Glycoxydation promotes vascular damage Via MAPK‐ERK/JNK pathways

Nigris, Filomena de; Rienzo, Monica; Sessa, Marcella; Infante, Teresa; Cesario, Elena; Ignarro, Louis J.; Al‐Omran, Mohammed; Giordano, Antonio; Palinski, Wulf; Napoli, Claudio

doi:10.1002/jcp.24070

Cited by 6 publications

(6 citation statements)

References 59 publications

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“…or more). We observed that very low levels of p-p38 and p-JNK were detected in vascular cells, this is consistent with the previous reports [33][34][35][36]. Compared with adult control, the expression levels of p-p38 and p-JNK seem to be higher in ageing groups.…”

Section: Discussionsupporting

confidence: 92%

Valsartan ameliorates ageing‐induced aorta degeneration via angiotensin II type 1 receptor‐mediated ERK activity

Huang

Zhang

et al. 2014

J Cellular Molecular Medi

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Angiotensin II (Ang II) plays important roles in ageing-related disorders through its type 1 receptor (AT1R). However, the role and underlying mechanisms of AT1R in ageing-related vascular degeneration are not well understood. In this study, 40 ageing rats were randomly divided into two groups: ageing group which received no treatment (ageing control), and valsartan group which took valsartan (selective AT1R blocker) daily for 6 months. 20 young rats were used as adult control. The aorta structure were analysed by histological staining and electron microscopy. Bcl-2/Bax expression in aorta was analysed by immunohistochemical staining, RT-PCR and Western blotting. The expressions of AT1R, AT2R and mitogen-activated protein kinases (MAPKs) were detected. Significant structural degeneration of aorta in the ageing rats was observed, and the degeneration was remarkably ameliorated by long-term administration of valsartan. With ageing, the expression of AT1R was elevated, the ratio of Bcl-2/Bax was decreased and meanwhile, an important subgroup of MAPKs, extracellular signal-regulated kinase (ERK) activity was elevated. However, these changes in ageing rats could be reversed to some extent by valsartan. In vitro experiments observed consistent results as in vivo study. Furthermore, ERK inhibitor could also acquire partial effects as valsartan without affecting AT1R expression. The results indicated that AT1R involved in the ageing-related degeneration of aorta and AT1R-mediated ERK activity was an important mechanism underlying the process.

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Section: Discussionsupporting

confidence: 92%

Valsartan ameliorates ageing‐induced aorta degeneration via angiotensin II type 1 receptor‐mediated ERK activity

Huang

Zhang

et al. 2014

J Cellular Molecular Medi

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“…The MAPK signaling pathway plays an important role in vascular damage. 18 Therefore, we examined the effect of H. parasuis on activation of the MAPK signaling pathway in PAVECs. The PAVECs were infected with H. parasuis , and phosphorylation of MAPK was measured using phospho-specific Abs.…”

Section: Resultsmentioning

confidence: 99%

Baicalin modulates apoptosis via RAGE, MAPK, and AP-1 in vascular endothelial cells during Haemophilus parasuis invasion

Zhao

Xiong

et al. 2019

Innate Immun

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Glässer’s disease, caused by Haemophilus parasuis, is a chronic disease related to an inflammatory immune response. Baicalin exerts important biological functions. In this study, we explored the protective efficacy of treatment with baicalin and the potential mechanism of activation of the MAPK signaling pathway in porcine aortic vascular endothelial cells (PAVECs) induced by H. parasuis. H. parasuis stimulated expression of receptor for advanced glycation end products, induced a significant increase in the level of protein kinase-α and protein kinase-δ phosphorylation, and significantly up-regulated ERK, c-Jun N-terminal kinase, and p38 phosphorylation in PAVECs. H. parasuis also up-regulated the levels of apoptotic genes ( Bax, C-myc, and Fasl) and the expression levels of c-Jun and c-Fos, and induced S-phase arrest in PAVECs. However, treatment with baicalin inhibited expression of RAGE, suppressed H. parasuis-induced protein kinase-α and protein kinase-δ phosphorylation, reduced ERK, c-Jun N-terminal kinase, and p38 phosphorylation, down-regulated apoptotic genes ( Bax, C-myc, and Fasl), attenuated phospho-c-Jun production from the extracellular to the nuclei, and reversed S-phase arrest in PAVECs. In conclusion, baicalin treatment inhibited the MAPK signaling pathway, thereby achieving its anti-inflammatory responses, which provides a new strategy to control H. parasuis infection.

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“…MAPK1 is a component of MAP kinase family which is involved in a wide variety of cellular processes such as proliferation, differentiation, and transcription regulation and development. Many researchers have determined the MAPK signaling participate in the biological processes of vascular system such as proliferation of vascular endothelial cell [32] and vascular damage [33]. COL4A3 is a subunit of Type IV collagen and is the major structural component of basement membranes.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA/mRNA profiling and regulatory network of intracranial aneurysm

Jiang

Zhang

et al. 2013

BMC Med Genomics

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BackgroundIntracranial aneurysm (IA) is one of the most lethal forms of cerebrovascular diseases characterized by endothelial dysfunction, vascular smooth muscle cell phenotypic modulation, inflammation and consequently loss of vessel cells and extracellular matrix degradation. Besides environmental factors, genetics seem to be a very important factor in the genesis of this disease. Previous mRNA expression studies revealed a large number of differentially expressed genes between IA and control tissue. However, microRNAs (miRNA), small non-coding RNAs which are post-transcriptional regulators of gene expression, have been barely studied. Studying miRNAs could provide a hypothetical mechanism underlying rupture of IA.MethodsA microarray study was carried out to determine difference in microRNAs and mRNA between patients’ IA tissues and controls. Quantitative RT-PCR assay compared the expression level between two groups (14 IA domes vs. 14 controls) were used for validation. Validated miRNAs were analyzed using Ingenuity Pathway Analysis (IPA) to identify the networks and pathways.Results18 miRNAs were confirmed by qPCR to be robustly down-regulated in 14 ruptured IA patients including hsa-mir-133b, hsa-mir-133a, hsa-mir-1, hsa-mir-143-3p, hsa-mir-145-3p, hsa-mir-145-5p, hsa-mir-455-5p, hsa-mir-143-5p, hsa-mir-23b-3p etc., of which 11 miRNAs are clusters: hsa-mir-1/has-mir-133a, hsa-mir-143/hsa-mir-145, hsa-mir-23b/hsa-mir-24-1, and hsa-mir-29b-2/hsa-mir-29c. 12 predicted functions were generated using IPA which showed significant associations with migration of phagocytes, proliferation of mononuclear leukocytes, cell movement of mononuclear leukocytes, cell movement of smooth muscle cells etc.ConclusionThese data support common disease mechanisms that may be under miRNA control and provide exciting directions for further investigations aimed at elucidating the miRNA mechanisms and targets that may yield new therapies for IA.

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Glycoxydation promotes vascular damage Via MAPK‐ERK/JNK pathways

Cited by 6 publications

References 59 publications

Valsartan ameliorates ageing‐induced aorta degeneration via angiotensin II type 1 receptor‐mediated ERK activity

Valsartan ameliorates ageing‐induced aorta degeneration via angiotensin II type 1 receptor‐mediated ERK activity

Baicalin modulates apoptosis via RAGE, MAPK, and AP-1 in vascular endothelial cells during Haemophilus parasuis invasion

MicroRNA/mRNA profiling and regulatory network of intracranial aneurysm

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