Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

Zhong, Zhiying; Tang, Yu

doi:10.1159/000445606

Cited by 23 publications

(20 citation statements)

References 33 publications

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“…Several studies have shown that other adhesion molecules, such as VE-cadherin and PECAM-1 (CD31), can be modulated by TRPM4 [28] and TRPM7 [29]. Endothelial dysfunction is a complex and multistep process that includes endothelial cell migration [30-33]. Our data clearly demonstrate that H 2 O 2 considerably promotes EC migration and that inhibition of TRPM4 with 9-phenanthrol significantly inhibits H 2 O 2 -induced migration of HUVECs.…”

Section: Discussionsupporting

confidence: 57%

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Ding

Ban

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: The present study investigated whether the transient receptor potential melastatin 4 (TRPM4) channel plays a role in high salt diet (HSD)-induced endothelial injuries. Methods: Western blotting and immunofluorescence were used to examine TRPM4 expression in the mesenteric endothelium of Dahl salt-sensitive (SS) rats fed a HSD. The MTT, TUNEL, and transwell assays were used to evaluate the cell viability, cell apoptosis, and cell migration, respectively, of human umbilical vein endothelial cells (HUVECs). Enzyme-linked immunosorbent assays were used to determine the concentrations of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), and E-selectin. Carboxy-H2DCFDA, a membrane-permeable reactive oxygen species (ROS)-sensitive fluorescent probe, was used to detect intracellular ROS levels. Results: TRPM4 was mainly expressed near the plasma membrane of mesenteric artery endothelial cells, and its expression level increased in SS hypertensive rats fed a HSD. Its protein expression was significantly upregulated upon treatment with exogenous hydrogen peroxide (H₂O₂) and aldosterone in cultured HUVECs. Cell viability decreased upon treatment with both agents in a concentration-dependent manner, which could be partially reversed by 9-phenanthrol, a specific TRPM4 inhibitor. Exogenous H₂O₂ induced apoptosis, enhanced cell migration, and increased the release of adhesion molecules, including ICAM-1, VCAM-1, and E-selectin, all of which were significantly attenuated upon treatment with 9-phenanthrol. Aldosterone and H₂O₂ induced the accumulation of intracellular ROS, which was significantly inhibited by 9-phenanthrol, suggesting that oxidative stress is one of the mechanisms underlying aldosterone-induced endothelial injury. Conclusions: Given the fact that oxidative stress and high levels of circulating aldosterone are present in hypertensive patients, we suggest that the upregulation of TRPM4 in the vascular endothelium may be involved in endothelial injuries caused by these stimuli.

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Section: Discussionsupporting

confidence: 57%

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Ding

Ban

Liu

et al. 2017

Cell Physiol Biochem

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“…Conversely, periostin inhibits glucose-induced ROS production in endothelial cells (316). Growth of human umbilical vein endothelial cells in medium containing 33 mM glucose for 2 days induced periostin expression and apoptosis.…”

Section: B Periostinmentioning

confidence: 95%

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Roberts

Kaur

Isenberg

2017

Antioxidants & Redox Signaling

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Significance: In contrast to structural elements of the extracellular matrix, matricellular proteins appear transiently during development and injury responses, but their sustained expression can contribute to chronic disease. Through interactions with other matrix components and specific cell surface receptors, matricellular proteins regulate multiple signaling pathways, including those mediated by reactive oxygen and nitrogen species and H 2 S. Dysregulation of matricellular proteins contributes to the pathogenesis of vascular diseases and cancer. Defining the molecular mechanisms and receptors involved is revealing new therapeutic opportunities. Recent Advances: Thrombospondin-1 (TSP1) regulates NO, H 2 S, and superoxide production and signaling in several cell types. The TSP1 receptor CD47 plays a central role in inhibition of NO signaling, but other TSP1 receptors also modulate redox signaling. The matricellular protein CCN1 engages some of the same receptors to regulate redox signaling, and ADAMTS1 regulates NO signaling in Marfan syndrome. In addition to mediating matricellular protein signaling, redox signaling is emerging as an important pathway that controls the expression of several matricellular proteins. Critical Issues: Redox signaling remains unexplored for many matricellular proteins. Their interactions with multiple cellular receptors remains an obstacle to defining signaling mechanisms, but improved transgenic models could overcome this barrier. Future Directions: Therapeutics targeting the TSP1 receptor CD47 may have beneficial effects for treating cardiovascular disease and cancer and have recently entered clinical trials. Biomarkers are needed to assess their effects on redox signaling in patients and to evaluate how these contribute to their therapeutic efficacy and potential side effects. Antioxid. Redox Signal. 27, 874-911.

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“…The activity of caspase-3 was detected by a colorimetric caspase-3 assay kit (Sigma, St. Louis, MO, USA) according to the manufacturer's protocol [20]. HCAECs (2 × 10 5 /well) were cultured in 6-well plates with QL (0-1 µg/ml) and ox-LDL (150 μg/ml) for 24 h. The cell lysate were added with caspase-3 substrate at 37°C for 90 min.…”

Section: Measurement Of Caspase-3 Activitymentioning

confidence: 99%

Qiliqiangxin improves oxidized low-density lipoprotein-induced human coronary artery endothelial cells injury

Du¹,

Lv²,

Meng³

et al. 2018

biomedicalresearch

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Qiliqiangxin (QL) has protective effect for the cardiovascular diseases treatment. This study aim to evaluate the effect of QL on the cell viability, cell apoptosis and caspase-3 activity in oxidized LDL (oxLDL)-induced Human Coronary Artery Endothelial Cells (HCAECs). HCAECs were treated with QL (0-1µg/ml) and oxLDL (150 μg/ml). The HCAECs viability was detected by cell proliferation assay and Lactate Dehydrogenase (LDH) release assay. The HCAECs apoptosis was evaluated by the annexin V-FITC assay. The activity of caspase-3 of HCAECs was measured by colorimetric caspase-3 assay. Cell migration assay and capillary-like tube formation assay on Matrigel were performed. Treatment of HCAECs to ox-LDL (150 μg/ml) decreased cell viability, stimulated apoptosis and enhanced caspase-3 activity. In addition, treatment with QL (0.5 µg/ml) alone did not affect cell viability and LDH release. Furthermore, the treatment with QL (0.5 µg/ml) significantly increased ox-LDL (150 μg/ml) decreased cell viability. Treatment with QL (0.5 µg/ml) reduced ox-LDL-stimulated apoptosis and caspase-3 activity in HCAECs in a dose-dependent manner. QL (0.5 µg/ml) attenuated ox-LDL (150 μg/ml) abolished cell migration and tube formation. Our study demonstrated that QL prevents ox-LDLinduced HCAECs injury by decreasing the apoptosis via caspase-3 activity.

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Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

Cited by 23 publications

References 33 publications

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Transient Receptor Potential Melastatin 4 (TRPM4) Contributes to High Salt Diet-Mediated Early-Stage Endothelial Injury

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Qiliqiangxin improves oxidized low-density lipoprotein-induced human coronary artery endothelial cells injury

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