Exposure to endosulfan increases endothelial permeability by transcellular and paracellular pathways in relation to cardiovascular diseases

Xu, Dan; Liu, Tong; Lin, Limei; Li, Shuai; Hang, Xiaoming; Sun, Yeqing

doi:10.1016/j.envpol.2016.12.051

Cited by 18 publications

(4 citation statements)

References 59 publications

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“… 34 We found that LAMC1 could regulate cell proliferation and cytoskeleton changes through FAK signaling in endosulfan-exposed cells. 23 Here, we confirmed LAMC1 is a novel target gene of miR-22. LAMC1 siRNAs (si-2, 3) significantly decreased cell adhesion rate and each LAMC1 siRNA disrupted the formation of stress fibers.…”

Section: Discussionsupporting

confidence: 63%

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The subsequent biological effects of simulated microgravity on endothelial cell growth in HUVECs

Guo

Zhang

et al. 2018

Chinese Journal of Traumatology

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PurposeMicrogravity is known to cause endothelium dysfunction in astronauts returning from spaceflight. We aimed to reveal the regulatory mechanism in alterations of human endothelial cells after simulated microgravity (SMG).MethodsWe utilized the rotary cell culture system (RCCS-1) to explore the subsequent effects of SMG on human umbilical vein endothelial cells (HUVECs).ResultsSMG-treated HUVECs appeared obvious growth inhibition after return to normal gravity, which might be attributed to a set of responses including alteration of cytoskeleton, decreased cell adhesion capacity and increased apoptosis. Expression levels of mTOR and its downstream Apaf-1 were increased during subsequent culturing after SMG. miR-22 was up-regulated and its target genes SRF and LAMC1 were down-regulated at mRNA levels. LAMC1 siRNAs reduced cell adhesion rate and inhibited stress fiber formation while SRF siRNAs caused apoptosis.ConclusionSMG has the subsequent biological effects on HUVECs, resulting in growth inhibition through mTOR signaling and miR-22-mediated mechanism.

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Section: Discussionsupporting

confidence: 63%

“… 22 The laminin γ-1 chain is the most ubiquitously expressed γ subunit, encoded by LAMC1 that can influence intracellular pathway to regulate the cytoskeleton changes and interfere endothelial barrier function. 23 …”

Section: Introductionmentioning

confidence: 99%

The subsequent biological effects of simulated microgravity on endothelial cell growth in HUVECs

Guo

Zhang

et al. 2018

Chinese Journal of Traumatology

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“…After that, FAK activates and triggers subsequent signaling cascades in a variety of cellular activities [10,11]. FAK can also participate in the signal transduction process in tumor vessel, mediating the vessel permeability [12][13][14]. The FERM domain of FAK can combine with the cytoplasmic region of vascular endothelial calcium mucin.…”

Section: Introductionmentioning

confidence: 99%

The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review

Zhou

Qian

Tang

2019

J Exp Clin Cancer Res

235

160

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FAK is a tyrosine kinase overexpressed in cancer cells and plays an important role in the progression of tumors to a malignant phenotype. Except for its typical role as a cytoplasmic kinase downstream of integrin and growth factor receptor signaling, related studies have shown new aspects of the roles of FAK in the nucleus. FAK can promote p53 degradation through ubiquitination, leading to cancer cell growth and proliferation. FAK can also regulate GATA4 and IL-33 expression, resulting in reduced inflammatory responses and immune escape. These findings establish a new model of FAK from the cytoplasm to the nucleus. Activated FAK binds to transcription factors and regulates gene expression. Inactive FAK synergizes with different E3 ligases to promote the turnover of transcription factors by enhancing ubiquitination. In the tumor microenvironment, nuclear FAK can regulate the formation of new blood vessels, affecting the tumor blood supply. This article reviews the roles of nuclear FAK in regulating gene expression. In addition, the use of FAK inhibitors to target nuclear FAK functions will also be emphasized.

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“…Lipid profile abnormalities play a significant role in atherosclerosis and cardiovascular disease. The findings of the present investigation indicate that exposure to endosulfan alters the metabolism of cholesterol and thus increases the risk of cardiovascular disease and atherosclerosis in mice (Vandenberg 2020;Xu et al, 2017). Medicinal plants have a potent protective effect in controlling the hyperlipidemic effect (Deokar, 1998;Cuvelier et al, 1992…”

Section: Resultsmentioning

confidence: 74%

Efficacy of Withania somnifera on lipid profile of endosulfan induced toxicity in Swiss albino mice

Jha

Paul

2020

JANS

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India is an agrarian country with crops cultivated at a huge scale. Pesticides in recent times have caused serious health hazards in the population which are widely used by the farmers for the better yield of crops. Endosulfan is an organochlorine pesticide, which is widely used by the farmers. But, in the present times, it has caused serious health hazards in the exposed population causing various diseases, including cancer. Hence, the present study on animal aims to observe the protective effect of Withania somnifera against endosulfan induced toxicity in Swiss albino mice. Endosulfan at the dose of 3mg/Kg body weight per day was administered orally to Swiss albino mice for 4 weeks. Then after, W. somnifera at the dose of 1000 mg/Kg b.w. was orally administered for 4 weeks. Mice were sacrificed after the completion of the entire treatment. After dissection, the blood samples were collected for biochemical assay, especially for lipid profile analysis. The lipid profile study showed inclination in the Total cholesterol level (117±6.686 mg/dl), Cholesterol (LDL) (78.83±4.151mg/dl), level and Triglycerides level (60.83±2.613mg/dl), while declination in Cholesterol (HDL) (13.50±1.33mg/dl), level after Endosulfan exposure. But, upon W. somnifera treatment to the endosulfan treated group showed significant (p<0.001) normalisation in the lipid profile levels. Therefore, it was concluded that W. somnifera played a vital role to control the endosulfan induced toxicity.

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Exposure to endosulfan increases endothelial permeability by transcellular and paracellular pathways in relation to cardiovascular diseases

Cited by 18 publications

References 59 publications

The subsequent biological effects of simulated microgravity on endothelial cell growth in HUVECs

The subsequent biological effects of simulated microgravity on endothelial cell growth in HUVECs

The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review

Efficacy of Withania somnifera on lipid profile of endosulfan induced toxicity in Swiss albino mice

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