7 research outputs found
Human breast milk exosomes accelerate mouse wound healing
P543
The healing of cutaneous wounds is a very efficient process despite being very complex. Under certain pathological conditions healing may be impaired, prolonging the healing process and eventually leading to medical intervention and the chronicity of the wound. Exosomes are secreted extracellular vesicles present in biological fluids where they play a key role in intercellular communication at the tissue, organ and organismal levels. Given that human breast milk contains abundant maternal extracellular vesicles (MEVs) with pro-regenerative and immunomodulatory properties, the aim of the present study was to evaluate if topical application ofMEVs into open wounds would be beneficial for healing. Full-thickness excision wounds of 4-mm diameter were created in the dorsal skin of C57BL/6 mice and topical application of 20 micrograms of human MEV isolated at weeks 9, 11, 12 and 15 postpartum of breastfeeding were placed onto the open wounds. Control wounds were vehicle-treated. Macroscopic measurements up to 7 days postwounding revealed that the area of the wound treated with MEV significantly decreased compared with controls. Histological analyses at day 7 post-wounding showed no differences in the granulation tissue area between groups. ..
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Addressing Food Loss and Waste : A Global Problem with Local Solutions
The report focuses on the role that food loss and waste (FLW) could play in reducing the environmental footprint of food systems while attempting to meet the caloric and nutrient needs of a population expected to increase by 3 billion people in the next 30 years. The performance of the global food system over the last century has been extraordinary. From a global population of 1.6 billion people in 1900 to nearly 8 billion in 2020, the agri-food sector has risen to the challenge of providing global caloric sufficiency, mainly by increasing yields of a few principal staple crops. However, this path is no longer sustainable
653 Topical use of exosomes from human maternal milk accelerates acute cutaneous wound healing
575 Characterization of aged dermal stem cell phenotype: implications for skin homeostasis
Lack of GDAP1 Induces Neuronal Calcium and Mitochondrial Defects in a Knockout Mouse Model of Charcot-Marie-Tooth Neuropathy
27 páginas, 9 figuras.Mutations in GDAP1, which encodes protein located in the mitochondrial outer membrane, cause axonal recessive (AR-CMT2), axonal dominant (CMT2K) and demyelinating recessive (CMT4A) forms of Charcot-Marie-Tooth (CMT) neuropathy. Loss of function recessive mutations in GDAP1 are associated with decreased mitochondrial fission activity, while dominant mutations result in impairment of mitochondrial fusion with increased production of reactive oxygen species and susceptibility to apoptotic stimuli. GDAP1 silencing in vitro reduces Ca2+ inflow through store-operated Ca2+ entry (SOCE) upon mobilization of endoplasmic reticulum (ER) Ca2+, likely in association with an abnormal distribution of the mitochondrial network. To investigate the functional consequences of lack of GDAP1 in vivo, we generated a Gdap1 knockout mouse. The affected animals presented abnormal motor behavior starting at the age of 3 months. Electrophysiological and biochemical studies confirmed the axonal nature of the neuropathy whereas histopathological studies over time showed progressive loss of motor neurons (MNs) in the anterior horn of the spinal cord and defects in neuromuscular junctions. Analyses of cultured embryonic MNs and adult dorsal root ganglia neurons from affected animals demonstrated large and defective mitochondria, changes in the ER cisternae, reduced acetylation of cytoskeletal α-tubulin and increased autophagy vesicles. Importantly, MNs showed reduced cytosolic calcium and SOCE response. The development and characterization of the GDAP1 neuropathy mice model thus revealed that some of the pathophysiological changes present in axonal recessive form of the GDAP1-related CMT might be the consequence of changes in the mitochondrial network biology and mitochondria-endoplasmic reticulum interaction leading to abnormalities in calcium homeostasis.This work has been funded by grants from the Spanish Ministry of Economy and Competitiveness, grants no. SAF2009-07063 and SAF2012-32425 (to FP), the Collaborative Joint Project awarded by IRDiRC and funded by ISCIII grant IR11/TREAT-CMT, Instituto de Salud Carlos III (to both FP and JMC), the Generalitat Valenciana Prometeo Programme 2009/059 and 2014/029 (to FP) and the Swiss National Science Foundation, grant no. 31003A_135735/1 (to RC). This work has also been funded by the CIBERER, an initiative from the Instituto de Salud Carlos III. MB-M is the recipient of a FPI fellowship, from the Spanish Ministry of Economy and Competitiveness. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewe