Role of Autophagy in Angiogenesis Induced by a High-Glucose Condition in RF/6A Cells

2017 ◽  
Vol 237 (2) ◽  
pp. 85-95 ◽  
Author(s):  
Jun-Hui Du ◽  
Xia Li ◽  
Rong Li ◽  
Bai-Xiang Cheng ◽  
Manzila Kuerbanjiang ◽  
...  
Keyword(s):  
High Glucose ◽  
High Glucose Condition ◽  
Glucose Condition

scholarly journals Long non-coding RNA MEG3 serves as a ceRNA for microRNA-145 to induce apoptosis of AC16 cardiomyocytes under high glucose condition

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Yiwei Chen ◽  
Zhifang Zhang ◽  
Diqi Zhu ◽  
Wenchuo Zhao ◽  
Fen Li
Keyword(s):  
High Glucose ◽  
Human Cardiomyocytes ◽  
Non Coding Rna ◽  
High Glucose Condition ◽  
Promising Therapeutic Target ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Long Non Coding Rna ◽  
Glucose Condition

AbstractDiabetic cardiomyopathy (DCM) is one of the most serious complications of diabetes, but its pathogenesis remains largely unclear. In the present study, we aimed to explore the potential role of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and to investigate the underlying mechanisms in human AC16 cardiomyocytes under high glucose (HG) condition. The results demonstrated that MEG3 was overexpressed in HG-treated AC16 cells, and MEG3 knockdown suppressed the HG-induced apoptosis in AC16 cells. Mechanistically, MEG3 directly binds to miR-145 in AC16 cells, thereby up-regulating the expression of PDCD4. Rescue experiments showed that the role of MEG3 in HG-treated AC16 cells was partly dependent on its suppression on miR-145. In summary, our findings suggested that the role of MEG3 in HG-treated human cardiomyocytes is to serve as a competing endogenous RNA (ceRNA), which negatively regulates miR-145. These findings may provide a valuable and promising therapeutic target for the treatment of DCM in the future.

scholarly journals Asymmetric dimethylarginine (ADMA) accelerates renal cell fibrosis under high glucose condition through NOX4/ROS/ERK signaling pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Isaivani Jayachandran ◽  
Saravanakumar Sundararajan ◽  
Saravanakumar Venkatesan ◽  
Sairaj Paadukaana ◽  
Muthuswamy Balasubramanyam ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Kidney Cell ◽  
High Glucose ◽  
Renal Cell ◽  
Asymmetric Dimethylarginine ◽  
Cell Injury ◽  
High Glucose Condition ◽  
Erk Activity ◽  
Glucose Condition

Abstract We previously reported that the circulatory level of Asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide synthase, was increased in diabetic kidney disease patients. However, the mechanism and the role of ADMA in diabetic kidney injury remain unclear. Hence, our principal aim is to investigate the causal role of ADMA in the progression of renal cell fibrosis under high glucose (HG) treatment and to delineate its signaling alterations in kidney cell injury. High Glucose/ADMA significantly increased fibrotic events including cell migration, invasion and proliferation along with fibrotic markers in the renal cells; whereas ADMA inhibition reversed the renal cell fibrosis. To delineate the central role of ADMA induced fibrotic signaling pathway and its downstream signaling, we analysed the expression levels of fibrotic markers, NOX4, ROS and ERK activity by using specific inhibitors and genetic manipulation techniques. ADMA stimulated the ROS generation along with a significant increase in NOX4 and ERK activity. Further, we observed that ADMA activated NOX-4 and ERK are involved in the extracellular matrix proteins accumulation. Also, we observed that ADMA induced ERK1/2 phosphorylation was decreased after NOX4 silencing. Our study mechanistically demonstrates that ADMA is involved in the progression of kidney cell injury under high glucose condition by targeting coordinated complex mechanisms involving the NOX4- ROS-ERK pathway.

Effect of metformin and celecoxib on cytotoxicity and release of GDF-15 from human mesenchymal stem cells in high glucose condition

2017 ◽  
Vol 35 (7) ◽  
pp. 407-413 ◽  
Author(s):  
Elaheh Zafarvahedian ◽  
Azam Roohi ◽  
Mohammad Reza Sepand ◽  
Seyed Nasser Ostad ◽  
Mohammad Hossein Ghahremani
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
High Glucose ◽  
Human Mesenchymal Stem Cells ◽  
High Glucose Condition ◽  
Glucose Condition

scholarly journals PPARβ/δ accelerates bone regeneration in diabetic mellitus by enhancing AMPK/mTOR pathway-mediated autophagy

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Miao Chen ◽  
Dian Jing ◽  
Rui Ye ◽  
Jianru Yi ◽  
Zhihe Zhao
Keyword(s):  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Bone Healing ◽  
High Glucose ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Regulatory Effect ◽  
Compound C ◽  
High Glucose Condition ◽  
Glucose Condition

Abstract Background Diabetic patients are more vulnerable to skeletal complications. Peroxisome proliferators-activated receptor (PPAR) β/δ has a positive regulatory effect on bone turnover under physiologic glucose concentration; however, the regulatory effect in diabetes mellitus has not been investigated yet. Herein, we explored the effects of PPARβ/δ agonist on the regeneration of diabetic bone defects and the osteogenic differentiation of rat bone marrow mesenchymal stem cells (rBMSCs) under a pathological high-glucose condition. Methods We detected the effect of PPARβ/δ agonist on osteogenic differentiation of rBMSCs in vitro and investigated the bone healing process in diabetic rats after PPARβ/δ agonist treatment in vivo. RNA sequencing was performed to detect the differentially expressed genes and enriched pathways. Western blot was performed to detect the autophagy-related protein level. Laser confocal microscope (LSCM) and transmission electron microscope (TEM) were used to observe the formation of autophagosomes. Results Our results demonstrated that the activation of PPARβ/δ can improve the osteogenic differentiation of rBMSCs in high-glucose condition and promote the bone regeneration of calvarial defects in diabetic rats, while the inhibition of PPARβ/δ alleviated the osteogenic differentiation of rBMSCs. Mechanistically, the activation of PPARβ/δ up-regulates AMPK phosphorylation, yielding mTOR suppression and resulting in enhanced autophagy activity, which further promotes the osteogenic differentiation of rBMSCs in high-glucose condition. The addition of AMPK inhibitor Compound C or autophagy inhibitor 3-MA inhibited the osteogenesis of rBMSCs in high-glucose condition, suggesting that PPARβ/δ agonist promotes osteogenic differentiation of rBMSCs through AMPK/mTOR-regulated autophagy. Conclusion In conclusion, our study demonstrates the potential role of PPARβ/δ as a molecular target for the treatment of impaired bone quality and delayed bone healing in diabetic patients for the first time.

ERM Complex, a Therapeutic Target for Vascular Leakage Induced by Diabetes

2021 ◽  
Vol 28 ◽  
Author(s):  
Olga Simó-Servat ◽  
Hugo Ramos ◽  
Patricia Bogdanov ◽  
Marta García-Ramírez ◽  
Jordi Huerta ◽  
...  
Keyword(s):  
High Glucose ◽  
Therapeutic Target ◽  
Vascular Leakage ◽  
Cell Permeability ◽  
Diabetic Patients ◽  
Diabetic Mice ◽  
Erm Proteins ◽  
High Glucose Condition ◽  
Tnf Α ◽  
Glucose Condition

Background: Ezrin, radixin, and moesin (the ERM complex) interact directly with membrane proteins regulating their attachment to actin filaments. ERM protein activation modifies cytoskeleton organization and alters the endothelial barrier function, thus favoring vascular leakage. However, little is known regarding the role of ERM proteins in diabetic retinopathy (DR). Objective: This study aimed to examine whether overexpression of the ERM complex exists in db/db mice and its main regulating factors. Methods: 9 male db/db mice and 9 male db/+ aged 14 weeks were analyzed. ERM proteins were assessed by western blot and by immunohistochemistry. Vascular leakage was determined by the Evans blue method. To assess ERM regulation, HRECs were cultured in a medium containing 5.5 mM D-glucose (mimicking physiological conditions) and 25 mM D-glucose (mimicking hyperglycemia that occurs in diabetic patients). Moreover, treatment with TNF-α, IL-1β, or VEGF was added to a high glucose condition. The expression of ERM proteins was quantified by RT-PCR. Cell permeability was evaluated by measuring movements of FITC-dextran. Results: A significant increase of ERM in diabetic mice in comparison with non-diabetic mice was observed. A high glucose condition alone did not have any effect on ERM expression. However, TNF-α and IL-1β induced a significant increase in ERM proteins. Conclusion: The increase of ERM proteins induced by diabetes could be one of the mechanisms involved in vascular leakage and could be considered as a therapeutic target. Moreover, the upregulation of the ERM complex by diabetes is induced by inflammatory mediators rather than by high glucose itself.

The Effect of High-Glucose Condition on Insulin Binding to IM-9 Lymphocytes

1987 ◽  
Vol 19 (07) ◽  
pp. 316-318 ◽  
Author(s):  
N. Watanabe ◽  
M. Kobayashi ◽  
M. Iwasaki ◽  
O. Ishibashi ◽  
Y. Takata ◽  
...  
Keyword(s):  
High Glucose ◽  
Insulin Binding ◽  
High Glucose Condition ◽  
Glucose Condition
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