Myricetin inhibits advanced glycation end product (AGE)-induced migration of retinal pericytes through phosphorylation of ERK1/2, FAK-1, and paxillin in vitro and in vivo

“…Specifically, AGEs mediate PPARg via ERK phosphorylation [54], and regulate the migration of retinal pericytes through ERK phosphorylation during the development of diabetic retinopathy [55]. It has been demonstrated that MEK/ERK promotes cardiac hypertrophy in transgenic mice [56], which is a characteristic of diabetic cardiomyopathy [57,58].…”

Section: Discussionmentioning

confidence: 98%

Suppression of antioxidant Nrf-2 and downstream pathway in H9c2 cells by advanced glycation end products (AGEs) via ERK phosphorylation

Chang

Lin

et al. 2015

Biochimie

View full text Add to dashboard Cite

“…Pericyte migration is a key cellular feature of a wide variety of physiologic processes (67). AGE-induced pericyte migration is likely mediated through the RAGE-Src-ERK1/2-FAK-1paxillin signaling pathway (68). Our own group has shown that pericyte loss can also be caused by increased angiopoietin-2 expression (37), induced by MG modification of mSin3A (38).…”

Section: Discussionmentioning

confidence: 99%

Methylglyoxal induces retinopathy‐type lesions in the absence of hyperglycemia: studies in a rat model

et al. 2018

View full text Add to dashboard Cite

The aim of this study was to evaluate whether damage to the neurovascular unit in diabetes depends on reactive metabolites such as methylglyoxal (MG), and to assess its impact on retinal gene expression. Male Wistar rats were supplied with MG (50 mM) by drinking water and compared with age‐matched streptozotocin‐diabetic animals and untreated controls. Retinal damage was evaluated for the accumulation of MG‐derived advanced glycation end products, changes in hexosamine and PKC pathway activation, microglial activation, vascular alterations (pericyte loss and vasoregression), neuroretinal function assessed by electroretinogram, and neuro‐degeneration. Retinal gene regulation was studied by microarray analysis, and transcription factor involvement was identified by upstream regulator analysis. Systemic application of MG by drinking water increased retinal MG to levels comparable with diabetic animals. Elevated retinal MG resulted in MG‐derived hydroimidazolone modifications in the ganglion cell layer, inner nuclear layer, and outer nuclear layer, a moderate activation of the hexosamine pathway, a pan‐retinal activation of microglia, loss of pericytes, increased formation of acellular capillaries, decreased function of bipolar cells, and increased expression of the crystallin gene family. MG mimics important aspects of diabetic retinopathy and plays a pathogenic role in microglial activation, vascular damage, and neuroretinal dysfunction. In response to MG, the retina induces expression of neuroprotective crystalline.—Schlotterer, A., Kolibabka, M., Lin, J., Acunman, K., Dietrich, N., Sticht, C., Fleming, T., Nawroth, P., Hammes, H.‐P. Methylglyoxal induces retinopathy‐type lesions in the absence of hyperglycemia: studies in a rat model. FASEB J. 33, 4141–4153 (2019). http://www.fasebj.org

show abstract

Myricetin inhibits advanced glycation end product (AGE)-induced migration of retinal pericytes through phosphorylation of ERK1/2, FAK-1, and paxillin in vitro and in vivo

Cited by 31 publications

References 41 publications

The common dietary flavonoid myricetin attenuates liver fibrosis in carbon tetrachloride treated mice

The common dietary flavonoid myricetin attenuates liver fibrosis in carbon tetrachloride treated mice

Suppression of antioxidant Nrf-2 and downstream pathway in H9c2 cells by advanced glycation end products (AGEs) via ERK phosphorylation

Methylglyoxal induces retinopathy‐type lesions in the absence of hyperglycemia: studies in a rat model

Contact Info

Product

Resources

About