Reconstruction and Correction of the Rice Mitochondrial Reference Genome.
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Journal Article↗
Biomedical subjects
Yi Zou
Publications and source records attributed to Yi Zou.
Generation of eight-cell embryo-like cells from human pluripotent stem cells.
Mammalian embryonic development is a highly orchestrated process initiated by the fusion of the oocyte with sperm to generate the zygote. In humans, the zygote remains transcriptionally quiescent until the major wave of zygotic genome activation (ZGA) occurs around the eight-cell (8C) stage (day 3 after fertilization). These cells and the derived morula cells are totipotent: they have the capacity to form a whole individual. Our understanding of human totipotency is very limited because of ethical concerns using embryos and the scarcity of material available for research. Recently, we established a controllable transgene-free methodology to generate totipotent eight-cell embryo-like cells (8CLCs) from human pluripotent stem cells (PSCs) in vitro. These 8CLCs are produced using a novel medium, formulated by us, containing specific chemical compounds and cytokines. Here, we provide a detailed protocol for inducing, isolating and characterizing 8CLCs generated with this medium. The induction process can be done either in a stepwise manner (primed-naive-8CLC) that requires only 5 d starting from naive PSCs or directly from primed PSCs, which takes ~7 d. The resulting 8CLCs exhibit transcriptional and epigenetic features resembling those of human 8C embryo cells. On the basis of our experience, we expect that an individual with ~1 year of experience working with human PSC culture would be able to carry out this protocol. Our approach provides a valuable model for studying human early embryogenesis, particularly the molecular events surrounding ZGA.
Journal Article↗
Early immune dysregulation in Mtb/SIV co-infection resists cART treatment at the single-cell level.
Using single-cell transcriptomics of bronchoalveolar lavage cells from Mtb/SIV co-infected rhesus macaques on cART, we reveal profound immune dysregulation during early SIV co-infection of latent tuberculosis. SIV induces a sharp decline in CD4+ T cells, NK, and NKT cells, with incomplete recovery of Mtb-specific TH1 effector responses despite viral suppression. Instead, a persistent TH17-skewed environment emerges, alongside sustained myeloid inflammation driven by Type I interferon signaling and pro-inflammatory regulators such as KLF6 and NFKB1. Ligand-receptor network analyses demonstrate expanded CD4+ T cell-macrophage crosstalk and loss of immune homeostasis that cART fails to fully restore. These findings expose how SIV remodels the pulmonary immune landscape to impair protective immunity against Mtb, providing a transcriptomic framework to explain TB reactivation in HIV infection. Our work highlights the urgent need for adjunctive immunotherapies to complement cART, aiming to rebalance immune responses and improve TB control in co-infected individuals.
HIV↗
[Effects and mechanisms of ethanol extract of Salvia miltiorrhiza on liver fibrosis in mice].
To identify clinically advantageous TCMs for anti-hepatic fibrosis and to elucidate the effects and molecular mechanisms of Salvia miltiorrhiza ethanol extract in the intervention of liver fibrosis, this study screened high-frequency anti-hepatic fibrosis TCMs through a review of clinical literature. The S. miltiorrhiza active components, potential targets, and liver fibrosis-related disease targets were obtained using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP), the GeneCards database, and other databases. Gene Ontology(GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were performed on the shared targets between drugs and diseases. Molecular docking was conducted to evaluate the binding affinities between key components and core targets. In animal experiments, male Kunming mice were used to establish a liver fibrosis model induced by carbon tetrachloride(CCl_4). The mice were administered low, medium, and high doses of S. miltiorrhiza ethanol extract by gavage. The liver index, as well as serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) levels, were measured. Histopathological changes in liver tissue were observed using hematoxylin-eosin(HE) staining and Masson's trichrome staining. Western blot analysis was used to detect the protein expression levels of α-smooth muscle actin(α-SMA), Collagen Ⅰ, and heat shock protein 90 alpha family class A member 1(HSP90AA1) in liver tissue. The results showed that S. miltiorrhiza was the most frequently used TCM in clinical anti-hepatic fibrosis. A total of 65 active components and 135 potential targets were identified, and 109 common targets were obtained by intersecting these with liver fibrosis-related targets. The core targets included tumor protein p53(TP53), serine/threonine protein kinase AKT1(AKT1), Jun proto-oncogene(JUN), signal transducer and activator of transcription 3(STAT3), and HSP90AA1, which were mainly enriched in pathways related to cancer, hepatitis B, and the PI3K-AKT signaling pathway. Molecular docking indicated that the main active components of S. miltiorrhiza bound stably to the core targets, with the strongest binding affinity observed for HSP90AA1. Animal experiments demonstrated that the liver index, serum ALT and AST levels, and the expression of α-SMA, Collagen Ⅰ, and HSP90AA1 in liver tissue were significantly increased in the model group, accompanied by obvious pathological manifestations of fibrosis. Compared with the model group, different dose groups of S. miltiorrhiza ethanol extract reduced the liver index and serum ALT and AST levels to varying degrees, alleviated pathological damage and collagen deposition in liver tissue, and downregulated the protein expression of α-SMA, Collagen Ⅰ, and HSP90AA1. In conclusion, S. miltiorrhiza ethanol extract exerts a significant protective effect on CCl_4-induced liver fibrosis in mice, and its mechanisms may be related to the inhibition of HSP90AA1 expression and the regulation of liver fibrosis-related signaling pathways.
Animals↗