Establishment of in vitro model of erectile dysfunction for the study of high-glucose-induced angiopathy and neuropathy

Andrology ◽  
2016 ◽  
Vol 5 (2) ◽  
pp. 327-335 ◽  
Author(s):  
G. N. Yin ◽  
S.-H. Park ◽  
K.-M. Song ◽  
A. Limanjaya ◽  
K. Ghatak ◽  
...  
2014 ◽  
Vol 445 (1) ◽  
pp. 236-243 ◽  
Author(s):  
Tomoyuki Yuasa ◽  
Kikuko Amo ◽  
Shuhei Ishikura ◽  
Hisao Nagaya ◽  
Keiji Uchiyama ◽  
...  

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 512 ◽  
Author(s):  
Samuel Bernardo-Bermejo ◽  
Elena Sánchez-López ◽  
María Castro-Puyana ◽  
Selma Benito-Martínez ◽  
Francisco Javier Lucio-Cazaña ◽  
...  

Diabetic nephropathy is characterized by the chronic loss of kidney function due to high glucose renal levels. HK-2 proximal tubular cells are good candidates to study this disease. The aim of this work was to study an in vitro model of high glucose-induced metabolic alterations in HK-2 cells to contribute to the pathogenesis of this diabetic complication. An untargeted metabolomics strategy based on CE-MS was developed to find metabolites affected under high glucose conditions. Intracellular and extracellular fluids from HK-2 cells treated with 25 mM glucose (high glucose group), with 5.5 mM glucose (normal glucose group), and with 5.5 mM glucose and 19.5 mM mannitol (osmotic control group) were analyzed. The main changes induced by high glucose were found in the extracellular medium where increased levels of four amino acids were detected. Three of them (alanine, proline, and glutamic acid) were exported from HK-2 cells to the extracellular medium. Other affected metabolites include Amadori products and cysteine, which are more likely cause and consequence, respectively, of the oxidative stress induced by high glucose in HK-2 cells. The developed CE-MS platform provides valuable insight into high glucose-induced metabolic alterations in proximal tubular cells and allows identifying discriminative molecules of diabetic nephropathy.


Biochimie ◽  
2003 ◽  
Vol 85 (7) ◽  
pp. 701-705 ◽  
Author(s):  
Debora Donnini ◽  
Elisa Del Terra ◽  
Francesco Saverio Ambesi-Impiombato ◽  
Francesco Curcio

2018 ◽  
Vol 74 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Tugba Soydas ◽  
Elif Yaprak Sarac ◽  
Suzan Cinar ◽  
Sibel Dogan ◽  
Seyhun Solakoglu ◽  
...  

Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.


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