The Role of BCL-2 Family Members in Acute Kidney Injury

Borkan, Steven C.

doi:10.1016/j.semnephrol.2016.04.001

Cited by 43 publications

(33 citation statements)

References 157 publications

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“…MSCs have been shown to integrate into injury sites and differentiate into renal epithelial cells in cases of cisplatin‐ and glycerol‐induced AKI . The growing evidence has implicated that AKI induces an imbalance between the pro‐apoptotic (Bax and bid) and anti‐apoptotic (Bcl‐2 and Bcl‐xL) members in both animal models and humans . We have observed changes in the levels of Bcl‐2 mRNA, a decrease after IR‐induced AKI, and recovery after ADMSC transplantation, in agreement with previous reports that ADMSC treatment increases Bcl‐2 expression at the transcriptional and translational levels, although the increase in Bcl‐2 expression after ischemic ARF in rat was reported .…”

Section: Discussionsupporting

confidence: 91%

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Zhang

Wang

et al. 2017

Clin Exp Pharma Physio

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Acute kidney injury (AKI) represents a group of complicated syndromes with a high mortality rate. The administration of adipose-derived mesenchymal stem cells (ADMSCs) has been tested as a possible treatment method for AKI. The long-term evaluation of AKI induced by ischemia/reperfusion (IR) and the probable renal protection of ADMSCs are limited. In this study we have established a rat AKI model induced by IR and investigated the possible protective effects of ADMSCs. Adult Sprague-Dawley (SD) rats were divided into three groups (n = 6/each group). The MOCK group was as the normal control. Rats in the IR-AKI and IR-AKI+ADMSCs groups were subjected to IR injury by clamping both renal pedicles for 40 minutes. Rats in the MOCK and IR-AKI groups were injected with PBS via the tail vein as negative treatment controls. Rats in the IR-AKI+ADMSCs group received ADMSCs therapy (2 × 10 cells were injected into the rats via the tail vein). We found that ADMSC transplantation restored the pathologic morphology induced by IR-AKI to normal compared with the MOCK group, suggesting the reparative function of ADMSCs in kidney tissues. Compared with IR-induced AKI alone, ADMSC treatment significantly decreased the number of apoptotic cells, the level of total urinary protein and serum creatinine, the expression of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IFN-γ, TNF-α, IFN-γ, and TGF-β), and the inflammation-associated proteins (HGF and SDF1), but increased the expression of the anti-inflammatory cytokine, IL-10, and the anti-apoptotic regulator, Bcl-2. Our data have indicated that ADMSC transplantation may protect against IR-induced AKI by anti-apoptotic and anti-inflammatory effects.

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Section: Discussionsupporting

confidence: 91%

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Zhang

Wang

et al. 2017

Clin Exp Pharma Physio

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“…Bcl‐2 family members are major regulators by mitochondria. They can change their conformations to form mitochondrial permeability transition pores in the outer mitochondrial membrane (Borkan, ). In accordance with the previous theory, after F1012‐2 treatment, loss of ΔΨm in TNBC cells was observed, consistent with membrane depolarization.…”

Section: Discussionmentioning

confidence: 99%

F1012‐2 inhibits the growth of triple negative breast cancer through induction of cell cycle arrest, apoptosis, and autophagy

Tian

Yan

Yang

et al. 2018

Phytotherapy Research

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Sesquiterpene lactones (SLs) are plant-derived constituents that have been proved to have potential antitumour activity. However, the intracellular molecular targets of SLs and the underlying molecular mechanisms have not been well elucidated. Here, we report that F1012-2, a novel SL active fraction, isolated from Eupatorium lindleyanum DC., can significantly inhibit the growth of triple-negative breast cancer (TNBC) cells (MDA-MB-231 and MDA-MB-468) but has no obvious inhibitory effect on the growth of human mammary epithelial cells (MCF-10A). The related mechanisms on cell growth inhibition of F1012-2 were demonstrated by inducing apoptosis in a caspase-dependent manner through the intrinsic pathway and extrinsic pathway. F1012-2 could also activate autophagy in TNBC cells. Simultaneously, we found that F1012-2-induced apoptosis was enhanced by inhibition of autophagy. Furthermore, F1012-2 could induce cell cycle arrest at G2/M phase with decreasing expression of cyclin B1, cdc2, and upregulating p21, p-cdc2. Also, F1012-2 activated Akt and p38 signalling pathways. In vivo, F1012-2 exhibited a potential antitumour effect in MDA-MB-231 xenografts without apparent toxicity. Taken together, our results identified that F1012-2 inhibited cell growth via multiple signalling pathways in vitro and in vivo. These data suggest that F1012-2 may be a potential natural active fraction for the treatment of TNBC.

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“…Anti-apoptotic protein Bcl-2 is involved in apoptosis pathway by heterodimerization with Bax 25. Some evidence shows that the expression of Bcl-2 was suppressed in VPA-induced ASD rats 26.…”

Section: Discussionmentioning

confidence: 99%

Rapamycin modulated brain-derived neurotrophic factor and B-cell lymphoma 2 to mitigate autism spectrum disorder in rats

Zhang¹,

Li²,

Ni³

2017

NDT

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The number of children suffered from autism spectrum disorder (ASD) is increasing dramatically. However, the etiology of ASD is not well known. This study employed mammalian target of rapamycin inhibitor rapamycin to explore its effect on ASD and provided new therapeutic strategies for ASD. ASD rat model was constructed and valproic acid (VPA) was injected intraperitoneally into rats on pregnancy day 12.5. Offspring from VPA group were divided into ASD group and ASD + rapamycin (ASD + RAPA) group. Compared with normal group, the frequency and duration of social behavior and straight times of ASD group were shortened, but the grooming times were extended. Meanwhile, in ASD group, the average escape latency and the frequency of crossing plates were decreased, the apoptotic index (AI) detected by TUNEL assay was increased, and the expression of brain-derived neurotrophic factor (BDNF) and B-cell lymphoma 2 (Bcl-2) analyzed was decreased with great difference compared with normal group (P<0.01). However, rapamycin treatment in ASD rats mitigated the ASD-like social behavior, such as the frequencies of straight and grooming. Furthermore, rapamycin shortened the average escape latency, but increased the frequency of crossing plates of ASD rats. In hippocampus, rapamycin decreased the AI, but increased the levels of BDNF and Bcl-2 (P<0.01) of ASD rats. These findings revealed that rapamycin significantly mitigated the social behavior by enhancing the expression of BDNF and Bcl-2 to suppress the hippocampus apoptosis in VPA-induced ASD rats.

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The Role of BCL-2 Family Members in Acute Kidney Injury

Cited by 43 publications

References 157 publications

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

F1012‐2 inhibits the growth of triple negative breast cancer through induction of cell cycle arrest, apoptosis, and autophagy

Rapamycin modulated brain-derived neurotrophic factor and B-cell lymphoma 2 to mitigate autism spectrum disorder in rats

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