductive Health, School of Pharmaceutical Sciences, Hangzhou Medical College (Zhejiang Academy of Medical Sciences), Hangzhou, China.

Frontiers in Endocrinology
|January 23, 2024
PubMed
Summary

Soluble intercellular adhesion molecule-1 (sICAM-1) weakens the blood-testis barrier (BTB) and impairs sperm production. sICAM-1 may regulate BTB permeability by influencing SRC signaling, offering potential therapeutic targets for male infertility.

Keywords:
Sertoli cellsblood-testis barrier (BTB)cytoskeletonmale fertilitysoluble intercellular adhesion molecule-1 (sICAM-1)spermatogenesistestis

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Using Cell-substrate Impedance and Live Cell Imaging to Measure Real-time Changes in Cellular Adhesion and De-adhesion Induced by Matrix Modification

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Area of Science:

  • Reproductive Biology
  • Cell Biology
  • Immunology

Background:

  • Intercellular adhesion molecule-1 (ICAM-1) is a glycoprotein on immune and epithelial cells.
  • Soluble ICAM-1 (sICAM-1) is released from cell surfaces and linked to disease severity.
  • sICAM-1 regulates the blood-testis barrier (BTB) and spermatogenesis.

Purpose of the Study:

  • To investigate the role of sICAM-1 in regulating BTB integrity and spermatogenesis.
  • To explore the molecular mechanisms by which sICAM-1 affects BTB function.
  • To identify potential therapeutic targets for male infertility related to BTB dysfunction.

Main Methods:

  • In vitro and in vivo studies of sICAM-1 overexpression.
  • Analysis of BTB junction protein expression (N-cadherin, γ-catenin, connexin 43).
  • Assessment of SRC family kinase (SFK) signaling pathways.

Main Results:

  • sICAM-1 overexpression weakened the BTB, reduced junction proteins, and caused germ cell loss.
  • Membrane-bound ICAM-1 exhibited barrier-strengthening effects, contrasting with sICAM-1.
  • sICAM-1 overexpression phenocopied SRC inhibition, suggesting SRC acts downstream of sICAM-1.

Conclusions:

  • sICAM-1 acts as a molecular switch disrupting BTB integrity and Sertoli-germ cell adhesion.
  • SRC signaling is implicated in the downstream effects of sICAM-1 on BTB dynamics.
  • Targeting sICAM-1/SRC pathways may offer novel strategies for treating male infertility and barrier dysfunction.