Evidence for elevated (LIMK2 and CFL1) and suppressed (ICAM1, EZR, MAP2K2, and NOS3) gene expressions in metabolic syndrome

Tabur, Suzan; Öztuzcu, Serdar; Oğuz, Eli̇f; Demiryürek, Şeniz; Dağlı, Hasan; Alaşehirli, Belgin; Özkaya, Mesut; Demiryürek, Abdullah Tuncay

doi:10.1007/s12020-016-0910-0

Cited by 8 publications

(6 citation statements)

References 37 publications

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“…This may highlight that the serological cellular adhesion molecules may be modifiable with 16 weeks of exenatide treatment whereas RH-PAT may require more time to show a significant change, and clarification of these functional findings with longer studies involving serial measurement of the serum endothelial markers are required. The correlation of decreased ICAM-1 with triglycerides and p-selectin with hip circumference is in accord with their relationship with metabolic syndrome and their reduction that reflected the weight loss (37, 38).…”

Section: Discussionsupporting

confidence: 55%

The Effect of Exenatide on Cardiovascular Risk Markers in Women With Polycystic Ovary Syndrome

et al. 2019

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Background: Polycystic ovary syndrome (PCOS) is associated with an adverse cardiovascular risk profile including a prothrombotic state. Exenatide has been shown to be effective at improving insulin sensitivity and weight loss in PCOS; therefore this study was undertaken to assess its effects on weight, endothelial function, inflammatory markers, and fibrin structure/function in overweight/obese women with PCOS. Methods: Thirty overweight/obese anovulatory women with all 3 Rotterdam criteria received exenatide 5 mcg bd for 4 weeks then 10 mcg bd for 12 weeks. The primary outcome was change in weight; secondary outcomes were changes in endothelial function [Reactive Hyperemia-Peripheral Arterial Tonometry (RH-PAT)], serum endothelial markers (ICAM-1, VCAM-1, E-selectin, and P-selectin), change in inflammation (hsCRP), and alteration in clot structure and function [maximum absorbance (MA), and time from full clot formation to 50% lysis (LT)]. Results: Twenty patients completed the study. Exenatide reduced weight 111.8 ± 4.8 to 108.6 ± 4.6 kg p = 0.003. Serum endothelial markers changed with a reduction in ICAM-1 (247.2 ± 12.9 to 231.3 ± 11.5 ng/ml p = 0.02), p-selectin (101.1 ± 8.2 to 87.4 ± 6.6 ng/ml p = 0.01), and e-selectin (38.5 ± 3.3 to 33.6 ± 2.6 ng/ml p = 0.03), without an overt change in endothelial function. Inflammation improved (CRP; 8.5 ± 1.4 to 5.6 ± 0.8 mmol/L p = 0.001), there was a reduction in clot function (LT; 2,987 ± 494 to 1,926 ± 321 s p = 0.02) but not clot structure. Conclusion: Exenatide caused a 3% reduction in weight, improved serum markers of endothelial function, inflammation, and clot function reflecting an improvement in cardiovascular risk indices in these women with PCOS. This suggests exenatide could be an effective treatment for obese women with PCOS. Clinical Trial Registration: ISRCTN81902209.

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Section: Discussionsupporting

confidence: 55%

The Effect of Exenatide on Cardiovascular Risk Markers in Women With Polycystic Ovary Syndrome

et al. 2019

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“…The present study investigated epigenetic changes that occurred after nerve injury. Among the adhesion-associated differentially methylated genes identified in the present study, several important genes have been implicated in cell adhesion or proliferation, including Bcar1, Col5a3, Col18a1, Ezr, Col3a1 and Stat5a (59)(60)(61).…”

Section: Discussionmentioning

confidence: 76%

Identification of adhesion‑associated DNA methylation patterns in the peripheral nervous system

et al. 2020

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Schwann cells are unique glial cells in the peripheral nervous system. These cells provide a range of cytokines and nutritional factors to maintain axons and support axonal regeneration. However, little is known concerning adhesion-associated epigenetic changes that occur in Schwann cells after peripheral nerve injury (PNI). In the present study, adhesion-associated DNA methylation biomarkers were assessed between normal and injury peripheral nerve. Specifically, normal Schwann cells (NSCs) and activated Schwann cells (ASCs) were obtained from adult Wistar rats. After the Schwann cells were identified, proliferation and adhesion assays were used to assess differences between NSCs and ASCs. Methylated DNA immunoprecipitation-sequencing and bioinformatics analysis were used to identify and analyze the differentially methylated genes. Reverse transcription-quantitative PCR was performed to assess the expression levels of adhesion-associated genes. In the present study, the proliferation and adhesion assays demonstrated that ASCs had a more robust proliferative activity and adhesion compared with NSCs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to identify methylation-associated biological processes and signaling pathways. Protein-protein interaction network analysis revealed that Fyn, Efna1, Jak2, Vav3, Flt4, Epha7, Crk, Kitlg, Ctnnb1 and Ptpn11 were potential markers for Schwann cell adhesion. The expression levels of several adhesion-associated genes, such as vinculin, BCAR1 scaffold protein, collagen type XVIII α1 chain and integrin subunit β6, in ASCs were altered compared with those in NSCs. The current study analyzed adhesion-associated DNA methylation patterns of Schwann cells and identified candidate genes that may potentially regulate Schwann cell adhesion in Wistar rats before and after PNI.

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“…Generally, the positive association was due to three major mechanisms, including decreased testosterone, adipokine alterations and insulin resistance ( 2 , 16 ). Recently, several studies reported the involvement of ILK, β-parvin and cofilin in patients with obesity or metabolic syndromes ( 7 – 9 ). Meanwhile, a pioneering research conducted by Shibue et al firstly identified that the activation of ILK/β-parvin/cofilin pathway was critical in the formation of FLPs and the progression of carcinomas ( 6 ).…”

Section: Discussionmentioning

confidence: 99%

“…The researchers identified that the activation of integrin-linked kinase (ILK), β-parvin, cofilin pathway could promote caner progression, via enhancing the formation of FLPs and maintaining its existence, which raised a brand new perspective in cancer researches ( 6 ). Meanwhile, the signaling of ILK, β-parvin or cofilin were also involved in obesity and energy metabolism as recently proposed ( 7 – 9 ). Liu et al ( 7 ) discovered that oleic acid, with high levels in sera of obese patients, would activate ILK signaling pathway and therefore promote proliferation of renal cell carcinoma.…”

Section: Introductionmentioning

confidence: 87%

“…It was also demonstrated that ILK might promote diet-induced insulin resistance in obese mice, by impairing insulin signaling and insulin perfusion through capillaries via ILK-PINCH-parvin complex (IPP) ( 8 ). Besides, Cofilin 1 ( CFL1 ) gene expression was proved to be markedly elevated in patients with metabolic syndrome in Turkish population ( 9 ). Despite the complicated crosstalk and molecular network, these findings guided us to explore whether ILK/β-parvin/cofilin pathway played a role in obesity induced cancer progression.…”

Section: Introductionmentioning

confidence: 99%

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Differential expressions of integrin‑linked kinase, β‑parvin and cofilin 1 in high‑fat diet induced prostate cancer progression in a transgenic mouse model

Jiang

et al. 2018

Oncol Lett

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High-fat diet induced obesity was associated with more aggressive prostate cancer. Recent research has demonstrated that integrin-linked kinase (ILK), β-parvin and downstream cofilin 1 jointly affected cancer progression. Meanwhile, these proteins were also involved in energy metabolism. Therefore, the present study was conducted to investigate the potential function of ILK, β-parvin and cofilin 1 in the high-fat diet-induced progression of prostate cancer. Transgenic mice with prostate cancer were employed, fed with different diets and sacrificed at 20 and 28 weeks. Tumor differentiation, extracapsular extension and metastasis were compared between the groups. Expression levels of ILK, β-parvin and cofilin 1 in prostate were evaluated by immunohistochemical analysis and determined by an immunoreactivity score. Public databases were applied for analysis and validation. It was detected that high-fat diet feeding promoted cancer progression in transgenic mice with prostate cancer, with increased expressions of β-parvin (P=0.038) and cofilin 1 (P=0.018). Higher expressions of ILK, β-parvin and cofilin 1 were also associated with poorer cancer differentiation. Additionally, higher mRNA levels of CFL1 were correlated with a worse disease-free survival in patients of certain subgroups from The Cancer Genome Atlas database. Further studies were warranted in discussing the potential roles of ILK, β-parvin and cofilin 1 in high-fat diet feeding induced progression of prostate cancer.

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Evidence for elevated (LIMK2 and CFL1) and suppressed (ICAM1, EZR, MAP2K2, and NOS3) gene expressions in metabolic syndrome

Cited by 8 publications

References 37 publications

The Effect of Exenatide on Cardiovascular Risk Markers in Women With Polycystic Ovary Syndrome

The Effect of Exenatide on Cardiovascular Risk Markers in Women With Polycystic Ovary Syndrome

Identification of adhesion‑associated DNA methylation patterns in the peripheral nervous system

Differential expressions of integrin‑linked kinase, β‑parvin and cofilin 1 in high‑fat diet induced prostate cancer progression in a transgenic mouse model

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