[The normal functions of integrins and their involvement in pathology]. / Functiile normale ale integrinelor si implicarea lor în patologie.

Ordered cell-cell and cell-matrix adhesive interactions are a fundamental feature of all multicellular organisms. Numerous studies in recent years have confirmed that both types of cell adhesion are mediated by cell surface receptors known as "adhesion molecules". These receptors can be divided into a limited number of families. Knowledge gained from basic research into cell adhesion is now being applied to clinical problems, and some of these have been summarized here. Integrins are heterodimeric proteins mediating cell-cell and cell-extracellular matrix adhesive connections and signal transduction across the plasma membrane. The important roles of integrins are in Leukocyte Adhesion Deficiency, in viral diseases, neural development and cancer. Suggestive data now points to roles in functions characterized in part by morphological rearrangements, such as learning and memory, and injury responses.

The diminution of platelet activity in vitamin E-treated diabetic rats.

BACKGROUND: Because vitamin E deficiency has been demonstrated in platelets obtained from diabetic subjects, in our research we investigated the platelet activity and the oxidative stress in alloxan diabetic rats supplemented with vitamin E. MATERIAL AND METHODS: The platelet activity was estimated by the adhesion index (AI) and the oxidative stress was correlated with the determined level of malondialdehyde (MDA) an end product of lipid peroxidation. RESULTS: We found that alloxanic diabetes was associated with significant increase in the both MDA level and AI (p < 0.01 and p < 0.05, respectively). The AI was better correlated to the MDA level (r = +0.60) than to the hyperglycemia. The administration of vitamin E before and after alloxan was accompanied by a significant decrease of both MDA level and AI comparing to untreated diabetic rats. CONCLUSIONS: Our study suggests that vitamin E supplementation may improve the increased platelet adhesion as a consequence of an increased oxidative stress and therefore the incidence of diabetic angiopathy may be reduced.

[Mechanotransduction and tensegrity (I)]. / Mecanotransductie si tensegritate (I).

The current review deals with mechanotransduction by means of an architectural model of cell function called tensegrity. This concept was introduced by D. E. Ingber in order to frame more focused mechanisms of mechano-transduction, i.e. different signaling pathways, which are less able to predict global cellular behaviour in response to stress, into a coherent mechano-chemical theory of cell function. Tensegrity structures are made and held up by interconnecting a continuous series of tension elements with a discontinuous series of compression resistant struts, in a simple "stick and string" model. These structures develops an intrinsic stabilizing tension called prestress and reacts by global rearrangements of their configuration to a local action of a mechanical stress. The only requirement of a tensegrity network is that tension is continuous and compression is local. At the cellular level the theory assumes that membrane, nucleus and all the organelles are hard-wired by the insoluble cytoskeletal (CSK) scaffold. More than that, the interconnection between CSK and the extracellular matrix (ECM) provides an efficient mechanical couple responsible for changes in cell shape and movement. Cell shape, in turn, regulates cellular function. Focal adhesion complexes, which mediate the CSK-ECM interaction are viewed as integrative devices for both mechanical signaling and soluble factor-dependent signaling. Furthermore, the tensegral molecular network is considered to be a solid-state regulatory system of all cell functions. The way tensegrity influences molecular mechanics, cellular response tuning and coordinated behaviour of large scale structures are also discussed. Besides its conceptual importance, the tensegrity model has multiple applications, being used in combined approach of cell biology, bioengineering, architecture, and biomechanics in order both to improve cell culture and its subsequent applications and the open the way to a more complex technology of tissular engineering.