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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
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G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
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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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The Adhesion GPCR ADGRL2/LPHN2 Can Protect Against Cellular and Organismal Dysfunction.

Philipp Jakobs1, Anne Rafflenbeul2, Willem Berend Post3

  • 1Cardiovascular Degeneration, Haendeler Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.

Cells
|November 27, 2024
PubMed
Summary

ADGRL2 protein protects endothelial cells from sepsis triggers like LPS by preserving eNOS activity and enhancing antioxidant responses. This protective role against oxidative stress is conserved across species, suggesting therapeutic potential.

Keywords:
ADGRL2/LPHN2Caenorhabditis elegansNRF2eNOSendothelial cellslipopolysaccharidereactive oxygen speciesskn-1

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Sepsis and septic shock are often triggered by bacterial lipopolysaccharide (LPS).
  • Endothelial cells are crucial for vascular integrity but are compromised during sepsis.
  • Reduced endothelial NO Synthase (eNOS) activity contributes to vascular leakage in septic shock.

Purpose of the Study:

  • To investigate the role of Adhesion GPCRs (aGPCRs), specifically ADGRL2/LPHN2, in endothelial cell function during sepsis.
  • To elucidate the protective mechanisms of ADGRL2 against LPS-induced endothelial cell damage.
  • To explore the evolutionary conservation of ADGRL2's protective functions.

Main Methods:

  • Overexpression of ADGRL2 in endothelial cells.
  • Treatment of cells with LPS to mimic septic conditions.
  • Analysis of eNOS activity, apoptosis, migration, and antioxidative responses (NRF2 activity).
  • Utilizing Caenorhabditis elegans models to study the homolog lat-2.

Main Results:

  • ADGRL2 overexpression protected endothelial cells from LPS-induced activation, apoptosis, and impaired migration.
  • ADGRL2 preserved eNOS activity by altering its binding partners and enhanced NRF2-mediated antioxidative responses.
  • The protective function of ADGRL2 against oxidative stress was conserved in C. elegans lat-2 mutants, which exhibited increased ROS and reduced lifespan.

Conclusions:

  • ADGRL2 plays a significant protective role in endothelial cells against LPS-induced damage and oxidative stress.
  • ADGRL2 mechanism involves preserving eNOS activity and boosting antioxidative pathways.
  • The findings suggest ADGRL2 as a potential therapeutic target for sepsis and related vascular complications.