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Centro de Investigaciones Biológicas (CIB-CSIC)
Autophagy in Development and Disease
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Wimasis is wondeful since we no longer have to spend our valuable time counting dots inside cells!
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Dr. Patricia Boya
Head of laboratory
Our lab uses cellular and animal models to understand the physiological roles of autophagy and its implications during disease.

Autophagy is an essential intracelullar degradation pathway that recycles cell components generating new building blocks and energy to maintain cellular homeostasis. Autophagy plays an important role in the response to nutrient starvation; the recycling of damaged organelles and is a survival mechanism under stress conditions. In addition, autophagy could as well participate in programmed cell death.

We are interested in the implication of autophagy during development and in the relationship of autophagy with basic processes such as proliferation, differentiation and cell death. Moreover we want to understand how autophagy deregulation may play a role in several pathological situations such as cancer and neurodegenerative conditions.

We have several projects with pharmaceutical companies to screen for new drugs that modulate autophagy with the aim to find new treatments for cancer, neurodegenerative diseases and other pathological conditions.

Wimasis has allowed us to speed up and standardize the process of autophagosome quantification in cells and tissues.
Products they are using
The Ludwig-Maximilians-University (LMU) Munich
The division of clinical pharmacology (Prof. Dr. Stefan Endres, work group of Dr. David Anz)
For the homeostasis of the immune system communication between the different types of immune cells is of major importance. Communication takes place via soluble factors like cytokines and via direct cell-cell-interaction.

For example during the generation of an immune response, where antigen presenting cells that have processed an antigen and got maturated by pathogen-associated-molecular-patterns secret different types of cytokines in order to activate surrounding immune cells and attract t-helper-cells. Only if these t-helper-cells express the right t-cell-receptor for the specific antigen, an immune response can be evoked. This process is important in the context of defense against invading pathogens, but also for example in the context of immunological recognition and eventually rejection of tumor cells.

In cooperation with Wimasis we were able to develop a new method which can be used to automatically analyze migration and interaction of cells.
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University of Córdoba
Department of Cell Biology Physiology and Immunology, Faculty of Sciences
In this case we study alterations in mitochondrial ultrastructure and dynamics in kidney cells of mice submitted to calorie restriction. It has been proofed in a wide range of animal species, that caloric restriction without malnutrition (RC) is the most robust experimental intervention that increases longevity and delays the onset of cancer, kidney disease, cataracts, diabetes, hypertension, etc... Although the extension of the maximum longevity has not been fully tested in primates, other beneficial effects accepted that this intervention occurs in these animals and in humans. However, it has not been fully elucidated the mechanisms through which the RC operates to produce these effects.

Currently "Theory of Free Radicals” propose that the cellular aging occurs due to the accumulation of reactive oxygen species (ROS), this theory appears to be the most logical to explain the effects of the RC, because as it has been shown, that the intervention RC drastically decreases the production of ROS in cells, supporting the idea that a decrease in oxidative stress may be a mechanism that contributes to delay aging. Moreover, it has been found that it is the organelle mitochondria where the increased production and accumulation of ROS occurs, and thus constitutes a special target for studies on aging and caloric restriction. Furthermore, numerous alterations have been detected in mitochondria during aging (reduction of mitochondrial biogenesis and ATP synthesis, increased leakage of H + , etc.), many of which are reversed when the animals are subjected to periods of RC.

Other studies have found an inverse correlation between longevity and the degree of unsaturation of membrane phospholipids , having assumed that polyunsaturated fatty acids are more susceptible to lipid peroxidation and other changes that would result in the accumulation of ROS in the cells. Finding least amount of polyunsaturated fatty acids after CR periods support this idea. Therefore, it is possible to assume that the decrease in the number of double bonds in fatty acids in the membranes can be an adaptation of the longest species to prevent the development and accumulation of oxidative damage.

Previous studies conducted in our group have shown that CR produces alterations in the ultrastructure and dynamics of fission / fusion of mouse liver mitochondria, and these effects are modulated by dietary fat composition in CR . However, it is completely unknown whether alterations in kidney mitochondria, specifically in cells of the proximal convoluted tubule, a structure that plays a key role in the reabsorption of molecules and electrolytes and therefore the proper functioning of the body, which physiology also altered during aging.

In cooperation with Wimasis we were able to develop an automatic method for automatic detection of mitochondria in kidney tissue and isolated monocyte cells, providing us with thousands of planimetrics and stereologycs parameters in a record time. Wimasis “Stereology” software makes the improvement of data recompilation possible, in a fast,and reliable way, and ensuring the reproducibility of our material.
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