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MiRNA Nanostring Data on a Silk Scaffold model following CCI injury

ABSTRACT: This study investigates the effects of controlled cortical impact (CCI), a form of traumatic brain injury (TBI), using a 3D silk scaffold cell culture model. Human induced neural stem cells (iNSCs), human induced astrocytes, and HMC3 microglial cells were seeded onto the silk scaffolds and allowed to grow under controlled conditions. A subset of these cell cultures was then subjected to CCI to simulate injury. The primary aim of the study was to assess the cellular and molecular response to CCI, particularly focusing on miRNA expression profiles. miRNA Nanostring technology was employed to quantify differential expression patterns associated with CCI exposure, providing insights into neuroinflammatory, regenerative, and apoptotic pathways impacted by the injury. These data contribute to a better understanding of miRNA's role as a biomarker for TBI and its potential involvement in cellular recovery and neuroprotection processes following traumatic injury.

ORGANISM(S): Homo sapiens

PROVIDER: GSE280043 | GEO | 2024/12/11

REPOSITORIES: GEO

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Project description:Traumatic brain injury (TBI) initiates not only complex neurovascular and glial changes within the brain but also pathophysiological responses that extend beyond the central nervous system. The peripheral response to TBI has become an intensive area of research, as these systemic perturbations can induce dysfunction in multiple organ systems. As there are no approved therapeutics for TBI, it is imperative that we investigate the peripheral response to TBI to identify targets for future intervention. Of particular interest is the gastrointestinal (GI) system. Even in the absence of polytrauma, brain-injured individuals are at increased risk of suffering from GI-related morbidity and mortality. Symptoms such as intestinal dysmotility, inflammation, ulceration, and fecal incontinence can drastically diminish quality of life. The GI tract is inhabited by trillions of microbes that have been implicated as modulators of many neurological disorders. Clinical and preclinical studies implicate gut dysbiosis, a pathological imbalance in the normally symbiotic microbiota, as both a consequence of TBI as well as a contributing factor to brain damage. However, our understanding of this interplay is still limited. While relatively little is known about the effects of TBI on the structure and function of the GI tract, prior studies report that experimental TBI induces intestinal barrier dysfunction and morphological changes. To confirm these findings in the current model of TBI, male C57BL/6J mice underwent a sham control or a controlled cortical impact (CCI) procedure to induce a contusive brain injury, and intestinal permeability was assessed at 4 h, 8 h, 1 d, and 3 d post-injury. An acute, transient increase in permeability was observed at 4 h after CCI. Histological analyses of the ileum and colon at multiple time points from 4 h to 4 wks revealed no overt morphological changes, suggesting that CCI induced a short-lived physiologic dysfunction without major structural alterations to the GI tract. As the microbiome is a modulator of GI physiology, we performed 16s gene sequencing on fecal samples collected prior to and over the first month after CCI or sham injury. Microbial community diversity was assessed using common metrics of alpha and beta diversity. Alpha diversity was lower in the CCI injury group and beta diversity differed among groups, although these effects were not observed in all metrics. Subsequent differential abundance analysis revealed that the phylum Verrucamicrobiota was increased in CCI mice at 1, 2, and 3 d post-injury when compared to sham mice. Subsequent qPCR identified the Verrucamicrobiota species as Akkermansia Muciniphila, an obligate anaerobe that resides in and helps regulate the intestinal mucus layer and barrier. To determine whether TBI promotes changes to the GI tract favorable for the proliferation of A. muciniphila, mucus-producing goblet cells and the level of GI hypoxia were evaluated. Goblet cell density in the medial colon was significantly increased at 1 d, while colon hypoxia was significantly increased at 3 d. Taken together, these studies show that CCI induces transient intestinal barrier dysfunction followed by increased goblet cell density and hypoxia in the colon with a concomitant increase in A. muciniphila that may suggest a compensatory response to systemic stress after TBI.

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MiRNA Nanostring Data on a Silk Scaffold model following CCI injury

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