Oleate protects macrophages from palmitate-induced apoptosis through the downregulation of CD36 expression

Kim, Dong Hee; Cho, Yoon Mi; Lee, Kyung Hye; Jeong, Seong-Whan; Kwon, Oh-Joo

doi:10.1016/j.bbrc.2017.05.066

Cited by 42 publications

(31 citation statements)

References 22 publications

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“…There was no change in palmitate uptake or palmitate incorporation into ceramide following overnight oleate treatment. This is counter to the recent report that oleate cotreatment of RAW264.7 macrophage cells prevented the palmitateinduced increase in the mRNA level of the FA transporter CD36 (Kim et al, 2017), hinting at cell type-specific mechanisms. Collectively, oleate and FA treatment influences MCF-7 and MDA-MB-231 cell palmitate metabolism and thereby avoid the deleterious effects of lipotoxicity.…”

Section: Discussioncontrasting

confidence: 99%

“…Palmitate also impairs MDA‐MB‐231 cell proliferation and activates apoptosis (Baumann et al ., 2016; Hardy et al ., 2000, 2003; Kourtidis et al ., 2009; Wu et al ., 2017) via a number of mechanisms, including ER stress (Baumann et al ., 2016; Boslem et al ., 2011), impaired autophagy (RostamiRad et al ., 2018; Wu et al ., 2017), altered NAD metabolism (Penke et al ., 2017), and ceramide synthesis (Luo et al ., 2017). Importantly, many of the deleterious effects of palmitate on cellular function are mitigated by cotreatment with other FAs, in particular the monounsaturated FA oleate (Colvin et al ., 2017; Kim et al ., 2017; Penke et al ., 2017; Sargsyan et al ., 2016), which itself is pro‐proliferative and activates phosphoinositide 3‐kinase signaling (Hardy et al ., 2000). …”

Section: Discussionmentioning

confidence: 99%

“…Our results shed new light on the contribution of FA oxidation in MCF‐7 cells where pharmacological inhibition of FA oxidation sensitized MCF‐7 cells to palmitate‐induced apoptosis and suggests that targeting FA oxidation is an attractive therapeutic strategy in BrCa. The addition or presence of oleate ameliorates the cytotoxic effects of palmitate (Capel et al ., 2016; Colvin et al ., 2017; Kim et al ., 2017; Kwon and Querfurth, 2015; Penke et al ., 2017; Sargsyan et al ., 2016). Proposed mechanisms for these observations include attenuating palmitate‐induced ER stress (Colvin et al ., 2017), preventing activation of the unfolded protein response (Sommerweiss et al ., 2013), activating prosurvival pathways of ER stress (Sargsyan et al ., 2016), restoring insulin stimulated protein kinase B (Akt) signaling (Capel et al ., 2016), and activating AMP‐activated protein kinase and mechanistic target of rapamycin signaling (Kwon and Querfurth, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…Exposure to elevated levels of the saturated FA palmitate induces apoptosis in a range of cells including 3T3 fibroblasts (Kamili et al, 2015), peripheral blood mononuclear cells (RostamiRad et al, 2018), human cardiac progenitor cells (Leonardini et al, 2017), pancreatic b cells (Boslem et al, 2011;Luo et al, 2017), macrophages (Kim et al, 2017), and hepatocytes (Penke et al, 2017). Palmitate also impairs MDA-MB-231 cell proliferation and activates apoptosis (Baumann et al, 2016;Hardy et al, 2000Hardy et al, , 2003Kourtidis et al, 2009;Wu et al, 2017) via a number of mechanisms, including ER stress (Baumann et al, 2016;Boslem et al, 2011), impaired autophagy (RostamiRad et al, 2018Wu et al, 2017), altered NAD metabolism (Penke et al, 2017), and ceramide synthesis (Luo et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

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Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

et al. 2018

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Breast cancer (BrCa) metabolism is geared toward biomass synthesis and maintenance of reductive capacity. Changes in glucose and glutamine metabolism in BrCa have been widely reported, yet the contribution of fatty acids (FAs) in BrCa biology remains to be determined. We recently reported that adipocyte coculture alters MCF‐7 and MDA‐MB‐231 cell metabolism and promotes proliferation and migration. Since adipocytes are FA‐rich, and these FAs are transferred to BrCa cells, we sought to elucidate the FA metabolism of BrCa cells and their response to FA‐rich environments. MCF‐7 and MDA‐MB‐231 cells incubated in serum‐containing media supplemented with FAs accumulate extracellular FAs as intracellular triacylglycerols (TAG) in a dose‐dependent manner, with MDA‐MB‐231 cells accumulating more TAG. The differences in TAG levels were a consequence of distinct differences in intracellular partitioning of FAs, and not due to differences in the rate of FA uptake. Specifically, MCF‐7 cells preferentially partition FAs into mitochondrial oxidation, whereas MDA‐MB‐231 cells partition FAs into TAG synthesis. These differences in intracellular FA handling underpin differences in the sensitivity to palmitate‐induced lipotoxicity, with MDA‐MB‐231 cells being highly sensitive, whereas MCF‐7 cells are partially protected. The attenuation of palmitate‐induced lipotoxicity in MCF‐7 cells was reversed by inhibition of FA oxidation. Pretreatment of MDA‐MB‐231 cells with FAs increased TAG synthesis and reduced palmitate‐induced apoptosis. Our results provide novel insight into the potential influences of obesity on BrCa biology, highlighting distinct differences in FA metabolism in MCF‐7 and MDA‐MB‐231 cells and how lipid‐rich environments modulate these effects.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

et al. 2018

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“…CD36, also known as platelet glycoprotein 4, fatty acid translocase (FAT), is a multifunctional membrane protein found on the surfaces of various cell types including cardiomyocytes. Kim, et al have reported that the saturated fatty acid, palmitate, signi icantly induced lipotoxic cell death in RAW264.7 macrophages, which was antagonized by the monounsaturated fatty acid, oleate, through the down-regulation of CD36 expression [67]. In addition, the treatment of high density lipoprotein (HDL) reversed palmatic acid-induced lipotoxicity and energy metabolism imbalance in H9c2 cardiomyoblast cells and in neonatal rat cardiomyocytes [68].…”

Section: Low-density Lipoprotein Receptorsmentioning

confidence: 99%

Lipid-induced cardiovascular diseases

Manandhar¹,

Ju²,

Choi³

et al. 2017

J Cardiol Cardiovasc Med

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Cardiovascular diseases are the leading cause of death worldwide. There are many evidences that the dysfunctioning lipotoxicity is the one of major factors of cardiovascular diseases such as, atherosclerosis, hypertension, and coronary heart disease. Obesity and diabetes increase circulating lipids that are likely with more generation of toxic intermediates, which leading to the complications associated with cardiovascular diseases. Indeed, lipotoxicity is a metabolic syndrome caused by abnormal lipid accumulation, which leads to cellular dysfunction and necrosis. Here we review the factors that induced pathogenesis of cardiovascular diseases by lipid accumulation and the mechanisms underlying the lipotoxicity.

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Pequi Oil, a MUFA/Carotenoid‐Rich Oil, Exhibited Protective Effects against DSS‐Induced Ulcerative Colitis in Mice

Moreno

Evangelista‐Silva

Santos

et al. 2021

Euro J Lipid Sci & Tech

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Inflammatory bowel diseases (IBD) affect the gastrointestinal tract, and the imbalance of intestinal immune homeostasis can trigger them. Pequi oil (PO), a monounsaturated (MUFA) and carotenoid-rich food with nutraceutical potential, could help reshape the intestinal immune response, ameliorating IBD outcomes. This study investigates the effects of a 28 days intake of PO on elements of the intestinal immune response of mice with DSS-induced ulcerative colitis (disease activity index, colonic damage, inflammatory cells and markers). PO reduces body weight, colonic crypt and goblet cell losses and ameliorates diarrhea. In the colon, it increases T cells and secretory-IgA and decreases CD8+T cells. In lymphoid organs, it reduces CD8+T cells. Moreover, it also reduces the IL-17 and CRP in plasma. PO oil promotes a less cytotoxic response that may protect mice from immunological injuries caused by an IBD in the intestinal mucosa, improving the disease prognosis. Practical applications: This study demonstrates that the intake of pequi oil contributes to the regulation of immune response and improves clinical and histological signs of DSS-induced ulcerative colitis in mice. Its effects in cytotoxic cell reduction and other inflammatory markers and stimulation of regulatory cells, and preservation of mucus-producing cells, provide news insights about the importance of the regular intake of this food to better prognosis of ulcerative colitis acute episodes. In addition, these findings encourage further studies with foods with a protective potential for the intestinal mucosa.

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Oleate protects macrophages from palmitate-induced apoptosis through the downregulation of CD36 expression

Cited by 42 publications

References 22 publications

Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

Lipid-induced cardiovascular diseases

Pequi Oil, a MUFA/Carotenoid‐Rich Oil, Exhibited Protective Effects against DSS‐Induced Ulcerative Colitis in Mice

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