Triacsin C reduces lipid droplet formation and induces mitochondrial biogenesis in primary rat hepatocytes

Dechandt, Carlos Roberto Porto; Reis, Fernando M. C. V.; Teodoro, Bruno Gonzaga; Fernandes, Anna Maria A. P.; Eberlin, Marcos N.; Kettelhut, Ísis C.; Curti, Carlos; Alberici, Luciane C.

doi:10.1007/s10863-017-9725-9

Cited by 22 publications

(15 citation statements)

References 40 publications

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“…Cell death, including apoptosis, seems important in the progression of NAFLD and NASH (Figure 1 ). Recently, several inhibitors of apoptosis have been suggested as potential treatments for NASH (Table 1 )[ 112 - 124 ]. Clinical trials for the treatment of NASH are currently being conducted[ 125 ] and some are targeting apoptosis in NASH patients.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis and non-alcoholic fatty liver diseases

Kanda

Matsuoka

Yamazaki

et al. 2018

WJG

195

130

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The number of patients with nonalcoholic fatty liver diseases (NAFLD) including nonalcoholic steatohepatitis (NASH), has been increasing. NASH causes cirrhosis and hepatocellular carcinoma (HCC) and is one of the most serious health problems in the world. The mechanism through which NASH progresses is still largely unknown. Activation of caspases, Bcl-2 family proteins, and c-Jun N-terminal kinase-induced hepatocyte apoptosis plays a role in the activation of NAFLD/NASH. Apoptotic hepatocytes stimulate immune cells and hepatic stellate cells toward the progression of fibrosis in the liver through the production of inflammasomes and cytokines. Abnormalities in glucose and lipid metabolism as well as microbiota accelerate these processes. The production of reactive oxygen species, oxidative stress, and endoplasmic reticulum stress is also involved. Cell death, including apoptosis, seems very important in the progression of NAFLD and NASH. Recently, inhibitors of apoptosis have been developed as drugs for the treatment of NASH and may prevent cirrhosis and HCC. Increased hepatocyte apoptosis may distinguish NASH from NAFLD, and the improvement of apoptosis could play a role in controlling the development of NASH. In this review, the association between apoptosis and NAFLD/NASH are discussed. This review could provide their knowledge, which plays a role in seeing the patients with NAFLD/NASH in daily clinical practice.

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Section: Discussionmentioning

confidence: 99%

Apoptosis and non-alcoholic fatty liver diseases

Kanda

Matsuoka

Yamazaki

et al. 2018

WJG

195

130

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“…See also Movie S3). On the other hand, when cells were pre-treated with triacsin C and 2-bromooctanoate, which are inhibitors of lipogenesis, 43,46 the de novo formation of mLDs was suppressed (Movie S4). This observation implies that free FAs, generated by lipolysis, are re-metabolized to TAGs, which are then accumulated in the ER to form mLDs.…”

Section: Resultsmentioning

confidence: 99%

A Fused Thiophene-S,S-Dioxide-Based Super-Photostable Fluorescent Marker for Lipid Droplets

Taki¹,

Kajiwara²,

Yamaguchi³

et al. 2020

Preprint

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Lipid droplets (LDs) are essential organelle in most eukaryotes, and tracking intracellular LDs dynamics using synthetic small molecules is crucial for biological studies. However, only a limited number of fluorescent markers that satisfy all requirements, such as the selective staining of LDs, high photostability, and sufficient biocompatibility, have been developed. Herein, we report a series of donor-p-acceptor dyes based on the thiophene-containing fused polycyclic scaffold [1]benzothieno[3,2-b][1]benzothiophene (BTBT), in which either or both thiophene rings are oxidized into thiophene-S,S-dioxide to form an electron-accepting building block. Among these dyes, LAQ1 satisfied all the aforementioned requirements, and allowed us capturing ultra-small LDs on the endoplasmic reticulum (ER) membrane by stimulation emission depletion (STED) microscopy with a super-resolution below the diffraction limit of light. Moreover, the extremely high photostability of LAQ1 enabled recording the lipolysis of LDs and the concomitant lipogenesis as well as long-term trajectory analysis of micro LDs at the single particle level in living cells.

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“…4A). Therefore, we treated RGB-FLAG cells with T.C, one of the few compounds that inhibit the formation of lipid droplets ( 37 , 38 ). To assess the effect of T.C, we detected the expression of perilipin 2 that is a prominent protein associated with the surface of lipid droplets and participates in the formation and stabilization of lipid droplets (fig.…”

Section: Resultsmentioning

confidence: 99%

Viperin catalyzes methionine oxidation to promote protein expression and function of helicases

et al. 2019

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Helicases play pivotal roles in fundamental biological processes, and posttranslational modifications regulate the localization, function, and stability of helicases. Here, we report that methionine oxidation of representative helicases, including DNA and RNA helicases of viral (ORF44 of KSHV) and cellular (MCM7 and RIG-I) origin, promotes their expression and functions. Cellular viperin, a major antiviral interferon-stimulated gene whose functions beyond host defense remain largely unknown, catalyzes the methionine oxidation of these helicases. Moreover, biochemical studies entailing loss-of-function mutations of helicases and a pharmacological inhibitor interfering with lipid metabolism and, hence, decreasing viperin activity indicate that methionine oxidation potently increases the stability and enzyme activity of these helicases that are critical for DNA replication and immune activation. Our work uncovers a pivotal role of viperin in catalyzing the methionine oxidation of helicases that are implicated in diverse fundamental biological processes.

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Triacsin C reduces lipid droplet formation and induces mitochondrial biogenesis in primary rat hepatocytes

Cited by 22 publications

References 40 publications

Apoptosis and non-alcoholic fatty liver diseases

Apoptosis and non-alcoholic fatty liver diseases

A Fused Thiophene-S,S-Dioxide-Based Super-Photostable Fluorescent Marker for Lipid Droplets

Viperin catalyzes methionine oxidation to promote protein expression and function of helicases

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