1.Effect of hemeoxygenase system on Nogo-A expression in rat oligodendrocytesin vitro after carbon monoxide poisoning
Xiaohong WANG ; Suping WANG ; Juhua CHE ; Hong WANG ; Cui WANG ; Tao WANG ; Yanling ZHU
Chinese Journal of Tissue Engineering Research 2016;(2):230-235
BACKGROUND:Cerebral white matter demyelination is outstanding in the images of delayed encephalopathy after acute carbon monoxide (CO) poisoning. Since Nogo-A and Nogo-receptor are expressed in onoligodendrocytes and neurons respectively, we infer that Nogo-A system is involved in brain injury after acute CO poisoning and related to delayed encephalopathy after acute CO poisoning. Endogenous CO is a gaseous messenger, which is the metabolic product of hemeoxygenase. There is no report about the CO effect on Nogo-A system til now. OBIECTIVE: To in vitro culture oligodendrocytes using endogenous CO, inhibit the activity of hemeoxygenase system using zinc protoporphyrin-IX (ZnPPIX) and observe the variation of Nogo-A in oligodendrocytes at mRNA and protein levels. METHODS: Rat oligodendrocytes cultured in vitro were divided into control, CO, ZnPPIX groups. Cels in the CO and ZnPPIX groups were treated with 1% CO directly, In the ZnPPIX group, 10 μmol/L ZnPPIX was added into the culture medium before CO treatment. The expressions of Nogo-A mRNA and protein at 6, 24, 48 hours after culture were compared. Differences in the peak levels of Nogo-A mRNA and protein between CO and ZnPPIX groups were detected using RT-PCR and immunohistochemistry respectively. RESULTS: The expression levels of Nogo-A mRNA and protein were significantly higher in the CO group than the control group and reached the peak at 24 hours of culture. Compared with the CO group, oligodendrocytes cultured with ZnPPIX showed higher expressions of Nogo-A mRNA and protein at 24 hours of culture. These findings suggest that except the influence of hypoxia occurring in CO poisoning, exogenous CO increases the expression of Nogo-A in cultured oligodendrocytes in vitro, and the heme oxygenase system can inhibit the expression of Nogo-A mRNA and protein.
2.Ultrasound for assisting acupuncture therapy
Yang LIU ; Yanling CHE ; Yile XU ; Jiashuo LI
Chinese Journal of Interventional Imaging and Therapy 2024;21(3):179-181
Acupuncture therapy needs to cause enough somatosensory stimulation to achieve therapeutic effect.How to identify the site and depth before acupuncture,assess therapeutic effect after acupuncture and ensure the safety of treatment are the points for clinical application of acupuncture therapy,but no standard objective and quantitative access has been achieved.Under assistance of ultrasound,precise positioning before acupuncture,visualization of anatomical structures and quantification of the depth during acupuncture became feasible.The research progresses of ultrasound for assisting acupuncture therapy were reviewed in this article.
3.Single-nucleus transcriptomics reveals a gatekeeper role for FOXP1 in primate cardiac aging.
Yiyuan ZHANG ; Yandong ZHENG ; Si WANG ; Yanling FAN ; Yanxia YE ; Yaobin JING ; Zunpeng LIU ; Shanshan YANG ; Muzhao XIONG ; Kuan YANG ; Jinghao HU ; Shanshan CHE ; Qun CHU ; Moshi SONG ; Guang-Hui LIU ; Weiqi ZHANG ; Shuai MA ; Jing QU
Protein & Cell 2023;14(4):279-293
Aging poses a major risk factor for cardiovascular diseases, the leading cause of death in the aged population. However, the cell type-specific changes underlying cardiac aging are far from being clear. Here, we performed single-nucleus RNA-sequencing analysis of left ventricles from young and aged cynomolgus monkeys to define cell composition changes and transcriptomic alterations across different cell types associated with age. We found that aged cardiomyocytes underwent a dramatic loss in cell numbers and profound fluctuations in transcriptional profiles. Via transcription regulatory network analysis, we identified FOXP1, a core transcription factor in organ development, as a key downregulated factor in aged cardiomyocytes, concomitant with the dysregulation of FOXP1 target genes associated with heart function and cardiac diseases. Consistently, the deficiency of FOXP1 led to hypertrophic and senescent phenotypes in human embryonic stem cell-derived cardiomyocytes. Altogether, our findings depict the cellular and molecular landscape of ventricular aging at the single-cell resolution, and identify drivers for primate cardiac aging and potential targets for intervention against cardiac aging and associated diseases.
Aged
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Animals
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Humans
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Aging/genetics*
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Forkhead Transcription Factors/metabolism*
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Myocytes, Cardiac/metabolism*
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Primates/metabolism*
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Repressor Proteins/metabolism*
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Transcriptome
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Macaca fascicularis/metabolism*