High glucose promotes annulus fibrosus cell apoptosis through activating the JNK and p38 MAPK pathways

Shan, Peng-Fei; Yang, Di; Zhu, Danjie; Feng, Fabo; Li, Xin

doi:10.1042/bsr20190853

Cited by 27 publications

(30 citation statements)

References 36 publications

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“…Because normal AF cell viability is responsible for maintaining of the ECM in AF tissue, inhibiting high glucose-induced AF cell apoptosis may be a potential way to retard disc degeneration in DM patients. In line with us, several previous studies have shown that high glucose significantly affected biological behaviors of intervertebral disc cells, such as promoting cell apoptosis [15,19], accelerating autophagy [37], decreasing matrix biosynthesis [14] and inducing cellular senescence [15,38]. Together, these studies indicate that a high glucose environment is harmful to the healthy cellular activities of disc cells.…”

Section: Discussionsupporting

confidence: 81%

“…DM often induces many complications including cardiovascular issue, renal failure and neuropathy [9]. Several studies have reported that DM is a potential etiological factor of intervertebral disc degeneration [10][11][12][13][14][15]. Moreover, some researchers have demonstrated that high glucose can promote apoptosis of disc cartilage endplate cells and notochordal cells, and ultimately accelerate the progression of disc degeneration [16,17].…”

Section: Introductionmentioning

confidence: 99%

“…Annulus fibrosus (AF) is the peripheral region of an intact intervertebral disc, which often exhibits tears and fissures in the degenerative discs [18]. Similarly, previous studies have shown that high glucose induces apoptosis or premature senescence of AF cells [19,20]. However, the mechanism behind the effects of high glucose on AF cell apoptosis remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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High-glucose environment accelerates annulus fibrosus cell apoptosis by regulating endoplasmic reticulum stress

2020

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Diabetes mellitus (DM) is an important risk factor of intervertebral disc degeneration. However, how DM affects annulus fibrosus (AF) biology remains unclear. The present study was aimed to investigate the effects and mechanism of high glucose on AF cell biology. Rat AF cells were cultured in baseline medium and culture medium with 0.2 M glucose. The inhibitor 4-PBA was added along with the high glucose culture medium to study the role of endoplasmic reticulum (ER) stress in this process. Compared with the control cells, high glucose significantly increased cell apoptosis ratio and caspase-3/9 activity, up-regulated mRNA/protein expression of Bax and caspase-3/cleaved caspase-3, but down-regulated mRNA/protein expression of Bcl-2. Moreover, high glucose increased mRNA and protein expression of CHOP, ATF-6 and GRP78. However, once ER stress was inhibited by the inhibitor 4-PBA in the high glucose group, cell apoptosis ratio and caspase-3/9 activity were decreased, mRNA/protein expression of Bax and caspase-3/cleaved caspase-3 was down-regulated, but mRNA/protein expression of Bcl-2 was up-regulated. In conclusion, high glucose condition can promote AF cell apoptosis through inducing ER stress. The present study helps us understand the mechanism of disc degeneration in DM patients.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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High-glucose environment accelerates annulus fibrosus cell apoptosis by regulating endoplasmic reticulum stress

2020

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“…For example, FoxO1 overexpress in cardiomyocyte with DM, resulting in cardiac metabolic disorders, activation of caspases, and increased mitochondrial apoptosis [81]. In addition, high glucose activates JNK and p38 MAPK and promotes the apoptosis of annulus fibrosus cell in intervertebral disc [82].…”

Section: Various Pathways In Dm Maymentioning

confidence: 99%

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Kawaguchi

2020

Contrast Media & Molecular Imaging

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Contrast-induced acute kidney injury (CI-AKI) is the third most common hospital-acquired AKI after AKI induced by renal perfusion insufficiency and nephrotoxic drugs, taking great adverse effects on the prognosis and increasing hospital stay and medical cost. Diabetes nephropathy (DN) is a common chronic complication of DM (diabetes mellitus), and DN is an independent risk factor for chronic kidney disease (CKD) and CI-AKI. The incidence of CI-AKI significantly increases in patients with renal injury, especially in DM-related nephropathy. The etiology of CI-AKI is not fully clear, and research studies on how DM becomes a facilitated factor of CI-AKI are limited. This review describes the mechanism from three aspects. ① Pathophysiological changes of CI-AKI in kidney under high-glucose status (HGS). HGS can enhance the oxidative stress and increase ROS which next causes stronger vessel constriction and insufficient oxygen supply in kidney via vasoactive substances. HGS also aggravates some ion pump load and the latter increases oxygen consumption. CI-AKI and HGS are mutually causal, making the kidney function continue to decline. ② Immunological changes of DM promoting CI-AKI. Some innate immune cells and pattern recognition receptors (PRRs) in DM and/or DN may respond to some damage-associated molecular patterns (DAMPs) formed by CI-AKI. These effects overlap with some pathophysiological changes in hyperglycemia. ③ Signaling pathways related to both CI-AKI and DM. These pathways involved in CI-AKI are closely associated with apoptosis, inflammation, and ROS production, and some studies suggest that these pathways may be potential targets for alleviating CI-AKI. In conclusion, the pathogenesis of CI-AKI and the mechanism of DM as a predisposing factor for CI-AKI, especially signaling pathways, need further investigation to provide new clinical approaches to prevent and treat CI-AKI.

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“…Patients with diabetes experience decreased physiological function of intervertebral discs compared with patients without dM. recent studies have also revealed that high glucose concentrations lead to apoptosis of intervertebral disc cells, including NP and AF cells (31,32). A previous study demonstrated that high glucose concentrations can enhance oxidative stress, impair mitochondrial functions and ultimately lead to rat ceP cell apoptosis in a concentrationand time-dependent (12).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

Jiang

Zeng

et al. 2020

Mol Med Report

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diabetes mellitus (dM) contributes to intervertebral disc degeneration (idd). The long non-coding rna MalaT1 has been revealed to play an important role in diabetes-associated complications. However, the specific role of MALAT1 in diabetes-associated idd has not been determined. The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. rat ceP cells were cultured in high-glucose medium (25 mM glucose) for 24 or 72 h. Cells cultured in medium containing 5 mM glucose were used as a control. Flow cytometry was used to detect the degree of apoptosis. Reverse transcription-quantitative PCR was used to measure the expression of MALAT1 mRNA. In addition, CEP cells were treated with different conditions (high glucose, high glucose + MalaT1 negative control, high glucose + MALAT1 RNAi, normal control) for 72 h. Flow cytometry was subsequently used to detect apoptosis and western blotting was used to measure the expression levels of total and phosphorylated p38. The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Furthermore, MALAT1 knockout decreased the expression levels of total and phosphorylated p38 and reduced the apoptosis of rat CEP cells. The results obtained in the present study indicated that MALAT1 may serve as an important therapeutic target for curing or delaying idd in patients with diabetes.

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High glucose promotes annulus fibrosus cell apoptosis through activating the JNK and p38 MAPK pathways

Cited by 27 publications

References 36 publications

High-glucose environment accelerates annulus fibrosus cell apoptosis by regulating endoplasmic reticulum stress

High-glucose environment accelerates annulus fibrosus cell apoptosis by regulating endoplasmic reticulum stress

The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Long non‑coding RNA MALAT1 promotes high glucose‑induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway

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