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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Shear-Sensing by C-Reactive Protein: Linking Aortic Stenosis and Inflammation.

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Shear stress causes C-reactive protein (CRP) to dissociate into inflammatory monomers (mCRP), contributing to aortic valve stenosis (AS). This dissociation activates cells involved in AS development and other vascular diseases.

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Area of Science:

  • Cardiovascular Biology
  • Protein Biochemistry
  • Mechanobiology

Background:

  • C-reactive protein (CRP) exists as a pentameric form (pCRP) but can dissociate into monomeric subunits (mCRP).
  • Monomeric CRP (mCRP) exhibits prothrombotic and proinflammatory properties.
  • Pathophysiological shear rates, common in aortic valve stenosis (AS), can alter protein structure and function.

Purpose of the Study:

  • To investigate if shear stress modifies CRP conformation and induces inflammatory effects relevant to AS pathogenesis.
  • To explore the role of shear-induced CRP dissociation in the development of AS.

Main Methods:

  • Subjecting human pCRP to pathophysiologically relevant shear rates in vitro.
  • Utilizing biophysical and biochemical analyses to assess CRP conformation and function.
  • Employing a mouse model of arterial stenosis to study in vivo shear effects.
  • Measuring mCRP and pCRP levels in severe AS patients before and after transcatheter aortic valve implantation.
  • Examining CRP presence on excised stenotic aortic valves.
  • Using microfluidic models to simulate AS shear rates and investigate mCRP's inflammatory function.

Main Results:

  • High shear rates induced pCRP dissociation into mCRP and aggregation into larger particles.
  • In vivo studies confirmed mCRP deposition post-stenosis in a mouse model.
  • AS patients showed elevated circulating mCRP levels pre-transcatheter aortic valve implantation.
  • Excised human stenotic aortic valves exhibited mCRP deposition.
  • Shear-stressed pCRP in a microfluidic AS model activated endothelial cells (increased ICAM-1, P-selectin) and platelets (increased TGF-β).

Conclusions:

  • Identified a novel mechanism of shear-induced pCRP dissociation to mCRP, activating key cells in AS development.
  • This mechanosensing mechanism of pCRP dissociation is likely relevant to other conditions with increased shear rates, such as atherosclerosis.