Advanced glycation endproducts produced by in vitro glycation of type I collagen modulate the functional and secretory behavior of dorsal root ganglion cells cultivated in two-dimensional system
| Autor: | Vanessa Zambelli, Morena Brazil Sant'Anna, Maira Estanislau Soares De Almeida, Isabella Araujo Franca, Sandra Coccuzzo Sampaio, Aline Carolina Giardini, Yara Cury, Louise F. Kimura, Michelle Cristiane Bufalo |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Glycation End Products
Advanced Male 0301 basic medicine MAPK/ERK pathway Glycosylation Cell Survival MAP Kinase Signaling System Receptor for Advanced Glycation End Products Cell Culture Techniques Biology Collagen Type I RAGE (receptor) Extracellular matrix Mice 03 medical and health sciences 0302 clinical medicine Dorsal root ganglion In vivo Glycation Ganglia Spinal medicine Animals Phosphorylation Rats Wistar Cells Cultured Nitrites Tumor Necrosis Factor-alpha Cell Biology Actins Cell biology Enzyme Activation Actin Cytoskeleton 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Neuron Type I collagen |
| Zdroj: | Experimental Cell Research. 382:111475 |
| ISSN: | 0014-4827 |
| DOI: | 10.1016/j.yexcr.2019.06.020 |
| Popis: | Advanced glycation end-products (AGEs) are proteins/lipids that are glycated upon sugar exposure and are often increased during inflammatory diseases such as osteoarthritis and neurodegenerative disorders. Here, we developed an extracellular matrix (ECM) using glycated type I collagen (ECM-GC), which produced similar levels of AGEs to those detected in the sera of arthritic mice. In order to determine whether AGEs were sufficient to stimulate sensory neurons, dorsal root ganglia (DRGs) cells were cultured on ECM-GC or ECM-NC-coated plates. ECM-GC or ECM-NC were favorable for DRG cells expansion. However, ECM-GC cultivated neurons displayed thinner F-actin filaments, rounded morphology, and reduced neuron interconnection compared to ECM-NC. In addition, ECM-GC did not affect RAGE expression levels in the neurons, although induced rapid p38, MAPK and ERK activation. Finally, ECM-GC stimulated the secretion of nitrite and TNF-α by DRG cells. Taken together, our in vitro glycated ECM model suitably mimics the in vivo microenvironment of inflammatory disorders and provides new insights into the role of ECM impairment as a nociceptive stimulus. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect