Browsing by Author "Martinez, Agustin"
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Item Diseases associated with leaky hemichannels(Frontiers Research Foundation, 2015) Retamal, Mauricio; Reyes, Edison; Garcia, Isaac; Pinto, Bernardo; Martinez, Agustin; Gonzalez, CarlosHemichannels (HCs) and gap junction channels (GJCs) formed by protein subunits called connexins (Cxs) are major pathways for intercellular communication. While HCs connect the intracellular compartment with the extracellular milieu, GJCs allow the interchange of molecules between cytoplasm of two contacting cells. Under physiological conditions, HCs are mostly closed, but they can open under certain stimuli allowing the release of autocrine and paracrine molecules. Moreover, some pathological conditions, like ischemia or other inflammation conditions, significantly increase HCs activity. In addition, some mutations in Cx genes associated with human diseases, such as deafness or cataracts, lead to the formation of more active HCs or "leaky HCs." In this article we will revise cellular and molecular mechanisms underlying the appearance of leaky HCs, and the consequences of their expression in different cellular systems and animal models, in seeking a common pattern or pathological mechanism of disease.Item Gap junction channels and hemichannels in the CNS: regulation by signaling molecules(Elsevier, 2013) Orellana, Juan; Martinez, Agustin; Retamal, MauricioCoordinated interaction among cells is critical to develop the extremely complex and dynamic tasks performed by the central nervous system (CNS). Cell synchronization is in part mediated by connexins and pannexins; two different protein families that form gap junction channels and hemichannels. Whereas gap junction channels connect the cytoplasm of contacting cells and coordinate electric and metabolic activities, hemichannels communicate intra- and extra-cellular compartments and serve as diffusional pathways for ions and small molecules. Cells in the CNS depend on paracrine/autocrine communication via several extracellular signaling molecules, such as, cytokines, growth factors, transmitters and free radical species to sense changes in microenvironment as well as to adapt to them. These signaling molecules modulate crucial processes of the CNS, including, cellular migration and differentiation, synaptic transmission and plasticity, glial activation, cell viability and microvascular blood flow. Gap junction channels and hemichannels are affected by different signaling transduction pathways triggered by these paracrine/autocrine signaling molecules. Most of the modulatory effects induced by these signaling molecules are specific to the cell type and the connexin and pannexin subtype expressed in different brain areas. In this review, we summarized and discussed most of the relevant and recently published information on the effects of signaling molecules on connexin or pannexin based channels and their possible relevance in CNS physiology and pathology. This article is part of the Special Issue Section entitled 'Current Pharmacology of Gap Junction Channels and Hemichannels'.Item Redox-mediated regulation of connexin proteins; focus on nitric oxide(Elsevier, 2017) Garcia, Isaac; Sanchez, Helmuth; Martinez, Agustin; Retamal, MauricioConnexins are membrane proteins that form hemichannels and gap junction channels at the plasma membrane. Through these channels connexins participate in autocrine and paracrine intercellular communication. Connexin-based channels are tightly regulated by membrane potential, phosphorylation, pH, redox potential, and divalent cations, among others, and the imbalance of this regulation have been linked to many acquired and genetic diseases. Concerning the redox potential regulation, the nitric oxide (NO) has been described as a modulator of the hemichannels and gap junction channels properties. However, how NO regulates these channels is not well understood. In this mini-review, we summarize the current knowledge about the effects of redox potential focused in NO on the trafficking, formation and functional properties of hemichannels and gap junction channels.