Publications by authors named "Huihui Tu"

2 Publications

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Elevated pulmonary tuberculosis biomarker miR-423-5p plays critical role in the occurrence of active TB by inhibiting autophagosome-lysosome fusion.

Emerg Microbes Infect 2019 ;8(1):448-460

a Institute of Cell Biology , Zhejiang University School of Medicine , Hangzhou , People's Republic of China.

Rapid diagnosis of pulmonary tuberculosis is an effective measure to prevent the spread of tuberculosis. However, the grim fact is that the new, rapid, and safe methods for clinical diagnosis are lacking. Moreover, although auto-lysosome is critical in clearing Mycobacterium tuberculosis, the pathological significance of microRNAs, as biomarkers of tuberculosis, in autophagosome maturation is unclear. Here, these microRNAs were investigated by Solexa sequencing and qPCR validation, and a potential diagnostic model was established by logistic regression. Besides that, the mechanism of one of the microRNAs involved in the occurrence of tuberculosis was studied. The results showed that the expression of miR-423-5p, miR-17-5p, and miR-20b-5p were significantly increased in the serum of patients with tuberculosis. The combination of these three microRNAs established a model to diagnose tuberculosis with an accuracy of 78.18%, and an area under the curve value of 0.908. Bioinformatics analysis unveiled miR-423-5p as the most likely candidate in regulating autophagosome maturation. The up-regulation of miR-423-5p could inhibit autophagosome maturation through suppressing autophagosome-lysosome fusion in macrophages. Further investigations showed that VPS33A was the direct target of miR-423-5p, and the two CUGCCCCUC domains in VPS33A 3'-UTR were the direct regulatory sites for miR-423-5p. In addition, an inverse correlation between VPS33A and miR-423-5p was found in peripheral blood mononuclear cells of patients with tuberculosis. Since the inhibition of autolysosome formation plays a critical role in tuberculosis occurrence, our findings suggests that miR-423-5p could suppress autophagosome-lysosome fusion by post-transcriptional regulation of VPS33A, which might be important for the occurrence of active tuberculosis.
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http://dx.doi.org/10.1080/22221751.2019.1590129DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6455132PMC
August 2019

Interplay between Heightened Temporal Variability of Spontaneous Brain Activity and Task-Evoked Hyperactivation in the Blind.

Front Hum Neurosci 2016 20;10:632. Epub 2016 Dec 20.

School of Life Science, South China Normal University Guangzhou, China.

The brain's functional organization can be altered by visual deprivation. This is observed by comparing blind and sighted people's activation response to tactile discrimination tasks, like braille reading. Where, the blind have higher activation than the sighted upon tactile discrimination tasks, especially high activation difference is seen in ventral occipitotemporal (vOT) cortex. However, it remains unknown, whether this vOT hyperactivation is related to alteration of spontaneous activity. To address this question, we examined 16 blind subjects, 19 low-vision individuals, and 21 normally sighted controls using functional magnetic resonance imaging (fMRI). Subjects were scanned in resting-state and discrimination tactile task. In spontaneous activity, when compared to sighted subjects, we found both blind and low vision subjects had increased local signal synchronization and increased temporal variability. During tactile tasks, compared to sighted subjects, blind and low-vision subject's vOT had stronger tactile task-induced activation. Furthermore, through inter-subject partial correlation analysis, we found temporal variability is more related to tactile-task activation, than local signal synchronization's relation to tactile-induced activation. Our results further support that vision impairment induces vOT cortical reorganization. The hyperactivation in the vOT during tactile stimulus processing in the blind may be related to their greater dynamic range of spontaneous activity.
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http://dx.doi.org/10.3389/fnhum.2016.00632DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5169068PMC
December 2016