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Related Concept Videos

Inflammatory Response I: Vascular and Cellular01:30

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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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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Related Experiment Video

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On-Chip Endothelial Inflammatory Phenotyping
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APOC3 induces endothelial dysfunction through TNF-α and JAM-1.

Yun Tao1, Yisong Xiong2, Huimin Wang1

  • 1Center of Laboratory Medicine, Affiliated Hospital, Nantong University, 20 Xi Si Road, Nantong, 226001, People's Republic of China.

Lipids in Health and Disease
|September 14, 2016
PubMed
Summary

Apolipoprotein C3 (APOC3) promotes cardiovascular disease (CVD) by increasing inflammation and endothelial cell (EC) dysfunction. Targeting APOC3-induced inflammation may offer a novel therapeutic strategy for CVD.

Keywords:
APOC3Cardiovascular diseaseEndothelial dysfunctionInflammation

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Area of Science:

  • Lipid metabolism and cardiovascular research
  • Endothelial cell biology
  • Inflammation and atherosclerosis

Background:

  • Cardiovascular disease (CVD) fatality rates are rising, with elevated triglycerides as a risk factor.
  • Endothelial cell (EC) dysfunction is a key contributor to CVD.
  • Apolipoprotein C3 (APOC3) is linked to hyperlipidemia and CVD risk, but its direct effects on ECs were unclear.

Purpose of the Study:

  • To determine the direct effects of APOC3 on ECs.
  • To investigate APOC3's role in EC inflammation, chemotaxis, and exudation.

Main Methods:

  • Utilized ELISA, qRT-PCR, immunofluorescence, flow cytometry, and transwell assays on human umbilical vein endothelial cells (HUVECs).
  • Employed siRNA to silence TNF-α and JAM-1 to analyze APOC3's influence on EC inflammatory processes.

Main Results:

  • APOC3 correlated with EC inflammation, marked by increased TNF-α expression.
  • APOC3 disrupted endothelial tight junctions (TJs) via elevated JAM-1, promoting leukocyte exudation and EC chemotaxis.
  • APOC3 increased THP-1 cell adhesion to HUVECs.

Conclusions:

  • Elucidated the mechanism of APOC3-induced EC inflammation, chemotaxis, and exudation.
  • Suggests targeting APOC3-mediated inflammatory pathways as a potential new therapeutic approach for CVD.