Person: Davis-Dusenbery, Brandi N
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Davis-Dusenbery
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Brandi N
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Davis-Dusenbery, Brandi N
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Publication Atrial natriuretic peptide is negatively regulated by microRNA-425(American Society for Clinical Investigation, 2013) Arora, Pankaj; Wu, Connie; Khan, Abigail May; Bloch, Donald; Davis-Dusenbery, Brandi N; Ghorbani, Anahita; Spagnolli, Ester; Martinez, Andrew; Ryan, Allicia; Tainsh, Laurel T.; Kim, Samuel M; Rong, Jian; Huan, Tianxiao; Freedman, Jane E.; Levy, Daniel; Miller, Karen; Hata, Akiko; Del Monte, Federica; Vandenwijngaert, Sara; Swinnen, Melissa; Janssens, Stefan; Holmes, Tara M.; Buys, Emmanuel; Bloch, Kenneth; Newton-Cheh, Christopher; Wang, Thomas Jue-FuuNumerous common genetic variants have been linked to blood pressure, but no underlying mechanism has been elucidated. Population studies have revealed that the variant rs5068 (A/G) in the 3′ untranslated region of NPPA, the gene encoding atrial natriuretic peptide (ANP), is associated with blood pressure. We selected individuals on the basis of rs5068 genotype (AG vs. AA) and fed them a low- or high-salt diet for 1 week, after which they were challenged with an intravenous saline infusion. On both diets, before and after saline administration, ANP levels were up to 50% higher in AG individuals than in AA individuals, a difference comparable to the changes induced by high-salt diet or saline infusion. In contrast, B-type natriuretic peptide levels did not differ by rs5068 genotype. We identified a microRNA, miR-425, that is expressed in human atria and ventricles and is predicted to bind the sequence spanning rs5068 for the A, but not the G, allele. miR-425 silenced NPPA mRNA in an allele-specific manner, with the G allele conferring resistance to miR-425. This study identifies miR-425 as a regulator of ANP production, raising the possibility that miR-425 antagonists could be used to treat disorders of salt overload, including hypertension and heart failure.Publication Pathways Disrupted in Human ALS Motor Neurons Identified through Genetic Correction of Mutant SOD1(Elsevier BV, 2014) Kiskinis, Evangelos; Sandoe, Jackson L; Williams, Lauren; Boulting, Gabriella; Moccia, Robert; Wainger, Brian; Han, Steve Sang-woo; Peng, Theodore; Thams, Sebastian; Mikkilineni, Shravani; Mellin, Cassidy; Merkle, Florian; Davis-Dusenbery, Brandi N; Ziller, Michael; Oakley, Derek; Ichida, Justin; Di Costanzo, Stefania; Atwater, Nick; Maeder, M; Goodwin, Marcus; Nemesh, James; Handsaker, Robert; Paull, Daniel; Noggle, Scott; McCarroll, Steven; Joung, Keith; Woolf, Carl; Brown, Robert H; Eggan, KevinDirect electrical recording and stimulation of neural activity using micro-fabricated silicon and metal micro-wire probes have contributed extensively to basic neuroscience and therapeutic applications; however, the dimensional and mechanical mismatch of these probes with the brain tissue limits their stability in chronic implants and decreases the neuron–device contact. Here, we demonstrate the realization of a three-dimensional macroporous nanoelectronic brain probe that combines ultra-flexibility and subcellular feature sizes to overcome these limitations. Built-in strains controlling the local geometry of the macroporous devices are designed to optimize the neuron/probe interface and to promote integration with the brain tissue while introducing minimal mechanical perturbation. The ultra-flexible probes were implanted frozen into rodent brains and used to record multiplexed local field potentials and single-unit action potentials from the somatosensory cortex. Significantly, histology analysis revealed filling-in of neural tissue through the macroporous network and attractive neuron–probe interactions, consistent with long-term biocompatibility of the device.Publication The mouse C9ORF72 ortholog is enriched in neurons known to degenerate in ALS and FTD(2014) Suzuki, Naoki; Maroof, Asif; Merkle, Florian; Koszka, Kathryn; Intoh, Atsushi; Armstrong, Ian; Moccia, Rob; Davis-Dusenbery, Brandi N; Eggan, KevinUsing transgenic animals harboring a targeted LacZ insertion, we studied the expression pattern of the C9ORF72 mouse ortholog. Unlike most genes mutated in ALS, which are ubiquitously expressed, the C9ORF72-ortholog was most highly transcribed in the neuronal populations sensitive to degeneration in ALS and FTD. Thus, our study provides a potential explanation for the cell type specificity of neuronal degeneration caused by C9ORF72 mutations.Publication ALS-Implicated Protein TDP-43 Sustains Levels of STMN2, a Mediator of Motor Neuron Growth and Repair(Springer Nature, 2019-01-14) Limone, Francesco; Guerra San Juan, Irune; Burberry, Aaron; Kirchner, Rory; Chen, Kuchuan; Eggan, Kevin; Klim, Joseph; Williams, Luis; Davis-Dusenbery, Brandi N; Mordes, Daniel; Steinbaugh, Michael; Gamage, Kanchana; Moccia, Rob; Cassel, Seth; Wainger, Brian; Woolf, CliffordThe discovery that TDP-43 mutations cause familial ALS and that many patients display pathological TDP-43 mislocalization has nominated altered RNA metabolism as a potential disease mechanism. Despite its importance, the identity of RNAs regulated by TDP-43 in motor neurons remains poorly understood. Here, we report transcripts whose abundances in human motor neurons are sensitive to TDP-43 depletion. Notably, we found STMN2, which encodes a microtubule regulator, declined after TDP-43 knockdown, in patient-specific motor neurons, following TDP-43 mislocalization, and in the postmortem patient spinal cords. Loss of STMN2 upon reduced TDP-43 function was due to the emergence of a cryptic exon, which is of substantial functional importance, as we further demonstrate that STMN2 is necessary for both axonal outgrowth and repair. Importantly, post-translational stabilization of STMN2 could rescue neurite outgrowth and axon regeneration deficits induced by TDP-43 depletion. We propose restoring STMN2 expression warrants future examination as an ALS therapeutic strategy.