In Vitro Biocompatibility of Surface-Modified Porous Alumina Particles for HepG2 Tumor Cells: Toward Early Diagnosis and Targeted Treatment

2015 ◽  
Vol 7 (33) ◽  
pp. 18600-18608 ◽  
Author(s):  
Elisabet Xifre-Perez ◽  
Sandra Guaita-Esteruelas ◽  
Malgorzata Baranowska ◽  
Josep Pallares ◽  
Lluis Masana ◽  
...  

2017 ◽  
Vol 32 (6) ◽  
pp. 775-787 ◽  
Author(s):  
Albert Jung ◽  
Preeti Makkar ◽  
Jhaleh Amirian ◽  
Byong-Taek Lee

The objective of the present study was to develop a novel hybrid multichannel biphasic calcium phosphate granule (MCG)-based composite system for cartilage regeneration. First, hyaluronic acid-gelatin (HG) hydrogel was coated onto MCG matrix (MCG-HG). Poly(lactic-co-glycolic acid) (PLGA) microspheres was separately prepared and modified with polydopamine subsequent to BMP-7 loading (B). The surface-modified microspheres were finally embedded into MCG-HG scaffold to develop the novel hybrid (MCG-HG-PLGA-PD-B) composite system. The newly developed MCG-HG-PLGA-PD-B composite was then subjected to scanning electron microscopy, energy dispersive X-ray spectroscopy, Fourier Transform infrared spectroscopy, porosity, compressive strength, swelling, BMP-7 release and in-vitro biocompatibility studies. Results showed that 60% of BMP-7 retained on the granular surface after 28 days. A hybrid MCG-HG-PLGA-PD-B composite scaffold exhibited higher swelling and compressive strength compared to MCG-HG or MCG. In-vitro studies showed that MCG-HG-PLGA-PD-B had improved cell viability and cell proliferation for both MC3T3-E1 pre-osteoblasts and ATDC5 pre-chondrocytes cell line with respect to MCG-HG or MCG scaffold. Our results suggest that a hybrid MCG-HG-PLGA-PD-B composite scaffold can be a promising candidate for cartilage regeneration applications.





1993 ◽  
Vol 24 (1) ◽  
pp. 148-155 ◽  
Author(s):  
Mauro Bologna ◽  
Carlo Vicentini ◽  
Giovanni Corrao ◽  
Paola Muzi ◽  
Andrea Tubaro ◽  
...  


1988 ◽  
Vol 14 (6) ◽  
pp. 474-476 ◽  
Author(s):  
Mauro Bologna ◽  
Carlo Vicentini ◽  
Claudio Festuccia ◽  
Paola Muzi ◽  
Tiziano Napolitano ◽  
...  


2010 ◽  
Vol 5 (5) ◽  
pp. 055007 ◽  
Author(s):  
Cem Bayram ◽  
Alpay Koray Mizrak ◽  
Selçuk Aktürk ◽  
Hurkan Kurşaklioğlu ◽  
Atila Iyisoy ◽  
...  


2000 ◽  
Vol 33 (4) ◽  
pp. 601-608 ◽  
Author(s):  
Shwu-Bin Lin ◽  
Li-Ching Wu ◽  
Siao-Ling Huang ◽  
Hui-Lun Hsu ◽  
Sung-Hwa Hsieh ◽  
...  


2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 



1984 ◽  
Vol 104 (4_Supplb) ◽  
pp. S55-S56 ◽  
Author(s):  
W. LUSTER ◽  
C. GROPP ◽  
H. F. KERN ◽  
K. HAVEMANN


Sign in / Sign up

Export Citation Format

Share Document