Biology subjects

Hidalgo-Figueroa, M.

Publications and source records attributed to Hidalgo-Figueroa, M..

3 recordsLinked to original sources

bioRxiv2026

The serum from critical COVID-19 patients induces proteomic changes in olfactory neuroepithelial cells that resemble post-covid neurological complications

Post-acute sequelae of SARS-CoV-2 infection (PASC), commonly referred to as Long COVID, comprise a constellation of persistent, recurrent, or newly emerging symptoms that may endure for months or years following acute infection. Beyond respiratory impairment, PASC is characterized by a wide spectrum of extrapulmonary manifestations, among which neurological and neuropsychiatric symptoms are highly prevalent. Reported features include olfactory dysfunction with loss of smell and taste, fatigue, neuroinflammation, cognitive and memory impairment, depression, and anxiety, with some symptoms persisting up to one year post-infection. Despite increasing recognition of these complications, the molecular mechanisms underlying post-COVID neurological sequelae remain poorly defined. In this study, we employed a label-free quantitative (LFQ) proteomics approach to investigate protein alterations in olfactory neuroepithelium-derived stem cells (ONEs), a unique population of neural progenitors located in the olfactory mucosa at the interface between the respiratory system and both the peripheral and central nervous systems. Due to their anatomical exposure and susceptibility to SARS-CoV-2, ONEs represent a highly relevant translational model for exploring virus-associated neurobiological processes. ONEs derived from healthy donors were incubated with serum from either asymptomatic PCR-positive individuals (AS; n=4) or critically ill hospitalized patients (CR; n=6). Proteomic profiling revealed a distinct differential protein expression pattern in ONEs exposed to CR serum compared with AS serum. Altered pathways were associated with viral infection responses, respiratory and cardiovascular dysfunction, and notably, cerebrovascular and nervous system disorders. These findings highlight the vulnerability of ONEs to systemic factors associated with severe COVID-19 and provide molecular insight into mechanisms potentially contributing to persistent neurological sequelae in PASC. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=110 SRC="FIGDIR/small/710460v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@12cfda5org.highwire.dtl.DTLVardef@c0636borg.highwire.dtl.DTLVardef@bf303eorg.highwire.dtl.DTLVardef@1f861e9_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2025

Neurotrophin-3 produced by motor neurons non-cell autonomously regulate the development of pre-motor interneurons in the developing spinal cord

The development of multicellular organisms requires proper interplays between cell-autonomous genetic programs controlled by combinations of transcription factors that regulate the differentiation of distinct cell populations and non-cell autonomous processes that coordinate the proliferation, the fate, the survival, the respective location, and the proper interactions of these populations. During the development of the nervous system, non-cell autonomous mechanisms determine neuronal fate, survival, distribution, axon guidance, and connectivity. Although similar processes are suggested to be at work in the formation of spinal motor circuits, the molecular mechanisms involved remain mostly elusive. Here, we provide evidence that the Onecut transcription factors regulate a non-cell autonomous mechanism that modulate pre-motor interneuron development. We show that conditional inactivation of the Onecut factors in spinal motor neurons affects the differentiation and the positioning of pre-motor interneuron populations. We identify that Neurotrophin-3 produced by motor neurons under the control of the Onecut factors non-cell autonomously regulate the production and the distribution of pre-motor interneuron populations. Thus, we elucidated one of the non-cell autonomous mechanisms that coordinate the formation of the spinal motor circuits.

neuroscience↗

bioRxiv2018

Onecut factors and Pou2f2 regulate diversification and migration of V2 interneurons in the mouse developing spinal cord

Acquisition of proper neuronal identity and position is critical for the formation of neural circuits. In the embryonic spinal cord, cardinal populations of interneurons diversify into specialized subsets and migrate to defined locations within the spinal parenchyma. However, the factors that control interneuron diversification and migration remain poorly characterized. Here, we show that the Onecut transcription factors are necessary for proper diversification and distribution of the V2 interneurons in the developing spinal cord. Furthermore, we uncover that these proteins restrict and moderate the expression of spinal isoforms of Pou2f2, a transcription factor known to regulate B-cell differentiation. By gain- or loss-of-function experiments, we show that Pou2f2 contribute to regulate the position of V2 populations in the developing spinal cord. Thus, we uncovered a genetic pathway that regulates the diversification and the distribution of V2 interneurons during embryonic development.\n\nSignificance statementIn this study, we identify the Onecut and Pou2f2 transcription factors as regulators of spinal interneuron diversification and migration, two events that are critical for proper CNS development.

developmental biology↗