Endoplasmic reticulum stress suppresses lipin-1 expression in 3T3-L1 adipocytes

Takahashi, Nobuhiko; Yoshizaki, Takayuki; Hiranaka, Natsumi; Suzuki, Takahiko; Yui, Tomoo; Akanuma, M; Kanazawa, Kaoru; Yoshida, Mika; Naito, Sumiyoshi; Fujiya, Mikihiro; Kohgo, Yutaka; Ieko, Masahiro

doi:10.1016/j.bbrc.2012.12.112

Cited by 7 publications

(5 citation statements)

References 37 publications

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“…Although some cytokines such as TNFα and IL1β reduce adipose Lipin-1 expression [ 27 ], the mechanism by which the expression of Lipin-1 was impaired in adipose tissue in obesity states remains unclear. Recently, endoplasmic reticulum stress has been shown to be involved in the pathogenesis of obesity through suppression of the Lipin-1 expression in 3T3-L1 adipocytes [ 28 ]. On the other hand, cytochromes P450, notably those belonging to the CYP1 family, can induce endoplasmic reticulum stress [ 29 ], and interestingly, our results show that combination of BaP and PCB118 induces CYP1A1 expression in adipocytes.…”

Section: Discussionmentioning

confidence: 99%

In Vitro Cocktail Effects of PCB-DL (PCB118) and Bulky PCB (PCB153) with BaP on Adipogenesis and on Expression of Genes Involved in the Establishment of a Pro-Inflammatory State

May¹,

Bremond²,

Sauzet³

et al. 2018

IJMS

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(1) Objective: Highlight the in vitro effects of 3T3-L1 cell exposure to polychlorinated biphenyls (PCB118 and 153) or benzo(a)pyrene (BaP) alone or as a cocktail on adipogenesis (ADG) by focusing on changes in lipid metabolism and inflammatory-related genes expression (INFG) and ADG-related genes expression (ADGG); (2) Results: Treatment from the early stage of cell differentiation by BaP alone or in combination with PCBs decreased the expression of some of the ADGG (PPARγ Glut-4, FAS, Lipin-1a, Leptin, and Adiponectin). BaP enhanced the INFG, especially MCP-1 and TNFα. Co-exposure to BaP and PCB153 showed a synergistic effect on TNFα and IL6 expression. Treatment with BaP and PCBs during only the maturation period up-regulated the INFG (IL6, TNFα, CXCL-10 & MCP-1). PCB118 alone also enhanced TNFα, CXCL-10, and PAI-1 expression. The change in MCP-1 protein expression was in agreement with that of the gene. Finally, the BaP-induced up-regulation of the xenobiotic responsive element (XRE)-controlled luciferase activity was impaired by PCB153 but not by PCB118; (3) Conclusion: BaP and PCBs down-regulate a part of ADGG and enhance INFG. The direct regulatory effect of PCBs on both ADGG and INFG is usually rather lower than that of BaP and synergistic or antagonistic cocktail effects are clearly observed.

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Section: Discussionmentioning

confidence: 99%

In Vitro Cocktail Effects of PCB-DL (PCB118) and Bulky PCB (PCB153) with BaP on Adipogenesis and on Expression of Genes Involved in the Establishment of a Pro-Inflammatory State

May¹,

Bremond²,

Sauzet³

et al. 2018

IJMS

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“…Studies have shown that lipin1 expression is inhibited by treatment with ER stress inducers (tunicamycin and thapsigargin) in 3T3-L1 adipocytes, while activation of PPAR-γ restores the ER stress-induced lipin1 suppression, suggesting the involvement of PPAR-γ in the inhibitory effect of ER stress on lipin1 expression [60]. In addition, ER stress induces lipin2 expression in the liver, but has a limited effect on lipin2 expression in adipocytes, indicating that the role of ER stress in the expression of lipin family genes is tissue-dependent [60,61]. The expression of lipin1 in the uterus and liver is remarkably suppressed by estrogen, demonstrating that there is a potential role for lipin1 in uterine function and reproductive biology [62].…”

Section: Regulation Of Lipin Proteins Activity and Expressionmentioning

confidence: 99%

Lipin Family Proteins - Key Regulators in Lipid Metabolism

Chen

Rui²,

Tang³

et al. 2014

Ann Nutr Metab

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Background: Proteins in the lipin family play a key role in lipid synthesis due to their phosphatidate phosphatase activity, and they also act as transcriptional coactivators to regulate the expression of genes involved in lipid metabolism. The lipin family includes three members, lipin1, lipin2, and lipin3, which exhibit tissue-specific expression, indicating that they may have distinct roles in mediating disease. To date, most studies have focused on lipin1, whereas the roles of lipin2 and lipin3 are less understood. Summary: This review introduces the structural characteristics, physiological functions, relationship to lipid metabolism, and patterns of expression of the lipin family proteins, highlighting their roles in lipid metabolic homeostasis. © 2014 S. Karger AG, Basel

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“…In addition to regulation of autophagy, lipin-1 has been implicated in circadian rhythms and ER stress response (80–82). Aberrant circadian rhythms and ER stress are associated with pathogenesis of alcoholic liver disease (2,3,40,83–85).…”

Section: Resultsmentioning

confidence: 99%

Signal Transduction Mechanisms of Alcoholic Fatty Liver Disease: Emer ging Role of Lipin-1

You¹,

Jogasuria²,

Lee³

et al. 2017

CMP

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Lipin-1, a mammalian phosphatidic acid phosphatase (PAP), is a bi-functional molecule involved in various signaling pathways via its function as a PAP enzyme in the triglyceride synthesis pathway and in the nucleus as a transcriptional co-regulator. In the liver, lipin-1 is known to play a vital role in controlling the lipid metabolism and inflammation process at multiple regulatory levels. Alcoholic fatty liver disease (AFLD) is one of the earliest forms of liver injury and approximately 8–20% of patients with simple steatosis can develop into more severe forms of liver injury, including steatohepatitis, fibrosis/cirrhosis, and eventually hepatocellular carcinoma (HCC). The signal transduction mechanisms for alcohol-induced detrimental effects in liver involves alteration of complex and multiple signaling pathways largely governed by a central and upstream signaling system, namely, sirtuin 1 (SIRT1)-AMP activated kinase (AMPK) axis. Emerging evidence suggests a pivotal role of lipin-1 as a crucial downstream regulator of SIRT1-AMPK signaling system that is likely to be ultimately responsible for development and progression of AFLD. Several lines of evidence demonstrate that ethanol exposure significantly induces lipin-1 gene and protein expression levels in cultured hepatocytes and in the livers of rodents, induces lipin-1-PAP activity, impairs the functional activity of nuclear lipin-1, disrupts lipin-1 mRNA alternative splicing and induces lipin-1 nucleocytoplasmic shuttling. Such impairment in response to ethanol leads to derangement of hepatic lipid metabolism, and excessive production of inflammatory cytokines in the livers of the rodents and human alcoholics. This review summarizes current knowledge about the role of lipin-1 in the pathogenesis of AFLD and its potential signal transduction mechanisms.

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Endoplasmic reticulum stress suppresses lipin-1 expression in 3T3-L1 adipocytes

Cited by 7 publications

References 37 publications

In Vitro Cocktail Effects of PCB-DL (PCB118) and Bulky PCB (PCB153) with BaP on Adipogenesis and on Expression of Genes Involved in the Establishment of a Pro-Inflammatory State

In Vitro Cocktail Effects of PCB-DL (PCB118) and Bulky PCB (PCB153) with BaP on Adipogenesis and on Expression of Genes Involved in the Establishment of a Pro-Inflammatory State

Lipin Family Proteins - Key Regulators in Lipid Metabolism

Signal Transduction Mechanisms of Alcoholic Fatty Liver Disease: Emer ging Role of Lipin-1

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