In addition, the scientist highlighted the strong parallels existing between the apoptotic microenvironment in cardiovascular disease and those present in the tissues of a few degenerative diseases. In the long run, these data could provide better understanding of other untreatable human pathologies.
The sequence of reactions triggered by apoptosis was presented today, September 19th, at the Fourth Annual Meeting of the European Vascular Genomics Network (EVGN, www.evgn.org), the Network of excellence on cardiovascular disease, which is running in parallel with the 4th European Meeting on Vascular Biology and Medicine (EMVBM).
With more than 400 attendants from all over Europe and representatives from the rest of the world, among whom there are cardiologists, diabetes researchers, hematologists, thrombosis scientists, gene therapists and oncologists, the Bristol Meeting offers a stimulating environment for discussion and future planning.
Apoptosis, the programmed cell death that occurs when a cell has accumulated sufficient DNA damages that it is unable to repair its DNA, is centrally involved in the pathogenesis of a whole range of human illnesses and injury states, and atherosclerosis is no exception. However, until recently, its exact role in this pathology was unclear.
Martin Bennett, a leading cardiologist and atherosclerosis expert, set up a series of targeted experiments aimed at understanding the precise mechanism of action of this, otherwise useful, process.
“We decided – explained Bennett – to elucidate the role that VSMCs death has in the timeline of atherosclerosis progression. Using a mouse model that reproduces the human condition, we induced apoptosis of VSMCs only inside the vessel wall, observing, at first, a clear enlargement of the atherosclerotic plaques that almost doubled their size. This is a bad prognostic factor, as the more they grow the more the plaques become brittle”. That was exactly the second observation made: after the initial growth, the fibrous cap that encloses a typical plaque became thinner, whereas the plaque core increased. “All these signals – points out Bennett – could be useful at the bedside, for a real-time monitoring of atherosclerosis progression”. Not enough, after these first events, the researchers confirmed that the whole region involved in the apoptotic process undergoes calcification. This, in turn, prevents the remodelling of a vessel and, when occurs in a patient, it worsens his or her prognosis.
Furthermore, from Bennett’s investigation emerged striking analogies with two degenerative diseases: Marfan’s syndrome and Hutchinson Gilford Progeria. In both these diseases the tissues look much similar to the one analysed by Bennett in the atherosclerotic settings, with areas of calcifications, and the same kind of infiltrating cells.
“Early as they are, these data rise hope that apoptosis could be targeted at different levels, in order to prevent the cascade of reactions so noxious for the health. And that, possibly, it will help to find novel therapies also for other ailments”.
The “TRiC” to folding actin
10.08.2018 | Max-Planck-Institut für Biochemie
SERSitive: New substrates make it possible to routinely detect one molecule in a million
10.08.2018 | Institute of Physical Chemistry of the Polish Academy of Sciences
Proteins must be folded correctly to fulfill their molecular functions in cells. Molecular assistants called chaperones help proteins exploit their inbuilt folding potential and reach the correct three-dimensional structure. Researchers at the Max Planck Institute of Biochemistry (MPIB) have demonstrated that actin, the most abundant protein in higher developed cells, does not have the inbuilt potential to fold and instead requires special assistance to fold into its active state. The chaperone TRiC uses a previously undescribed mechanism to perform actin folding. The study was recently published in the journal Cell.
Actin is the most abundant protein in highly developed cells and has diverse functions in processes like cell stabilization, cell division and muscle...
Scientists have discovered that the electrical resistance of a copper-oxide compound depends on the magnetic field in a very unusual way -- a finding that could help direct the search for materials that can perfectly conduct electricity at room temperatur
What happens when really powerful magnets--capable of producing magnetic fields nearly two million times stronger than Earth's--are applied to materials that...
The quality of materials often depends on the manufacturing process. In casting and welding, for example, the rate at which melts solidify and the resulting microstructure of the alloy is important. With metallic foams as well, it depends on exactly how the foaming process takes place. To understand these processes fully requires fast sensing capability. The fastest 3D tomographic images to date have now been achieved at the BESSY II X-ray source operated by the Helmholtz-Zentrum Berlin.
Dr. Francisco Garcia-Moreno and his team have designed a turntable that rotates ultra-stably about its axis at a constant rotational speed. This really depends...
If certain signaling cascades are misregulated, diseases like cancer, obesity and diabetes may occur. A mechanism recently discovered by scientists at the Leibniz- Forschungsinstitut für Molekulare Pharmakologie (FMP) in Berlin and at the University of Geneva has a crucial influence on such signaling cascades and may be an important key for the future development of therapies against these diseases. The results of the study have just been published in the prestigious scientific journal 'Molecular Cell'.
Cell growth and cell differentiation as well as the release and efficacy of hormones such as insulin depend on the presence of lipids. Lipids are small...
You seem to be standing in the plasma vessel looking around: Where otherwise plasmas with temperatures of several million degrees are being investigated, with...
08.08.2018 | Event News
27.07.2018 | Event News
25.07.2018 | Event News
10.08.2018 | Physics and Astronomy
10.08.2018 | Life Sciences
10.08.2018 | Life Sciences