scholarly journals Chitosan nanoparticles as a promising candidate for liver injury induced by 2-nitropropane: Implications of P53, iNOS, VEGF, PCNA, and CD68 pathways

2021 ◽  
Vol 104 (2) ◽  
pp. 003685042110118
Author(s):  
Sameerah Shaheen ◽  
Maha M Arafah ◽  
Aliah R Alshanwani ◽  
Laila Mohammed Fadda ◽  
Ahlam M Alhusaini ◽  
...  
Keyword(s):  
Chitosan Nanoparticles ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Sod Activity ◽  
Tnf Α ◽  
Current Article ◽  
Hematoxylin And Eosin ◽  
Cluster Of Differentiation ◽  
Endothelial Growth Factor ◽  
Proliferating Cell

The current article was designed to assess the role of chitosan nanoparticles (CNPs) in the management of hepatic injury induced by the hepatocarcinogen 2-nitropropane (2-NP). Rats were divided into three groups. The first group served as a control, the second group was injected with 2-NP, while the third group was treated with CNPs 1 h before 2-NP injection every other day for 4 weeks. The 2-NP injection upregulated serum AST and ALT activities, as well as hepatic TNF- α, IL-6, and MDA levels and the expression of vascular endothelial growth factor (VEGF) and caspase-3, whereas GSH contents and SOD activity were decreased. Immunohistochemistry investigations revealed that the hepatic protein expression of collagen I, inducible nitric oxide synthetase, proliferating cell nuclear antigen, cluster of differentiation, and p53 were upregulated. hematoxylin and eosin (H&E) and Masson’s trichrome stains supported the previous parameters, and CNPs ameliorated most of the previous biochemical parameters. CNPs achieved promising results in the limitation of 2-NP hepatotoxicity.

scholarly journals Activated Microvessels Express Vascular Endothelial Growth Factor and Integrin αvβ3 During Focal Cerebral Ischemia

1999 ◽  
Vol 19 (9) ◽  
pp. 1038-1050 ◽  
Author(s):  
Takeo Abumiya ◽  
Jacinta Lucero ◽  
Ji Hoe Heo ◽  
Masafumi Tagaya ◽  
James A. Koziol ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Proliferating Cell Nuclear Antigen ◽  
Focal Cerebral Ischemia ◽  
Integrin Αvβ3 ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Primate Model ◽  
Endothelial Growth Factor ◽  
Proliferating Cell

Both vascular endothelial growth factor (VEGF) and integrin αvβ3 play roles in angiogenesis. In noncerebral vascular systems, VEGF can induce endothelial integrin αvβ3 expression. However, it is unknown whether VEGF, like integrin αvβ3, appears in the initial response of microvessels to focal brain ischemia. Their coordinate expression in microvessels of the basal ganglia after middle cerebral artery occlusion (MCAO) in the nonhuman primate model was examined quantitatively. Cells incorporating deoxyuridine triphosphate (dUTP+) by the polymerase I reaction at 1 hour (n = 3), 2 hours (n = 3), and 7 days (n = 4) after MCAO defined the ischemic core (Ic) and peripheral regions. Both VEGF and integrin αvβ3 were expressed by activated noncapillary (7.5- to 30.0-μm diameter) microvessels in the Ic region at 1 and 2 hours after MCAO. At 7 days after MCAO, the number of VEGF+, integrin αvβ3+, or proliferating cell nuclear antigen-positive microvessels had decreased within the Ic region. The expressions of VEGF, integrin αvβ3, and proliferating cell nuclear antigen were highly correlated on the same microvessels using hierarchical log-linear statistical models. Also, VEGF and subunit αv messenger ribonucleic acids were coexpressed on selected microvessels. Here, noncapillary microvessels are activated specifically early during a focal cerebral ischemic insult and rapidly express VEGF and integrin αvβ3 together.

scholarly journals Establishment of a Model of Microencapsulated SGC7901 Human Gastric Carcinoma Cells Cocultured with Tumor-Associated Macrophages

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Jin-Ming Zhu ◽  
Xiu-Lian Quan ◽  
Shi-Chao Han ◽  
Xue-Jun Fan ◽  
He-Ming Li ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Tumor Associated Macrophages ◽  
Successful Establishment ◽  
Endothelial Growth Factor ◽  
Proliferating Cell ◽  
Metalloproteinase 9 ◽  
Human Gastric Carcinoma Cells

The important factors of poor survival of gastric cancer (GC) are relapse and metastasis. For further elucidation of the mechanism, a culture system mimicking the microenvironment of the tumor in humans was needed. We established a model of microencapsulated SGC7901 human GC cells and evaluated the effects of coculturing spheres with tumor-associated macrophages (TAMs). SGC7901 cells were encapsulated in alginate-polylysine-sodium alginate (APA) microcapsules using an electrostatic droplet generator. MTT assays showed that the numbers of microencapsulated cells were the highest after culturing for 14 days. Metabolic curves showed consumption of glucose and production of lactic acid by day 20. Immunocytochemistry confirmed that Proliferating Cell Nuclear Antigen (PCNA) and Vascular Endothelial Growth Factor (VEGF) were expressed in microencapsulated SGC7901 cells on days 7 and 14. The expression of PCNA was observed outside spheroids; however, VEGF was found in the entire spheroids. PCNA and VEGF were increased after being cocultured with TAMs. Matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) expressions were detected in the supernatant of microencapsulated cells cocultured with TAMs but not in microencapsulated cells. Our study confirms the successful establishment of the microencapsulated GC cells. TAMs can promote PCNA, VEGF, MMP-2, and MMP-9 expressions of the GC cells.

Nitric oxide, VEGF, and VEGFR-2: interactions in activity-induced angiogenesis in rat skeletal muscle

2005 ◽  
Vol 289 (1) ◽  
pp. H336-H343 ◽  
Author(s):  
Malgorzata Milkiewicz ◽  
Olga Hudlicka ◽  
Margaret D. Brown ◽  
Haley Silgram
Keyword(s):  
Nitric Oxide ◽  
Nuclear Antigen ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Capillary Growth ◽  
Capillary Bed ◽  
Endothelial Growth Factor ◽  
Proliferating Cell ◽  
Increased Activity ◽  
Increased Blood Flow

Vascular endothelial growth factor (VEGF) is considered to be important in promotion of capillary growth in skeletal muscles exposed to increased activity. We studied its interactions with nitric oxide (NO) by examining the expression of endothelial NO synthase (NOS), VEGF, and VEGF receptor-2 (VEGFR-2) proteins in relation to capillary growth in rat extensor digitorum longus muscles electrically stimulated for 2, 4, or 7 days with and without NOS inhibition by Nω-nitro-l-arginine (l-NNA, 3 mg/day). Stimulation increased all proteins from 2 days onward, concomitantly with capillary proliferation (labeling for proliferating cell nuclear antigen). Capillary-to-fiber ratio was elevated by 25% after 7 days. Concurrent oral administration of l-NNA did not affect the increase in endothelial NOS but depressed its activity, as shown by increased blood pressure and decreased arteriolar diameters in 2-day-stimulated muscles. NOS inhibition eliminated the increased expression of VEGFR-2 and VEGF proteins in muscles stimulated for 2 and 4 days but not for 7 days. However, it depressed capillary proliferation and the increase in C/F at all time points. We conclude that, in stimulated muscles, NO, generated by activation of neuronal NOS by muscle activity or endothelial NOS by increased blood flow and capillary shear stress, may increase capillary proliferation in the early stages of stimulation through upregulation of VEGFR-2 and VEGF. With longer stimulation, capillary growth appears to require NO, and high levels of VEGF and VEGFR-2 may be contributing to maintenance of the increased capillary bed.

scholarly journals Autocrine/Paracrine Action of Pituitary Vasoactive Intestinal Peptide on Lactotroph Hyperplasia Induced by Estrogen

Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4403-4409 ◽  
Author(s):  
Oscar Gómez ◽  
José Antonio Balsa
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Receptor Antagonist ◽  
Proliferating Cell Nuclear Antigen ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Proliferating Cell ◽  
Tgf Β1 ◽  
Vip Receptor

Vasoactive intestinal polypeptide (VIP) content is increased in the hyperplastic pituitaries of estrogen (E)-treated rats, thus suggesting that this neuropeptide could mediate the E effect on lactotrophs. E also decreases pituitary TGF-β1 content, an autocrine/paracrine inhibitor of lactotroph proliferation, and induces pituitary angiogenesis. To elucidate the role of VIP in this context, lactotroph hyperplasia was induced in female Fisher 344 rats by implanting sc pellets of diethylstilbestrol (DES). Twenty-five days later, the rats were treated with three different increasing doses of a VIP receptor antagonist or the vehicle for 5 d. DES treatment resulted in a marked increase of serum prolactin (PRL), pituitary PRL content, PRL mRNA expression, pituitary weight, and pituitary proliferating cell nuclear antigen. DES treatment also increased pituitary VIP content and VIP mRNA levels, but not in the hypothalamus and cerebral cortex. Simultaneously, DES treatment decreased the pituitary TGF-β1 content and increased the pituitary content of vascular endothelial growth factor. VIP receptor antagonist partially reverted the effect of DES on serum PRL and pituitary PRL, proliferating cell nuclear antigen, TGF-β1, and vascular endothelial growth factor contents, as well as on pituitary weight, in a dose-dependent relation. These data suggest that pituitary VIP mediates the effect of E on lactotroph hyperplasia, pituitary TGF-β1, and angiogenesis.

Hypoxia-inducible Factor and Vascular Endothelial Growth Factor Are Expressed More Frequently in Embolized than in Nonembolized Cerebral Arteriovenous Malformations

Neurosurgery ◽  
2004 ◽  
Vol 55 (3) ◽  
pp. 663-670 ◽  
Author(s):  
Ulrich Sure ◽  
Elmar Battenberg ◽  
Astrid Dempfle ◽  
Wuttipong Tirakotai ◽  
Siegfried Bien ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Proliferating Cell Nuclear Antigen ◽  
Hypoxia Inducible Factor ◽  
Nuclear Antigen ◽  
Vascular Endothelial ◽  
Cerebral Arteriovenous Malformations ◽  
Hypoxia Inducible Factor 1Α ◽  
Endothelial Growth Factor ◽  
Proliferating Cell

Abstract OBJECTIVE: In previous studies, we documented a marked neoangiogenesis and endothelial proliferation in cerebral arteriovenous malformations (AVMs) that were embolized before surgery compared with those that were not embolized. We hypothesized that embolization caused a local hypoxia that promotes neoangiogenesis as a possible pathomechanism. To support this hypothesis, we now examined the angiogenesis-related proteins in a larger cohort of patients. In addition, we investigated hypoxia-inducible factor-1α as a possible protein operative during neoangiogenesis of cerebral AVMs. METHODS: Paraffin-embedded specimens of 56 AVMs obtained from surgical resection and 14 brain tissue controls were immunohistochemically stained with antibodies to proliferating cell nuclear antigen, MIB-1, vascular endothelial growth factor, Flk1, and hypoxia-inducible factor-1α by standard protocols. RESULTS: In AVMs treated with embolization before surgery (n = 35, 63%), the expression of hypoxia-inducible factor-1α (P = 0.0101) and vascular endothelial growth factor (P = 0.0007) was significantly higher (Fisher's exact test) than in patients who did not have previous endovascular treatment. Differences in the expression of Flk-1 (P = 0.0798) and proliferating cell nuclear antigen (P = 0.0423) were in the same direction but were not significant when corrected for multiple testing. CONCLUSION: Our results provide circumstantial evidence that a partial occlusion of cerebral AVMs might induce local hypoxia-related neoangiogenesis. To support these data, future animal studies should be performed.

Sign in / Sign up

Export Citation Format

Share Document