bioRxiv Science⌕ Search

Biology subjects

Valdez, G.

Publications and source records attributed to Valdez, G..

4 recordsLinked to original sources

A gavage-fomite based method to generate mouse models with natural microbiota

Laboratory-raised specific pathogen-free (SPF) mice have been indispensable for fundamental immunology research, yet their reliability in predicting human clinical outcomes has been questionable. A major factor contributing to this disconnect is the sanitized housing environment, which deprives laboratory mice of physiological microbial exposure critical for immune maturation. Various approaches have been developed to introduce microbes to SPF mice, aiming to mimic human-like microbial experiences and engender adult human-like immune traits. However, some of these methods, specifically the pet store mice cohousing approach suffer from significant variability in pathogen exposure driven by the uncontrolled nature of microbial exchange and is associated with heightened mortality. Here we present an alternative gavage-fomite (GaF) method that exposes mice to a similarly diverse array of pathogens and commensal as the pet store cohousing method while limiting mortality. GaF-treated mice exhibited consistent gut microbial composition, robust immune maturation characterized by mucosal T-cell distribution, elevated serum inflammatory cytokines, and a splenic immune transcriptional signature closely aligned with that of adult humans. Furthermore, these mice demonstrated enhanced protection against a virulent bacterial challenge. The simplicity, and effectiveness of the GaF method for generating mice with natural microbiota, may support broader use of these models in basic and translational immunological research across institutions.

immunology↗

The microRNA, miR-133b, functions to slow Duchenne muscular dystrophy pathogenesis

Duchenne muscular dystrophy (DMD) is characterized by progressive degeneration of skeletal muscles. To date, there are no treatments available to slow or prevent the disease. Hence, it remains essential to identify molecular factors that promote muscle biogenesis since they could serve as therapeutic targets for treating DMD. While the muscle enriched microRNA, miR-133b, has been implicated in the biogenesis of muscle fibers, its role in DMD remains unknown. To assess the role of miR-133b in DMD-affected skeletal muscles, we genetically ablated miR-133b in the mdx mouse model of DMD. In the absence of miR-133b, the tibialis anterior muscle of juvenile and adult mdx mice is populated by small muscle fibers with centralized nuclei, exhibits increased fibrosis, and thickened interstitial space. Additional analysis revealed that loss of miR-133b exacerbates DMD-pathogenesis partly by altering the number of satellite cells and levels of protein-encoding genes, including previously identified miR-133b targets as well as genes involved in cell proliferation and fibrosis. Altogether, our data demonstrate that skeletal muscles utilize miR-133b to mitigate the deleterious effects of DMD.

cell biology↗

Identification of a molecular fingerprint for synaptic glia

The inability to specifically identify and manipulate synaptic glial cells remains a major obstacle to understanding fundamental aspects of synapse formation, stability and repair. Using a combinatorial gene expression approach, we discovered molecular markers that allow us to specifically label perisynaptic Schwann cells (PSCs), glial cells at neuromuscular synapses. Using these markers, we demonstrate that PSCs fully-differentiate postnatally and have a unique molecular signature that includes genes predicted and known to play critical roles at synapses. These findings will serve as a springboard for unprecedented approaches for studying molecular determinants of PSC differentiation and function at neuromuscular synapses and possibly synapse-associated glia throughout the CNS.

neuroscience↗