In order to foresee the post-TBI outcomes of organelle function and its biochemicalresponses, it became apparent to investigate the biomechanical effects onjunctions where blood vessels and cellular networks meet 4, 5. This region isclassified as the blood-brain barrierwhich is just one of the primary pathways that will ultimately lead to calciumoverload and cell-death cascades, if mechanically injured 4, 5.
This is aresult of microvascular stenosis orblood that is restricted to the microcirculatory systems at the barrier due toa narrowing of the vessels, which cause the latched feet of astrocytes to swelland avoid glutamate intake 4. Therefore, the group of Ellis et al. prepared apopulation of astroglial cell monolayers (from neonatal rat pups) to study the homeostaticalterations of a mechanical insult 4, 9, 10. Their experiment setup isdepicted in Fig. 1.
2 with the main component being the 94A Cell InjuryController (Commonwealth Biotechnology, Richmond, VA, USA) 10. Furthermore,the well (Flexcell® culture plates, Dow Corning® corp.,Midland, MI, USA) is a circular, collagen-coated silicone elastomer (Silastic®)membrane which is readily flexible and assumed to be sufficiently adherent tothe cultured cells so that in the presence of a pressurized force, both willstretch in a similar manner 9-11. The advantage this device presents is thatthe user can control the duration and magnitude of the pulse 10. Moreover,astrocytes are particularly responsive to a focalized mechanical pulse,allowing the pressure waves to traverse their entire intercellular network 4.Overall, their goal was to create a reliable model that could inflict voluntaryinsults that are representable to forces experienced in vivo 10. Simply, the experiment was meant to demonstrate arapid application of force to induce invitro cell deformation and strain, rather than just uniformly compressingthe cells 10.