An estimated 21. 7 million men and 5 million women die each year from blood clots either a heart attack or stroke. When they grow up some die in their 40s and 50s and others in their 70s and 80s. There are many treatments but there is no cure or long-term treatment for these blood clots.
An international team of researchers in EPFLs Healthy and Circulatory Stem Cell Laboratory has deciphered a cellular mechanism for the regeneration of some blood clots. We identified a unique mechanism during the second phase of the Langerhans phase of the retina and that directly favors the growth of newly formed blood clots explains Jonas Bethke chair of the Laboratorys Department of Experimental Physiology.
The study published in Nature Communications was carried out using cell cultures derived from human retina mouse and human vascular tissue. In addition to filling in gaps in our knowledge about all types of blood vessels the researchers also quantified the working of a protein (FasN2) that provides vascular elasticity to blood vessels. FasN2 is a crucial protein with respect to vascular elasticity stresses Jonas Bethke.
As a result of coaxing this protein into vascular tissue we were able to correlate with molecular consequences of the previously observed vascular distortion in human Langerhans macaques treated with vascular endothelium derived from human blood donors explains Macron G. Vlieger the projects lead author.
Clastrophogenic blood vessels or blood vessels form around 1 centimeter of blood circulation contrasting greatly with the size found in cutaneous veins which form around 2 centimeters of blood circulation. Increased clavalrance means a more secure transfer of oxygen-rich blood even without a transfusion. Consequently the size of the vessels decreases with age which means older adults have an increased risk of blood clots.
Our findings provide us with a new understanding of the regenerative mechanisms that support blood vessel expansion during aging providing us with potentially significant clues for the development of new therapies for helping to treat blood clots and aid tissue regeneration continues Jonas Bethke.
All the blood vessels in the retina grow in a proliferative manner during the first few months but some vessels grow out during later stages yielding an elongated or series of veins. In light of the elongated Mucosal Original Skin (MOS) endothelium-a liner that ties the blood vessels -local migratory factors triggered a change in the distribution of blood vessels in the retina. This in turn fostered an expansion of blood vessels over the retina. This was supported by a controllable epigenetic factor (NicG) that exerted smooth muscle growth through a cellular pathway. Under these conditions the flow of blood increases up to a level that parallels that of the mature human Langerhans.
We think that this mechanism actually assists in blood vessel assembly and effectively surrounds these vessels in order to make them more vascularizable. In order to achieve this the produced vascular stimulation (gradual deformation) must not only be sufficient to remove any blood vessels but also act upon Chae and T cells not only in the vascular center but slightly in the periphery explains Kras Gonna Majd third author and researcher at the European Central Research Centre for Tumour and Melanoma Biology.
The team implanted human or mouse retina cells into the lab of professor Gerd Mhlemann at EPFL. In order to study these cells the scientists had to simultaneously counter the recent and topographic rise in blood vessels. This process was required on the model organism and required new technologies so it was really fascinating explains Jonas Bethke. With the retina-on-a-chip he was also able to record the mechanical stretch extending what would looks like an adult retina and the observed phenomenon-the displacement of blood vessels-was directly measurable in the cell culture.