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Biology subjects

Chang, M. Y.

Publications and source records attributed to Chang, M. Y..

3 recordsLinked to original sources

Molecular signatures of genetically defined jugular nociceptors and their responses to allergic airway inflammation

Abstract Rationale: Vagal sensory neurons are molecularly and functionally diverse, and they play critical roles in visceral sensation and homeostasis. The vagal system is anatomically divided into jugular and nodose ganglia, which exhibit distinct peripheral innervation patterns and physiological functions. Although recent transcriptomic studies have characterized nodose neuronal subtypes in detail, the molecular profiles of jugular sensory neurons remain poorly defined. Objectives: To define the molecular profiles of genetically identified jugular sensory neurons and determine the transcriptional responses of jugular and nodose airway afferents to allergic airway inflammation. Methods: We performed deep transcriptomic profiling of two genetically defined jugular nociceptor populations, MrgprC11 and MrgprD neurons, and compared them with airway-innervating P2ry1 nodose neurons and Phox2b nodose neurons. We further examined transcriptional changes of MrgprC11 and P2ry1 neurons following OVA-induced allergic airway inflammation. Measurements and Main Results: Transcriptomic analyses revealed distinct molecular signatures of jugular nociceptive neurons and identified subtype-specific genes across diverse functional categories. Following OVA challenge, MrgprC11 and P2ry1 neurons exhibited strikingly divergent transcriptional responses. More than 400 genes that were differentially expressed in both neuronal populations were regulated in opposite directions. GO enrichment analysis suggested that MrgprC11 jugular neurons adopted a metabolically restrained state with reduced translation and bioenergetic activities, whereas P2ry1 nodose neurons exhibited metabolically active state with enhanced translation and bioenergetic activities. Conclusions: These findings provide new insight into vagal sensory neuron diversity and reveal distinct transcriptional adaptations of jugular and nodose airway afferents during allergic inflammation.

neuroscience↗

Regulation of Versican Expression in Macrophages is Mediated byCanonical Type I Interferon Signaling via ISGF3

Growing evidence supports a role for versican as an important component of the inflammatory response, with both pro- and anti-inflammatory roles depending on the specific context of the system or disease under investigation. Our goal is to understand the regulation of macrophage-derived versican and the role it plays in innate immunity. In previous work, we showed that LPS triggers a signaling cascade involving TLR4, the Trif adaptor, type I interferons, and the type I interferon receptor, leading to increased versican expression by macrophages. In the present study, we used a combination of chromatin immunoprecipitation, siRNA, chemical inhibitors, and mouse model approaches to investigate the regulatory events downstream of the type I interferon receptor to better define the mechanism controlling versican expression. Results indicate that transcriptional regulation by canonical type I interferon signaling via the heterotrimeric transcription factor, ISGF3, controls versican expression in macrophages exposed to LPS. This pathway is not dependent on MAPK signaling, which has been shown to regulate versican expression in other cell types. The stability of versican mRNA may also contribute to prolonged versican expression in macrophages. These findings strongly support a role for macrophage-derived versican as a type I interferon-stimulated gene and further our understanding of versicans role in regulating inflammation.

cell biology↗

Inflation versus filling-in: why we feel we see more than we actually do in peripheral vision

Do we perceive fine details in the visual periphery? Here, we propose that phenomenology in the visual periphery can be characterized by an inflated sense of perceptual capacity, as observers overestimate the quality of their perceptual inputs. Distinct from the well-known perceptual phenomenon of \"filling-in\" where perceptual content is generated or completed endogenously, inflation can be characterized by incorrect introspection at the subjective level. The perceptual content itself may be absent or weak (i.e., not necessarily filled-in), and yet such content is mistakenly regarded by the system as rich. Behaviorally, this can be reflected by metacognitive deficits in the degree to which confidence judgments track task accuracy, and decisional biases for observers to think particular items are present, even when they are not. In two experiments using paradigms which exploit unique attributes of peripheral vision (crowding and summary statistics), we provide evidence that both types of deficits are present in peripheral vision, as observers reports are marked by overconfidence in discrimination judgments and high numbers of false alarms in detection judgments. We discuss potential mechanisms which may be the cause of inflation and propose future experiments to further explore this unique sensory phenomenon.

animal behavior and cognition↗