Cardiosome-mediated protection in myocardial ischemia.

Cardiosomes, exosomes released in cardiospheres by cardiomyocytes and progenitor cells, communicate locally and at a distance from different tissues, promoting beneficial cellular changes. For example, miRNAs have emerged as regulators of intercellular communication via transport by extracellular vesicles in general and cardiosomes specifically. Although cardiosomes are considered biomarkers owing to their immense biomedical application in various clinical fields, their role in cardiovascular diseases remains unclear. This mini-review examines the experimental and clinical evidence for cardiosomes as non-invasive diagnostic, treatment and prognostic tools in acute myocardial infarction, the novelty of which is often lost in medical practice. In addition, we discuss the potential role of cardiosomes in physiologic mechanisms and cell signaling in cardiac conditioning strategies against reperfusion injury.

Actin-Cytoskeleton Drives Caveolae Signaling to Mitochondria during Postconditioning.

Caveolae-associated signaling toward mitochondria contributes to the cardioprotective mechanisms against ischemia-reperfusion (I/R) injury induced by ischemic postconditioning. In this work, we evaluated the role that the actin-cytoskeleton network exerts on caveolae-mitochondria communication during postconditioning. Isolated rat hearts subjected to I/R and to postconditioning were treated with latrunculin A, a cytoskeleton disruptor. Cardiac function was compared between these hearts and those exposed only to I/R and to the cardioprotective maneuver. Caveolae and mitochondria structures were determined by electron microscopy and maintenance of the actin-cytoskeleton was evaluated by phalloidin staining. Caveolin-3 and other putative caveolae-conforming proteins were detected by immunoblot analysis. Co-expression of caveolin-3 and actin was evaluated both in lipid raft fractions and in heart tissue from the different groups. Mitochondrial function was assessed by respirometry and correlated with cholesterol levels. Treatment with latrunculin A abolishes the cardioprotective postconditioning effect, inducing morphological and structural changes in cardiac tissue, reducing F-actin staining and diminishing caveolae formation. Latrunculin A administration to post-conditioned hearts decreases the interaction between caveolae-forming proteins, the co-localization of caveolin with actin and inhibits oxygen consumption rates in both subsarcolemmal and interfibrillar mitochondria. We conclude that actin-cytoskeleton drives caveolae signaling to mitochondria during postconditioning, supporting their functional integrity and contributing to cardiac adaption against reperfusion injury.

Relevance of endoplasmic reticulum and mitochondria interactions in age-associated diseases.

Although the elixir of youth remains in the darkness, medical and scientific advances have succeeded in increasing human longevity; however, the predisposition to disease and its high economic cost are raising. Different strategies (e.g., antioxidants) and signaling pathways (e.g., Nrf2) have been identified to help regulate disease progression, nevertheless, there are still missing links that we need to understand. Contact sites called mitochondria-associated membranes (MAM) allow bi-directional communication between organelles as part of the essential functions in the cell to maintain its homeostasis. Different groups have deeply studied the role of MAM in aging; however, it's necessary to analyze their involvement in the progression of age-related diseases. In this review, we highlight the role of contact sites in these conditions, as well as the morphological and functional changes of mitochondria and ER in aging. We emphasize the intimate relationship between both organelles as a reflection of the biological processes that take place in the cell to try to regulate the deterioration characteristic of the aging process; proposing MAM as a potential target to help limit the disease progression with age.

Relevance of Membrane Contact Sites in Cancer Progression.

Membrane contact sites (MCS) are typically defined as areas of proximity between heterologous or homologous membranes characterized by specific proteins. The study of MCS is considered as an emergent field that shows how crucial organelle interactions are in cell physiology. MCS regulate a myriad of physiological processes such as apoptosis, calcium, and lipid signaling, just to name a few. The membranal interactions between the endoplasmic reticulum (ER)-mitochondria, the ER-plasma membrane, and the vesicular traffic have received special attention in recent years, particularly in cancer research, in which it has been proposed that MCS regulate tumor metabolism and fate, contributing to their progression. However, as the therapeutic or diagnostic potential of MCS has not been fully revisited, in this review, we provide recent information on MCS relevance on calcium and lipid signaling in cancer cells and on its role in tumor progression. We also describe some proteins associated with MCS, like CERT, STIM1, VDAC, and Orai, that impact on cancer progression and that could be a possible diagnostic marker. Overall, these information might contribute to the understanding of the complex biology of cancer cells.