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Differential Aortic and Mitral Valve Interstitial Cell Mineralization and the Induction of Mineralization by Lysophosphatidylcholine . | LitMetric

AI Article Synopsis

  • - The study examines how the lipid lysophosphatidylcholine (LPC) contributes to calcific aortic valve disease (CAVD) by analyzing its presence in calcified and non-calcified regions of diseased aortic valves.
  • - Researchers cultured porcine valvular interstitial cells (pVICs) from both aortic and mitral valves to see how different concentrations of LPC affect cellular processes related to mineralization, including phosphate mineralization and alkaline phosphatase activity.
  • - Results indicated that LPC promotes calcification in aortic valve cells more than in mitral valve cells, suggesting LPC is important in the development of CAVD and highlighting differences in the cellular behavior of valvular

Article Abstract

Purpose: Calcific aortic valve disease (CAVD) is a serious condition with vast uncertainty regarding the precise mechanism leading to valve calcification. This study was undertaken to examine the role of the lipid lysophosphatidylcholine (LPC) in a comparison of aortic and mitral valve cellular mineralization.

Methods: The proportion of LPC in differentially calcified regions of diseased aortic valves was determined using thin layer chromatography (TLC). Next, porcine valvular interstitial cells (pVICs) from the aortic (paVICs) and mitral valve (pmVICs) were cultured with LPC (10 - 10 nM) and analyzed for cellular mineralization, alkaline phosphatase activity (ALPa), proliferation, and apoptosis.

Results: TLC showed a higher percentage of LPC in calcified regions of tissue compared to non-calcified regions. In pVIC cultures, with the exception of 10 nM LPC, increasing concentrations of LPC led to an increase in phosphate mineralization. Increased levels of calcium content were exhibited at 10 nm LPC application compared to baseline controls. Compared to pmVIC cultures, paVIC cultures had greater total phosphate mineralization, ALPa, calcium content, and apoptosis, under both a baseline control and LPC-treated conditions.

Conclusions: This study showed that LPC has the capacity to promote pVIC calcification. Also, paVICs have a greater propensity for mineralization than pmVICs. LPC may be a key factor in the transition of the aortic valve from a healthy to diseased state. In addition, there are intrinsic differences that exist between VICs from different valves that may play a key role in heart valve pathology.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4235965PMC
http://dx.doi.org/10.1007/s13239-014-0197-3DOI Listing

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