Search Our Scientific Publications & Authors

Publications
find publications by category +
Translate page:

RAGE silencing deters CML-AGE induced inflammation and TLR4 expression in endothelial cells.

Authors:
Ravi Ramya Karunakaran Coral Subramaniam Rajesh Bharathidevi

Exp Eye Res 2021 Feb 25;206:108519. Epub 2021 Feb 25.

R.S. Mehta Jain Department of Biochemistry and Cell Biology, KBIRVO, Vision Research Foundation, Sankara Nethralaya, Chennai, 600006, India. Electronic address:

The N-(carboxymethyl)lysine (CML), the predominant advanced glycation end products (AGEs) in diabetes and its RAGE induced cytokine release has been well explored. But the CML mediated multiple AGEs receptor expression is still not understood and the role played by RAGE silencing in modulating CML generated pro-inflammatory cytokines in micro and macrovascular endothelial cells is yet to be studied. HUVEC and HREC cells were exposed with CML for 24 h. RAGE, AGER1, AGER2, Gal-3, TLR4, TLR2, CD36, FEEL-1, FEEL-2, and chemokine HMGB1 were quantified by either qPCR/western blotting. The receptor's expression was also determined in control vs diabetic retina. Expression of pro-inflammatory genes, ROS, and mitochondrial membrane potential change were assessed using ELISA, DCFDA, and JC-1 method respectively. RAGE expression was silenced either by Si-RAGE or neutralising antibody with anti-RAGE and expression of other AGE receptors, adaptors, and signalling pathway were studied compared with Si-Control. CML activated RAGE, TLR4, HMGB1(p < 0.001) and Gal-3 (p < 0.05) expression in both micro and macro vascular cells. Cadaveric diabetic retinal tissues also showed increased expression of RAGE, TLR4 and HMGB1 (p < 0.05). RAGE silencing significantly reduced TLR4, HMGB1 (p < 0.05) expression and inhibited the phosphorylation of NFκB and ERK1/2 in both these cells. The TLR4 adaptors MyD88 and TIRAP (p < 0.05) showed down regulation on RAGE silencing. This study shows CML induces AGE receptors expression as observed in diabetic retina and RAGE silencing down regulated TLR4 signalling and cytokine release by partly modulating TLR4 adaptors which needs further validation. From this study we speculate targeting the TLR4 adaptors like MyD88 and TIRAP can be a potential therapeutic target for reducing diabetic induced vascular complications.

Download full-text PDF

 Source
http://dx.doi.org/10.1016/j.exer.2021.108519DOI Listing
February 2021

Publication Analysis

Top Keywords

rage silencing
8
endothelial cells
8
expression
6
rage
6
cml
5
hmgb1 quantified
4
chemokine hmgb1
4
feel-2 chemokine
4
tlr2 cd36
4
cd36 feel-1
4
feel-1 feel-2
4
qpcr/western blotting
4
control diabetic
4
diabetic retina
4
retina expression
4
determined control
4
expression determined
4
blotting receptor's
4
receptor's expression
4
quantified qpcr/western
4

Keyword Occurance

Similar Publications

Loss of Basal Forebrain Cholinergic Neurons Following Adolescent Binge Ethanol Exposure: Recovery With the Cholinesterase Inhibitor Galantamine.

Authors:
Fulton T Crews Rachael Fisher Chloe Deason Ryan P Vetreno

Front Behav Neurosci 2021 26;15:652494. Epub 2021 Feb 26.

Bowles Center for Alcohol Studies, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

Binge drinking and alcohol abuse are common during adolescence and cause both cognitive deficits and lasting cholinergic pathology in the adult basal forebrain. Acetylcholine is anti-inflammatory and studies using the preclinical adolescent intermittent ethanol (AIE; 5.0 g/kg, i. Read More

View Article and Full-Text PDF
February 2021
Similar Publications

RAGE silencing deters CML-AGE induced inflammation and TLR4 expression in endothelial cells.

Authors:
Ravi Ramya Karunakaran Coral Subramaniam Rajesh Bharathidevi

Exp Eye Res 2021 Feb 25;206:108519. Epub 2021 Feb 25.

R.S. Mehta Jain Department of Biochemistry and Cell Biology, KBIRVO, Vision Research Foundation, Sankara Nethralaya, Chennai, 600006, India. Electronic address:

The N-(carboxymethyl)lysine (CML), the predominant advanced glycation end products (AGEs) in diabetes and its RAGE induced cytokine release has been well explored. But the CML mediated multiple AGEs receptor expression is still not understood and the role played by RAGE silencing in modulating CML generated pro-inflammatory cytokines in micro and macrovascular endothelial cells is yet to be studied. HUVEC and HREC cells were exposed with CML for 24 h. Read More

View Article and Full-Text PDF
February 2021
Similar Publications

LncRNA SNHG12 downregulates RAGE to attenuate hypoxia-reoxygenation-induced apoptosis in H9c2 cells.

Authors:
Ping Lu Shihui Xiao Shaoze Chen Youlin Fu Peng Zhang Yaner Yao Feng Chen

Biosci Biotechnol Biochem 2021 Mar;85(4):866-873

The Ganzhou Hospital Affiliated to Nanchang University (The Ganzhou People's Hospital), Ganzhou, China.

Ischemia-reperfusion (I/R) injury causes cardiac dysfunction through several mechanisms including the irregular expression of some long noncoding RNA. However, the role of SNHG12 in myocardial I/R injury remains unclear. Here, we found the increase of the SNHG12 level in hypoxia-reoxygenation (H/R)-injured-H9c2 cells. Read More

View Article and Full-Text PDF
March 2021
Similar Publications

Activation of the S100A7/RAGE Pathway by IGF-1 Contributes to Angiogenesis in Breast Cancer.

Authors:
Maria Grazia Muoio Marianna Talia Rosamaria Lappano Andrew H Sims Veronica Vella Francesca Cirillo Livia Manzella Marika Giuliano Marcello Maggiolini Antonino Belfiore Ernestina Marianna De Francesco

Cancers (Basel) 2021 Feb 4;13(4). Epub 2021 Feb 4.

Endocrinology, Department of Clinical and Experimental Medicine, University of Catania, Garibaldi-Nesima Hospital, 95122 Catania, Italy.

Background: Breast cancer (BC) mortality is increased among obese and diabetic patients. Both obesity and diabetes are associated with dysregulation of both the IGF-1R and the RAGE (Receptor for Advanced Glycation End Products) pathways, which contribute to complications of these disorders. The alarmin S100A7, signaling through the receptor RAGE, prompts angiogenesis, inflammation, and BC progression. Read More

View Article and Full-Text PDF
February 2021
Similar Publications

CML/RAGE Signal Bridges a Common Pathogenesis Between Atherosclerosis and Non-alcoholic Fatty Liver.

Authors:
Qiwen Pang Zhen Sun Chen Shao Honghua Cai Zhengyang Bao Lin Wang Lihua Li Lele Jing Lili Zhang Zhongqun Wang

Front Med (Lausanne) 2020 6;7:583943. Epub 2020 Nov 6.

Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.

Non-alcoholic fatty liver disease (NAFLD) has become a common chronic disease in the world. NAFLD is not only a simple intrahepatic lesion, but also affects the occurrence of a variety of extrahepatic complications. In particular, cardiovascular complications are particularly serious, which is the main cause of death in patients with NAFLD. Read More

View Article and Full-Text PDF
November 2020
Similar Publications