RESUMEN
Tardigrades are renowned for their ability to survive a wide array of environmental stressors. In particular, tardigrades can curl in on themselves while losing a significant proportion of their internal water content to form a structure referred to as a tun. In surviving varying conditions, tardigrades undergo distinct morphological transformations that could indicate different mechanisms of stress sensing and tolerance specific to the stress condition. Methods to effectively distinguish between morphological transformations, including between tuns induced by different stress conditions, are lacking. Herein, an approach for discriminating between tardigrade morphological states is developed and utilized to compare sucrose- and CaCl2-induced tuns, using the model species Hypsibius exemplaris. A novel approach of shadow imaging with confocal laser scanning microscopy enabled production of three-dimensional renderings of Hys. exemplaris in various physiological states resulting in volume measurements. Combining these measurements with qualitative morphological analysis using scanning electron microscopy revealed that sucrose- and CaCl2-induced tuns have distinct morphologies, including differences in the amount of water expelled during tun formation. Further, varying the concentration of the applied stressor did not affect the amount of water lost, pointing towards water expulsion by Hys. exemplaris being a controlled process that is adapted to the specific stressors.
Asunto(s)
Cloruro de Calcio , Sacarosa , Animales , Cloruro de Calcio/farmacología , Microscopía Confocal/métodos , Estrés Fisiológico , Invertebrados , Microscopía Electrónica de RastreoRESUMEN
Tardigrades, commonly known as 'waterbears', are eight-legged microscopic invertebrates renowned for their ability to withstand extreme stressors, including high osmotic pressure, freezing temperatures, and complete desiccation. Limb retraction and substantial decreases to their internal water stores results in the tun state, greatly increasing their ability to survive. Emergence from the tun state and/or activity regain follows stress removal, where resumption of life cycle occurs as if stasis never occurred. However, the mechanism(s) through which tardigrades initiate tun formation is yet to be uncovered. Herein, we use chemobiosis to demonstrate that tardigrade tun formation is mediated by reactive oxygen species (ROS). We further reveal that tuns are dependent on reversible cysteine oxidation, and that this reversible cysteine oxidation is facilitated by the release of intracellular reactive oxygen species (ROS). We provide the first empirical evidence of chemobiosis and map the initiation and survival of tardigrades via osmobiosis, chemobiosis, and cryobiosis. In vivo electron paramagnetic spectrometry suggests an intracellular release of reactive oxygen species following stress induction; when this release is quenched through the application of exogenous antioxidants, the tardigrades can no longer survive osmotic stress. Together, this work suggests a conserved dependence of reversible cysteine oxidation across distinct tardigrade cryptobioses.
Asunto(s)
Cisteína , Tardigrada , Animales , Especies Reactivas de Oxígeno , Invertebrados , CongelaciónRESUMEN
Photosynthesis relies on many easily oxidizable/reducible transition metals found in the metalloenzymes that make up much of the photosynthetic electron transport chain (ETC). One of these is manganese, an essential cofactor of photosystem II (PSII) and a component of the oxygen-evolving complex, the only biological entity capable of oxidizing water. Additionally, manganese is a cofactor in enzymatic antioxidants, notably the superoxide dismutases-which are localized to the chloroplastic membrane. However, unlike other metals found in the photosynthetic ETC, previous research has shown exposure to excess manganese enhances photosynthetic activity rather than diminishing it. In this study, the impact of PSII heterogeneity on overall performance was investigated using chlorophyll fluorescence, a rapid, non-invasive technique that probed for overall photosynthetic efficiency, reducing site activity, and antenna size and distribution. These measurements unveiled an enhanced plasticity of PSII following excess manganese exposure, in which overall performance and reducing center activity increased while antenna size and proportion of PSIIß centers decreased. This enhanced activity suggests manganese may hold the key to improving photosynthetic efficiency beyond that which is observed in nature.
Asunto(s)
Chlorella vulgaris , Manganeso , Fotosíntesis , Superóxido Dismutasa , CloroplastosRESUMEN
Epicardial fat is a continuously growing target of investigation in cardiovascular diseases due to both its anatomical proximity to the heart and coronary circulation and its unique physiology among adipose depots. Previous reports have demonstrated that epicardial fat plays key roles in coronary artery disease, but the non-coding RNA and transcriptomic alterations of epicardial fat in coronary artery disease have not been investigated thoroughly. Micro- and lncRNA microarrays followed by GO-KEGG functional enrichment analysis demonstrated sex-dependent unique mi/lncRNAs altered in human epicardial fat in comparison to subcutaneous fat in both patients with and without coronary artery disease (IRB approved). Among the 14 differentially expressed microRNAs in epicardial fat between patients with and without coronary artery disease, the hsa-miR-320 family was the most highly represented. IPW lncRNA interacted with three of these differentially expressed miRNAs. Next-generation sequencing and pathway enrichment analysis identified six unique mRNAs-miRNA pairs. Pathway enrichment identified inflammation, adipogenesis, and cardiomyocyte apoptosis as the most represented functions altered by the mi/lncRNAs and atherosclerosis and myocardial infarction among the highest cardiovascular pathologies associated with them. Overall, the epicardial fat in patients with coronary artery disease has a unique mi/lncRNA profile which is sex-dependent and has potential implications for regulating cardiac function.
Asunto(s)
Enfermedad de la Arteria Coronaria , ARN Largo no Codificante , Tejido Adiposo/metabolismo , Enfermedad de la Arteria Coronaria/metabolismo , Humanos , Pericardio/metabolismo , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Grasa Subcutánea/metabolismoRESUMEN
Angiotensin-converting enzyme 2 (ACE2) has been an increasingly prevalent target for investigation since its discovery 20 years ago. The finding that it serves a counterregulatory function within the traditional renin-angiotensin system, implicating it in cardiometabolic health, has increased its clinical relevance. Focus on ACE2's role in cardiometabolic health has largely centered on its apparent functions in the context of obesity. Interest in ACE2 has become even greater with the discovery that it serves as the cell receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), opening up numerous mechanisms for deleterious effects of infection. The proliferation of ACE2 within the literature coupled with its dual role in SARS-CoV-2 infection and obesity necessitates review of the current understanding of ACE2's physiological, pathophysiological, and potential therapeutic functions. This review highlights the roles of ACE2 in cardiac dysfunction and obesity, with focus on epicardial adipose tissue, to reconcile the data in the context of SARS-CoV-2 infection.
Asunto(s)
Tejido Adiposo/enzimología , Enzima Convertidora de Angiotensina 2/fisiología , COVID-19/enzimología , Obesidad/enzimología , Pericardio/enzimología , SARS-CoV-2 , COVID-19/epidemiología , Enfermedades Cardiovasculares/enzimología , Comorbilidad , Humanos , Inflamación/enzimología , Inflamación/virología , Obesidad/epidemiología , Proteínas Recombinantes , Sistema Renina-Angiotensina/fisiología , SARS-CoV-2/metabolismoRESUMEN
Adipose dysfunction with aging increases risk to insulin resistance and other chronic metabolic diseases. We previously showed functional changes in microRNAs involved in pre-adipocyte differentiation with aging resulting in adipose dysfunction. However, the mechanisms leading to this dysfunction in microRNAs in adipose tissue (adipomiRs) during aging are not well understood. We determined the longitudinal changes in expression of adipomiRs and studied their regulatory mechanisms, such as miRNA biogenesis and editing, in an aging rodent model, with Fischer344 × Brown-Norway hybrid rats at ages ranging from 3 to 30 months (male/females, n > 8). Expression of adipomiRs and their edited forms were determined by small-RNA sequencing. RT-qPCR was used to measure the mRNA expression of biogenesis and editing enzymes. Sanger sequencing was used to validate editing with aging. Differential expression of adipomiRs involved in adipocyte differentiation and insulin signaling was altered with aging. Sex- and age-specific changes in edited adipomiRs were observed. An increase in miRNA biogenesis and editing enzymes (ADARs and their splice variants) were observed with increasing age, more so in female than male rats. The adipose dysfunction observed with age is attributed to differences in editing of adipomiRs, suggesting a novel regulatory pathway in aging.