α-Linolenic acid protects renal cells against palmitic acid lipotoxicity via inhibition of endoplasmic reticulum stress

Katsoulieris, Elias; Mabley, Jon G.; Samai, Mohamed; Green, Irene C.; Chatterjee, Prabal K.

doi:10.1016/j.ejphar.2009.09.015

Cited by 61 publications

(47 citation statements)

References 54 publications

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“…2-DCB was also shown to induce single-strand DNA damage in LT97 and HT 29 human colon adenoma cells [6,7]. Additionally, some studies showed that PA can induce apoptosis in various cells such as human lung carcinoma cells, hepatocytes, and renal cells [8,10,11,14,31]. However, the effect of 2-DCB on apoptosis is not known.…”

Section: Discussionmentioning

confidence: 96%

“…The degrees of cytotoxicity and genotoxicity are dependent on fatty acid chain length and the degree of unsaturation of the fatty acid chain [7]. Recent studies showed that PA could induce apoptosis in human lung carcinoma cells, hepatocytes, renal cells, smooth muscle cells and endothelial progenitor cells [8][9][10][11][12]. The mechanisms of apoptosis induced by PA are involved in endoplasmic reticulum stress, mitochondrial dysfunction, PKC activation and increased oxidative stress [10,[13][14][15][16].…”

Section: Introductionmentioning

confidence: 98%

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Molecular mechanisms of apoptosis induction by 2-dodecylcyclobutanone, a radiolytic product of palmitic acid, in human lymphoma U937 cells

Zhao

Furuta

et al. 2012

Apoptosis

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The irradiation of fat-containing food forms 2-dodecylcyclobutanone (2-DCB) from palmitic acid (PA). In this study, we investigated whether 2-DCB and PA induce apoptosis in human lymphoma U937 cells. We found that cell viability decreased by 2-DCB and apoptosis was induced by 2-DCB and PA. 2-DCB and PA significantly enhanced the formation of intracellular reactive oxygen species (ROS). Apoptosis induced by 2-DCB and PA was strongly prevented by an antioxidant, N-acetyl-L: -cysteine. The treatment with 2-DCB and PA resulted in the loss of mitochondrial membrane potential, and Fas, caspase-8 and caspase-3 activation. Pretreatment with a pan-caspase inhibitor (z-VAD) significantly inhibited apoptosis induced by 2-DCB and PA. Moreover, 2-DCB and PA also induced Bax up-regulation, the reduction in Bcl-2 expression level, Bid cleavage and the release of cytochrome c from the mitochondria to the cytosol. In addition, an increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) was observed after the treatment with 2-DCB and PA. Our results indicated that intracellular ROS generation, the modulation of the Fas-mitochondrion-caspase-dependent pathway and the increase in [Ca(2+)](i) involved in apoptosis are induced by 2-DCB and PA in U937 cells.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 98%

Molecular mechanisms of apoptosis induction by 2-dodecylcyclobutanone, a radiolytic product of palmitic acid, in human lymphoma U937 cells

Zhao

Furuta

et al. 2012

Apoptosis

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“…A further study determined the potency of salubrinal in ameliorating neurotoxicity produced by cyclosporine-induced endoplasmic reticulum stress response in rats (Gasparetto et al, 2004). Furthermore, salubrinal has been used in the treatment of patients with urinary disease (Katsoulieris et al, 2009) and diabetes (Cnop et al, 2007). A more recent study has shown that salubrinal can effectively inhibit cardiomyocyte apoptosis induced by tunicamycin or hypoxia, possibly by its regulation of the pERK-eIF2α signaling pathway (Liu et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Role of salubrinal in protecting cardiomyocytes from doxorubicin-induced apoptosis

Gong¹,

Wu²,

Liang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We determined whether salubrinal can protect cardiomyocytes from doxorubicin-induced apoptosis and explored the related mechanisms to provide experimental evidence for exploring novel drug candidates to decrease cardiac toxicity. Neonatal rat cardiomyocytes were isolated, cultured in vitro, and pretreated with salubrinal (10, 20, or 40 μM) to observe their response to doxorubicin-induced cell apoptosis. Lactate dehydrogenase assay, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling staining, and flow cytometry were used to assess the extent of cardiomyocyte apoptosis. Fluorescent probes conjugated with 2',7'-dichlorofluorescein diacetate and a chemiluminescence assay were used to detect the production of reactive oxygen species. Western blotting was employed to quantify expression levels of cleaved caspase-3, cytosolic cytochrome c, and B-cell lymphoma-extra large (Bcl-xL). The mechanisms of salubrinal-related functions were also explored. Salubrinal effectively inhibited doxorubicin-induced reactive oxygen species production and N. Gong et al.

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“…Decreased SGLT2 expression in HFD mice indicated that HFD induced proximal renal tubule injury, while GLP-1 treatment attenuated the disorder. Fatty acids have been proved to activate ERS in animal and human mesangial cells, podocytes, proximal tubular cells, and the tubulointerstitium [3, 21, 22]. ERS contributed to the pathophysiology of renal injury according to aberrant metabolic conditions, such as hyperglycemia and hyperlipidemia [3].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Glucagon-Like Peptide-1 Analog on Renal Tubular Injury in Mice on High-Fat Diet

Guo

Wang

et al. 2017

Cell Physiol Biochem

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Aims: The study aimed to investigate the renoprotective effect of glucagon-like peptide-1 (GLP-1) against renal tubular injury in C57BL/6 mice induced by a high-fat diet (HFD). Methods: Twenty C57BL/6 mice were fed HFD for 12 weeks. Ten of these mice were treated with GLP-1 at 200 µg/kg subcutaneously twice daily for 4 weeks (HFDG group), and the other ten mice received vehicle only (HFD group). Ten mice fed standard rodent chow served as controls (Con group). Body weight, kidney weight, food intake, and systolic blood pressure were measured. The expression of endoplasmic reticulum stress (ERS) markers (BIP, p-eIF2α, ATF4, and CHOP) and apoptosis in the kidney were examined utilizing western blotting, immunohistochemistry and TUNEL, respectively. Angiotensin II and angiotensin II type 1 receptor (AT1R) were examined by ELISA. Human proximal tubule epithelial cells (HK2) were treated with GLP-1(150 nM) followed by treatment with palmitic acid (500 nM [PA]) for 24 h. HK2 cells treated with BSA were used as controls. The protein levels of ERS markers, apoptosis-associated protein, and AT1R were measured by western blotting. Results: Increase of body weight, food intake, and systolic blood pressure was less pronounced in GLP-1 treated HFDG mice compared to HFD mice. The levels of ERS markers (BIP, p-eIF2α, ATF4, and CHOP) and apoptosis decreased following GLP-1 treatment in vivo and in vitro (p<0.05). Increased AT1R induced by HFD and PA were blocked with GLP-1 treatment. In contrast, the level of angiotensin II after GLP-1 treatment was not significantly different between the HFD and HFDG mice. Conclusion: The study indicated that saturated fatty acids induced ERS and apoptosis in the kidney and increased AT1R expression. GLP-1 treatment exerted renoprotective effects against saturated fatty acid-induced kidney tubular cell ERS and apoptosis together with inhibition of AT1R expression in vivo and in vitro.

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α-Linolenic acid protects renal cells against palmitic acid lipotoxicity via inhibition of endoplasmic reticulum stress

Cited by 61 publications

References 54 publications

Molecular mechanisms of apoptosis induction by 2-dodecylcyclobutanone, a radiolytic product of palmitic acid, in human lymphoma U937 cells

Molecular mechanisms of apoptosis induction by 2-dodecylcyclobutanone, a radiolytic product of palmitic acid, in human lymphoma U937 cells

Role of salubrinal in protecting cardiomyocytes from doxorubicin-induced apoptosis

Protective Effects of Glucagon-Like Peptide-1 Analog on Renal Tubular Injury in Mice on High-Fat Diet

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