Bisphenols in Aquatic Products from South China: Implications for Human Exposure.

In this study, 245 representative samples of aquatic products were selected from local markets in Shenzhen by stochastic sampling. The samples comprised eight species and fell into three aquatic product categories: fish, crustaceans, and bivalves. A total of eight BPs were determined by liquid chromatography coupled with mass spectrometry, namely, bisphenol A (BPA), bisphenol AF (BPAF), bisphenol AP (BPAP), bisphenol B (BPB), bisphenol S (BPS), bisphenol P (BPP), bisphenol Z (BPZ), and bisphenol F (BPF). All BPs were detected in aquatic products, except for BPAF, indicating pervasive contamination by BPs in aquatic products. BPS demonstrated the highest detection rate both before and after enzymatic hydrolysis, whereas BPAP exhibited the lowest detection rate before enzymatic hydrolysis and BPB displayed the lowest detection rate after enzymatic hydrolysis. The concentration difference before and after enzymatic hydrolysis proved to be statistically significant. Moreover, 49-96% of BPs in aquatic products were found in the combined state, underscoring the essentiality of conducting detections on aquatic product samples following enzymatic hydrolysis. While the health risks associated with ingesting BPs residues through aquatic product consumption were found to be minimal for residents at risk of exposure, the results suggest the necessity for more stringent regulations governing the consumption of aquatic products.

C/EBPα-Mediated Transcriptional Activation of PIK3C2A Regulates Autophagy, Matrix Metalloproteinase Expression, and Phenotypic of Vascular Smooth Muscle Cells in Aortic Dissection.

Purpose: To investigate the function of C/EBPα in the development of aortic dissection (AD) and the underlying mechanism. Methods: Aortic vascular smooth muscle cells (VSMCs) were isolated, cultured, and identified from AD rats. Then, C/EBPα and PIK3C2A were knockdown or overexpressed by siRNA or plasmid transfection, respectively. Rapamycin or 3-MA was utilized to stimulate and restrain autophagy of VSMCs, respectively. Western blot was used to evaluate the expression levels of C/EBPα, PIK3C2A, LC3, Beclin-1, p62, MMP-2, MMP-9, α-SMA, SM-MHC, and OPN. The pathological status of aortic ring was evaluated by stretch stress, and ChIP assay was used to analyze the binding between C/EBPα and PIK3C2A. C/EBPα shRNA was injected into tail vein to observe the effect of C/EBPα knockdown in vivo on phenotype, autophagy of aortic vascular tissue by immunohistochemical staining and Western blot. Results: The protein levels of C/EBPα, PIK3C2A, MMP-2, MMP-9, and LC3 in the aorta of AD rats were all upregulated significantly. C/EBPα and rapamycin promoted notable upregulation of the synthesized proteins (OPN), PIK3C2A, matrix metalloproteinases, LC3, and Beclin-1 in VSMCs, while suppressed contractile proteins (α-SMA and SM-MHC) and p62. The opposite results were observed in the C/EBPα-knockdown VSMCs, PIK3C2A-knockdown VSMCs, or VSMCs treated with 3-MA. C/EBPα, PIK3C2A, and LC3 were dramatically upregulated by the stimulation of 3 g and 5 g stretch stress. The downregulated contractile proteins, upregulated synthetic proteins, activated autophagy, and aggravated pathological state in 5 g stretch stress-treated aortic rings were significantly reversed by the knockdown of C/EBPα. ChIP results indicated that there was a binding site for C/EBPα in the promoter of PIK3C2A. C/EBPα also downregulated α-SMA level and upregulated OPN levels in AD rats in vivo. Conclusion: Our data indicated that during the development of AD, C/EBPα regulated the transition of VSMC phenotype and extracellular matrix remodeling by activating autophagy through regulating the transcriptional activity of PIK3C2A promoter.

Mechanical stretch aggravates aortic dissection by regulating MAPK pathway and the expression of MMP-9 and inflammation factors.

This study aimed to explore whether mechanical stretch aggravated aortic dissection through regulating MAPK pathway, MMP-9, and inflammation factors. We first established aortic dissection model rats. Mechanical stretch (3 g) was exerted on vascular ring of aortic dissection which was also treated by inhibitors of MAPK pathway (SB203580, SP600125, and U0126). HE and Masson staining showed that aortic dissection severity with 3 g tension was worse than that without tension (0 g); after the treatments of diverse inhibitors, the fracture and breakage of the elastic fibers decreased. The expression of MMP-9, TNF-α, IL-1ß) p38/p-p38, JNK1/p-JNK1, and ERK1/2/p-ERK1/2 were determined by immunohistochemical analysis, RT-PCR, and western blot. No matter whether tension was exerted or inhibitors were added, there was no change in the expression of p38, JNK1, and ERK1/2. However, compared to the 0 g group, the expression of MMP-9, TNF-α, IL-1ß, p-p38, p-JNK1, and p-ERK1/2 was significantly upregulated in the 3 g group (P < 0.05). In both 0 g and 3 g groups, the expression of MMP-9, TNF-α, IL-1ß, p-p38, p-JNK1, and p-ERK1/2 was remarkably downregulated after inhibitors treatment (P < 0.05). In conclusion, mechanical stretch aggravated aortic dissection by regulating the MAPK pathway and the consequent expression of MMP-9 and inflammation factors.

Comparison of mesenchymal stromal cells from human bone marrow and adipose tissue for the treatment of spinal cord injury.

BACKGROUND AIMS: Bone marrow and subcutaneous adipose tissue are both considered prospective sources of mesenchymal stromal cells (MSCs), which can be used in cell therapy for spinal cord injury (SCI). The present study investigated whether human adipose tissue-derived mesenchymal stromal cells (hADSCs) transplanted into a rat model of SCI would lead to similar or improved neurologic effects compared with human bone marrow-derived mesenchymal stromal cells (hBMSCs). METHODS: hADSCs and hBMSCs were isolated from five adult donors. These MSCs were characterized using flow cytometry, immunocytochemistry, real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Immediately after SCI, 2 × 10(5) hBMSCs or hADSCs were injected into the injured spinal cord. Locomotor function, cell survival and differentiation, spinal cord tissue morphology and brain-derived neurotrophic factor (BDNF) expression were compared between groups. RESULTS: hADSCs and hBMSCs showed similar surface protein expression, and hADSCs showed higher proliferative activity with higher expression of vascular endothelial cell growth factor, hepatocyte growth factor and BDNF than hBMSCs. After transplant, both hADSCs and hBMSCs migrated within the injured spinal cord without differentiating into glial or neuronal elements. Administration of hADSCs was associated with marked changes in the SCI environment, with significant increases in BDNF levels. This was simultaneously associated with increased angiogenesis, preserved axons, decreased numbers of ED1-positive macrophages and reduced lesion cavity formation. These changes were accompanied by improved functional recovery. CONCLUSIONS: The present results suggest that hADSCs would be more appropriate for transplant to treat SCI than hBMSCs.