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Yuyan Zhu

Publications and source records attributed to Yuyan Zhu.

9 recordsLinked to original sources

Diet-dependent effects of an environmentally relevant dose of polyethylene and polyethylene terephthalate on white adipose tissue and systemic insulin resistance in mice.

As human exposure to micro- and nanoplastics (NPs) is unavoidable, it remains unclear whether dietary composition can modulate their health impacts. To address this, we investigated the metabolic effects of two common yet understudied polymers, polyethylene (PE) and polyethylene terephthalate (PET), in mice with either healthy or energy-dense diet. C57BL/6 J male mice were exposed to an environmentally relevant dose of PE or PET (100 nm, 25 mg/kg BW/day) for 29 weeks under either a normal diet (ND) or a high-fat diet (HFD). The metabolic consequence of NP exposure was highly diet-dependent. In ND-fed mice, PE and PET reduced white adipose tissue (WAT) mass, with PET inducing metabolic changes that toward a lipodystrophy-like state. Conversely, in HFD-fed mice, both polymers impaired systemic insulin sensitivity. Regardless of diet, PE and PET promoted immunoglobin G (IgG) accumulation in epididymal WAT, with PE-exposed lean mice exhibited the most robust IgG elevation, WAT fibrosis and impaired adipogenesis. These findings demonstrate that chronic, environmentally relevant PE or PET exposure disrupts metabolic health in male mice under both dietary contexts. While dietary composition dictates the specific metabolic phenotype, it does not prevent adverse outcomes. This complicates lifestyle-based mitigation strategies and underscores the urgent need for environmental source controls.

Insulin Sensitivity↗

The opioid receptor-ligand network in human cancers: pan-cancer multi-omics profiling and translational implications.

BACKGROUND: Opioid receptor-ligand signalling has been implicated in tumour biology and perioperative outcomes; however, its pan-cancer molecular landscape and clinical relevance remain incompletely defined. METHODS: We performed a pan-cancer multi-omics analysis of eight predefined opioid receptor-ligand genes across 33 tumour types from The Cancer Genome Atlas. Analyses included gene expression analysis using the linear models for microarray data (limma) package, genomic alterations, DNA methylation, regulatory network inference, pathway activity estimation using gene set variation analysis, and survival modelling. Multivariable Cox regression models were adjusted for age, sex, and tumour stage. RESULTS: Opioid receptor-ligand genes exhibited heterogeneous and generally low-to-moderate expression across tumour types. Genomic and epigenetic alterations were tumour-specific and variably associated with gene expression. Selected genes showed associations with overall survival in a tumour-dependent manner; however, these associations were attenuated after adjustment for clinical covariates and were accompanied by wide confidence intervals in some cohorts. Pathway analyses suggested associations with broader biological programmes, including epithelial-mesenchymal transition and immune-related pathways. Regulatory analyses identified candidate transcription factors and miRNAs, although these findings are exploratory. CONCLUSIONS: This pan-cancer analysis provides a systematic overview of opioid receptor-ligand gene features across human cancers. The observed associations are context-dependent and should be interpreted as hypothesis-generating. Further mechanistic and prospective studies are required to determine the clinical relevance of opioid signalling in cancer and perioperative settings.

Humans↗

Early increase in mRNA levels of pro-inflammatory cytokines and their interactions in the mouse hippocampus after transient global ischemia.

There is convincing evidence that cytokines are involved in the inflammatory response following cerebral ischemia, but the interactions among the pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6 in the early stage of ischemic reperfusion are not yet completely understood. In this study, we examined the early mRNA expressions of pro-inflammatory cytokines in the ischemic hippocampus after 30 min of bilateral common carotid artery occlusion in C57BL/6J wild-type (WT) and TNF-alpha, IL-1alpha/beta or IL-6 gene knockout (KO) mice utilizing real-time polymerase chain reaction. The mRNA expressions of the pro-inflammatory cytokines TNF-alpha, IL-6 and IL-1beta were significantly induced in ischemic WT mice compared with in the sham-operated mice. These increases peaked at 3 to 24 h for TNF-alpha, at 12 h for IL-1beta, and at 6 to 24 h for IL-6 after ischemia. The pattern of temporal expression of the cytokine mRNAs in ischemic gene KO mice, however, differed from that in WT mice. The TNF-alpha mRNA expression showed a similar temporal expression pattern in IL-6 KO mice compared to in WT mice following ischemic reperfusion, and the levels at all time points were lower than in WT mice. The IL-1beta mRNA level was very low in ischemic TNF-alpha KO mice and IL-6 KO mice in spite of a small peak observed in both at 24 h. The IL-6 mRNA level was significantly upregulated at all time points in both ischemic WT and TNF-alpha KO mice; however, the peak was delayed by 12-h in IL-1alpha/beta KO mice. In conclusion, the present study indicates that the rapid increases in cytokine levels are interdependent, interactive, and possibly modulate each other in the mouse hippocampus after transient global ischemia.

Analysis of Variance↗

Inhibition of tumor angiogenesis during cisplatin chemotherapy for bladder cancer improves treatment outcome.

OBJECTIVES: To investigate the effect of inhibiting tumor angiogenesis during cisplatinum-(II)-diamine dichloride (cisplatin) chemotherapy of bladder cancer (BC) in a rat model. METHODS: Bladder cancer was induced in 64 male rats using 0.05% N-butyl-N-(4-hydroxybutyl)-nitrosamine in their water supply for 20 weeks. The animals were then divided randomly into four groups of 16 rats each: a control BC group (group 1); a BC group treated with cisplatin (0.25 mg/kg body weight) by intraperitoneal injection twice every week (group 2); a BC group treated with the antiangiogenic factor TNP-470 (30 mg/kg body weight) by intraperitoneal injection twice every week (group 3); and a BC group treated with cisplatin plus TNP-470 (group 4, treatment regimens as described). Per group, 4 rats were killed weekly after the start of treatment, for 4 weeks. BC was confirmed using histologic characteristics, and the treatment outcomes were determined by measuring tumor microvascular density and cell proliferation and apoptosis indexes (PI and AI, respectively). RESULTS: All animals had confirmed BC. Both group 3 (TNP-470) and group 4 (cisplatin plus TNP-470) had significantly decreased microvascular density compared with group 1 (P <0.05). Although both the PI and AI were significantly different between group 4 (cisplatin plus TNP-470) and group 1 (control BC; P <0.05), neither the PI nor AI was significantly different between group 2 (cisplatin) and group 4 (cisplatin plus TNP-470; P >0.05). CONCLUSIONS: TNP-470 in conjunction with cisplatin chemotherapy resulted in a decrease in the microvascular density of BC in a rat model. However, TNP-470 did not appear to have a significant impact on the cisplatin effect against BC as measured by apoptosis and cell proliferation.

Angiogenesis Inhibitors↗

Role of protein kinase C-alpha in superficial bladder carcinoma recurrence.

OBJECTIVES: To investigate the role of protein kinase C-alpha (PKCalpha) in the recurrence of superficial bladder carcinoma. METHODS: Expression of PKCalpha was measured by Western blot analysis in 56 samples. A human RT-4 bladder cancer cell line stably expressing green fluorescent protein-PKCalpha (RT-4/PKCalpha) was established. The sensitivity of the RT-4/PKCalpha and parental cells to adriamycin (ADM) was determined by MTT assay. We also observed a change in the sensitivity of RT-4/PKCalpha to ADM under the conditions of PKCalpha upregulation and downregulation. RESULTS: PKCalpha expression and the ratio of PKCalpha expression in the membrane to that in cytosol were greater in cancerous tissues than in normal tissues (P <0.05). With an increase in tumor grade, the level of PKCalpha expression increased significantly in the membrane (P <0.01) and decreased in cytosol (P <0.01). Patients with superficial bladder carcinoma with a greater membrane/cytosol ratio of PKCalpha had a shorter recurrence-free period than did those with lower levels after standard ADM treatment at 2 years of follow-up (P <0.05). In vitro transfection of PKCalpha increased resistance of RT-4 cells to ADM (P<0.01). Activation of PKCalpha also greatly promoted resistance (P <0.001), and inhibition of PKCalpha decreased resistance (P <0.01). CONCLUSIONS: Our results have shown the correlation of PKCalpha overexpression/activation in superficial bladder carcinoma with the effect of ADM on tumor recurrence. PKCalpha may play an important role, not only in tumor differentiation, but also in intrinsic resistance to chemotherapy drugs by activation of the PKC pathway.

Aged↗

Increases in tumor necrosis factor-alpha following transient global cerebral ischemia do not contribute to neuron death in mouse hippocampus.

The actions of tumor necrosis factor-alpha (TNF-alpha) produced by resident brain cells and bone marrow-derived cells in brain following a transient global ischemia were evaluated. In wild-type mice (C57Bl/6J) following 20 min ischemia with bilateral common carotid artery occlusion (BCCAo), TNF-alpha mRNA expression levels in the hippocampus were significantly increased at 3 h and 36 h and exhibited a biphasic expression pattern. There were no hippocampal TNF-alpha mRNA expression levels at early time points in either wild-type mice bone marrow transplanted (BMT)-chimeric-TNF-alpha gene-deficient (T/W) or TNF-alpha gene-deficient mice BMT-TNF-alpha gene-deficient mice (T/T), although TNF-alpha mRNA levels were detectable in T/W BMT mice at 36 h. Histopathological findings showed no intergroup differences between wild-type and TNF-alpha gene-deficient mice at 4 and 7 days after transient ischemia. In addition, nuclear factor-kappaB (NF-kappaB) was activated within 12 h after global cerebral ischemia, but electrophoretic mobility shift assays (EMSA) showed no intergroup differences between wild type and TNF-alpha gene-deficient mice. In summary, early hippocampal TNF-alpha mRNA expression may not be related to bone marrow-derived cells, and secondary TNF-alpha expression as early as 36 h after ischemia probably resulted mainly from endogenous brain cells and possibly a few bone marrow-derived cells. Although we cannot exclude the possibility of the TNF-alpha contribution to the physiologic changes of hippocampus after transient global ischemia, these results indicate that TNF-alpha does not influence the morphological changes of the hippocampal neurons under our study condition.

Animals↗

Expression of lung resistance-related protein in transitional cell carcinoma of bladder.

OBJECTIVES: To determine the role of lung resistance-related protein (LRP) in intrinsic multidrug-resistance (MDR) of bladder cancer. METHODS: The study group consisted of 66 patients with newly diagnosed primary bladder cancer. No patient had been treated preoperatively with either radiotherapy or chemotherapy. Reverse transcriptase-polymerase chain reaction was performed to measure LRP, multidrug resistance-associated protein 1 (MDR1), and MRP1 mRNA expression. The expression of LRP, p53 proteins, and p63 proteins was examined by immunohistochemistry. We analyzed the correlation of LRP with the above indexes and the clinical pathologic parameters. RESULTS: The expression rate of LRP mRNA (63.6%) was the greatest among the three MDR markers in primary bladder cancer without exposure to chemotherapy. The LRP mRNA level was significantly greater in normal bladder tissue than in transitional cell carcinoma bladder tissue (P <0.01) and in superficial cancer than in invasive cancer (P = 0.013). LRP mRNA expression showed no association with either MDR1 or MRP1, but close correlation with the LRP level (P = 0.001). LRP was associated with low-grade (P <0.01) and low-stage (P <0.05) cancer but had no association with tumor suppressor p53 or p63. CONCLUSIONS: The grade and stage-related expression pattern of LRP indicates that it may be a predictive index for intrinsic MDR in early bladder cancer. Anticancer drugs out of the MDR spectrum of LRP may be more effective for patients with early bladder cancer.

Biomarkers, Tumor↗