Lipopolysaccharide induces human olfactory ensheathing glial apoptosis by promoting mitochondrial dysfunction and activating the JNK-Bnip3-Bax pathway

He, Maowei; Xiang, Zimin; Xu, Le; Duan, Yanran; Li, Fangqin; Chen, Jianmei

doi:10.1007/s12192-018-0945-7

Cited by 11 publications

(9 citation statements)

References 68 publications

(82 reference statements)

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“…It is well known that JNK pathway plays critical roles in the promotion of cell apoptosis under high glucose environment [35]. BNIP3 has also been reported to be associated with the regulation of JNK pathway in cells [36,37]. Here, we found that high glucose stimulation activated the JNK pathway in HK-2 cells.…”

Section: Discussionsupporting

confidence: 48%

RETRACTED ARTICLE: Silence of lncRNA GAS5 alleviates high glucose toxicity to human renal tubular epithelial HK-2 cells through regulation of miR-27a

Tian³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Renal tubular damage caused by persistent high glucose environment has been found to contribute to diabetic nephropathy. This study explored the effects of lncRNA growth arrest-specific 5 (GAS5) on high glucose-stimulated human renal tubular epithelial HK-2 damage, as well as the possible internal molecular mechanism. Viability and apoptosis of HK-2 cells were assessed with the help of CCK-8 assay and Annexin V-FITC/PI staining, respectively. Cell transfection was used to change the expression of GAS5, miR-27a and BNIP3. We found that high glucose stimulation suppressed HK-2 cell viability but induced cell apoptosis. The expression of GAS5 was increased in HK-2 cells under high glucose environment. Silence of GAS5 mitigated the high glucose-caused HK-2 cell viability reduction and apoptosis. Overexpression of miR-27a reversed the effects of GAS5 on high glucose-stimulated HK-2 cells. Overexpression of BNIP3 aggravated the high glucose-caused HK-2 cell viability reduction, apoptosis and activation of JNK pathway. Knockdown of BNIP3 had opposite effects. In conclusion, this research further confirmed the pro-apoptotic roles of GAS5 in renal tubular epithelial cells under high glucose environment. Silence of GAS5 alleviated high glucose toxicity to human renal tubular epithelial HK-2 cells might be via down-regulating miR-27a and BNIP3, and then inactivating JNK pathway. HIGHLIGHTS1. HG suppresses HK-2 cell viability, but promotes cell apoptosis; 2. HG enhances the expression of GAS5 in HK-2 cells; 3. Silence of GAS5 alleviates the HG-caused HK-2 cell toxicity; 4. miR-27a participates in the effects of GAS5 silencing on HG-stimulated HK-2 cells; 5. BNIP3 is regulated by miR-27a and related to the HG toxicity to HK-2 cells.

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Section: Discussionsupporting

confidence: 48%

RETRACTED ARTICLE: Silence of lncRNA GAS5 alleviates high glucose toxicity to human renal tubular epithelial HK-2 cells through regulation of miR-27a

Tian³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Mitochondrial dysfunction in the brain has been associated with the pathogenesis of several types of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease . Increased production of reactive oxygen species (ROS) and neurotoxins under pathological circumstances has a negative effect in mitochondrial abundance and the copy number of mitochondrial DNA (mtDNA) . Mitochondrial biogenesis plays a critical role in maintaining normal energy metabolism, mitochondrial homeostasis, and quality control .…”

Section: Introductionmentioning

confidence: 99%

“…2 Increased production of reactive oxygen species (ROS) and neurotoxins under pathological circumstances has a negative effect in mitochondrial abundance and the copy number of mitochondrial DNA (mtDNA). 3,4 Mitochondrial biogenesis plays a critical role in maintaining normal energy metabolism, mitochondrial homeostasis, and quality control. 5 Mitochondrial biogenesis is mainly regulated by the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and its downstream molecules nuclear respiratory factor 1 (NRF-1) and the mitochondrial transcription factor A (TFAM).…”

Section: Introductionmentioning

confidence: 99%

Sitagliptin promotes mitochondrial biogenesis in human SH‐SY5Y cells by increasing the expression of PGC‐1α/NRF1/TFAM

et al. 2019

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Mitochondrial dysfunction has been associated with the pathogenesis of a variety of neurodegenerative diseases. Sitagliptin is a dipeptidyl‐peptidase‐4 (DPP‐4) inhibitor that has been approved for the treatment of type 2 diabetes (T2DM). In the current study, we report that sitagliptin increased the expression of PGC‐1α, NRF1, and TFAM in human SH‐SY5Y neuronal cells. Notably, our data indicate that sitagliptin promoted mitochondrial biogenesis by increasing the amount of mtDNA, the levels of mitochondria‐related genes such as TOMM20, TOMM40, TIMM9, NDUFS3, ATP5C1, and the expression of oxidative phosphorylation subunits complex I and complex IV. Additionally, we found that sitagliptin induced a “gain of mitochondrial function” in SH‐SY5Y cells by increasing the mitochondrial respiratory rate and adenosine triphosphate (ATP) production. Significantly, our results demonstrate that sitagliptin activated the transcriptional factor CREB by inducing its phosphorylation at Ser133. Inhibition of CREB using its specific inhibitor H89 abolished the effects of sitagliptin on the expression of PGC‐1α, NRF1, and TFAM, as well as an increase in mtDNA amount and ATP production. These findings suggest that sitagliptin could become a potential agent for the treatment of neurological disorders.

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“…Bnip3 has been shown to suppress inflammation as well as apoptosis induced by LPS exposure in chondrocytes through the promotion of autophagy [ 30 ]. The JNK-Bnip3 pathway has been reported to act as an upstream mediator of Bax upregulation, which can be activated by LPS to induce apoptosis of human olfactory ensheathing glial cells [ 31 ]. When the JNK-Bnip3 pathway was inhibited, Bax activation by LPS was eliminated, which resulted in attenuation of cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway

Chen

Lai

et al. 2022

Canadian Respiratory Journal

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Dexmedetomidine (DEX), which is reported to be a newly discovered, novel α-2 adrenoceptor agonist, is known to exhibit anti-inflammatory properties in several diseases. DEX regulates inflammation-related signaling pathways and genes through interactions with several miRNAs. This study verified that expression levels of miR-140-3p were diminished when alveolar type II cells were exposed to LPS. However, the levels of miR-140-3p were confirmed as showing an increase with DEX treatment. These observations revealed that the expression of miR-140-3p was related to the beneficial effects that accompanied the DEX treatment of LPS-induced ALI. In addition, PD-1/PD-L1 expression increased extensively when RLE-6TN cells were induced by LPS. The increased expression was reduced after treatment with DEX. Thus, it appears that the PD-L1 expression was targeted directly by miR-140-3p, resulting in the partial repression of PD-L1 levels, which involved the inhibition of p-JNK and Bnip3 expression. Therefore, DEX was shown to inhibit the PD-L1 expression by promoting partially increased miR-140-3p levels in RLE-6TN cells. DEX also inactivated the JNK-Bnip3 pathway, resulting in the inhibition of inflammation and alleviating alveolar type II cell injury.

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Lipopolysaccharide induces human olfactory ensheathing glial apoptosis by promoting mitochondrial dysfunction and activating the JNK-Bnip3-Bax pathway

Cited by 11 publications

References 68 publications

RETRACTED ARTICLE: Silence of lncRNA GAS5 alleviates high glucose toxicity to human renal tubular epithelial HK-2 cells through regulation of miR-27a

RETRACTED ARTICLE: Silence of lncRNA GAS5 alleviates high glucose toxicity to human renal tubular epithelial HK-2 cells through regulation of miR-27a

Sitagliptin promotes mitochondrial biogenesis in human SH‐SY5Y cells by increasing the expression of PGC‐1α/NRF1/TFAM

Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells’ Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway

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