The cellular distribution of silica nanoparticles (NPs) in the liver is not well understood. Targeting specific cells is one of the most important issues in NP-based drug delivery to improve delivery efficacy. In this context, the present study analyzed the relative cellular distribution pattern of silica NPs in the liver, and the effect of surface energy modification on NPs. Hydrophobic NP surface modification enhanced NP delivery to the liver and liver sinusoid fFendothelial cells (LSECs). Conversely, hydrophilic NP surface modification was commensurate with targeting hepatic stellate cells (HSCs) rather than other cell types. There was no notable difference in NP delivery to Kupffer cells or hepatocytes, regardless of hydrophilic or hydrophobic NP surface modification, suggesting that both the targeting of hepatocytes and evasion of phagocytosis by Kupffer cells are not associated with surface energy modification of silica NPs. This study provides useful information to target specific cell types using silica NPs, as well as to understand the relationship between NP surface energy and the NP distribution pattern in the liver, thereby helping to establish strategies for cell targeting using various NPs.
Background/Aim: The pathological role of vascular endothelial growth factor receptor 2 (VEGFR-2) in chronic liver injury and liver regeneration is not fully understood. This study analysed the role of VEGFR-2 in liver fibrosis and its regeneration process. Materials and Methods: We administered intraperitoneally 50 mg/kg to 300 mg/kg thioacetamide (TAA) to 9-week-old male mice for 17 weeks. We measured levels of VEGFR-2 protein and identified the location of cells that specifically express VEGFR-2. Results: VEGFR-2 is rarely expressed in normal hepatocytes. However, high VEGFR-2 expression in liver sinusoidal endothelial cells was noted in the TAA group. Conversely, the group that experienced regeneration from liver fibrosis showed significantly higher VEGFR-2 expression in the nucleus of hepatocytes compared to the other groups. Conclusion: VEGFR-2 plays a pivotal role in the nucleus of hepatocytes during liver regeneration and VEGFR-2 may be closely related to cell division. Therefore, VEGFR-2 may be a new therapeutic target for liver regeneration.Liver fibrosis is marked by the formation of an abnormally large amount of scar tissue in the liver (1). Liver fibrosis represents the final common route of chronic liver disease, which eventually leads to cirrhosis (2). Chronic liver disease and cirrhosis result in approximately 35,000 deaths yearly in the United States and cirrhosis is the ninth leading cause of death (3). Therefore, it is very important that liver fibrosis does not progress to cirrhosis, an irreversible stage.Angiogenesis, which is the process of new blood vessel growth from existing vessels, is essential for the physiological functioning of tissues (4). Hepatic angiogenesis is closely associated with the progression of fibrosis in chronic liver diseases (5). According to a recent study, hepatic angiogenesis occurs in chronic liver disease, and is characterized by progressive fibrosis (6). Angiogenesis is a dynamic process regulated by the balance between pro-angiogenic and antiangiogenic factors. Vascular endothelial growth factor (VEGF) is one of the most important pro-angiogenic factors (4).Hepatocytes play a key role in angiogenesis, and have a close anatomical relationship with endothelial cells that secrete VEGF (7). VEGF regulates blood and lymphatic vessel development and maintains homeostasis (8). VEGF is primarily produced by endothelial cells in response to hypoxia and by stimulation of growth factors such as transforming growth factor, interleukins or platelet derived growth factor (9, 10). The biological function of VEGF is mediated upon binding to type III receptor tyrosine kinase (RTK), VEGF receptor 1 (VEGFR-1, Flt-1), VEGFR-2 (KDR/Flk-1), and VEGFR-3 (Flt-4) (11,12). VEGF stimulates angiogenesis by 1473 This article is freely accessible online.
A black bear of 29-year-old (Ursus americanus) died unexpectedly in captivity without any gross lesions or clinical signs. We identified a firm, lobulated, yellowish tan, and well-circumscribed mass embedded inside the testicular tissue at the time of necropsy. The tumor sections exhibited soft necrotic and hemorrhagic areas beneath its capsule. Histologically, the tumor comprised Sertoli cells arranged in tubules and solid sheets supported by prominent fibrous connective tissues. The Sertoli cells were positive for vimentin and ER-β expression, whereas it showed negative staining for inhibin-α, cytokeratin 19, and S-100. To the best of our knowledge, this is the rare case report of testicular Sertoli cell tumor in black bear.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.