Sodium hydrosulphide restores tumour necrosis factor-α-induced mitochondrial dysfunction and metabolic dysregulation in HL-1 cells

Ting I. Lee, Yu Hsun Kao, Lkhagva Baigalmaa, Ting Wei Lee, Yen Yu Lu, Yao Chang Chen, Tze Fan Chao, Yi Jen Chen

Research output: Contribution to journalArticle

Abstract

Tumour necrosis factor (TNF)-α induces cardiac metabolic disorder and mitochondrial dysfunction. Hydrogen sulphide (H2S) contains anti-inflammatory and biological effects in cardiomyocytes. This study investigated whether H2S modulates TNF-α-dysregulated mitochondrial function and metabolism in cardiomyocytes. HL-1 cells were incubated with TNF-α (25 ng/mL) with or without sodium hydrosulphide (NaHS, 0.1 mmol/L) for 24 hours. Cardiac peroxisome proliferator-activated receptor (PPAR) isoforms, pro-inflammatory cytokines, receptor for advanced glycation end products (RAGE) and fatty acid metabolism were evaluated through Western blotting. The mitochondrial oxygen consumption rate and adenosine triphosphate (ATP) production were investigated using Seahorse XF24 extracellular flux analyzer and bioluminescence assay. Fluorescence intensity using 2′, 7′-dichlorodihydrofluorescein diacetate was used to evaluate mitochondrial oxidative stress. NaHS attenuated the impaired basal and maximal respiration, ATP production and ATP synthesis and enhanced mitochondrial oxidative stress in TNF-α-treated HL-1 cells. TNF-α-treated HL-1 cells exhibited lower expression of PPAR-α, PPAR-δ, phosphorylated 5′ adenosine monophosphate-activated protein kinase-α2, phosphorylated acetyl CoA carboxylase, carnitine palmitoyltransferase-1, PPAR-γ coactivator 1-α and diacylglycerol acyltransferase 1 protein, but higher expression of PPAR-γ, interleukin-6 and RAGE protein than control or combined NaHS and TNF-α-treated HL-1 cells. NaHS modulates the effects of TNF-α on mitochondria and the cardiometabolic system, suggesting its therapeutic potential for inflammation-induced cardiac dysfunction.

Original languageEnglish
JournalJournal of Cellular and Molecular Medicine
DOIs
Publication statusAccepted/In press - Jan 1 2019

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Peroxisome Proliferator-Activated Receptors
Tumor Necrosis Factor-alpha
Adenosine Triphosphate
Cardiac Myocytes
Oxidative Stress
Diacylglycerol O-Acyltransferase
Smegmamorpha
Carnitine O-Palmitoyltransferase
Interleukin-6 Receptors
Acetyl-CoA Carboxylase
Mitochondrial Diseases
Hydrogen Sulfide
Cytokine Receptors
Adenosine Monophosphate
sodium bisulfide
Oxygen Consumption
Protein Kinases
Mitochondria
Protein Isoforms
Respiration

Keywords

  • fatty acid metabolism
  • HL-1 cardiomyocytes
  • peroxisome proliferator-activated receptors
  • proinflammatory cytokines
  • receptor for advanced glycation end
  • sodium hydrosulphide

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology

Cite this

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title = "Sodium hydrosulphide restores tumour necrosis factor-α-induced mitochondrial dysfunction and metabolic dysregulation in HL-1 cells",
abstract = "Tumour necrosis factor (TNF)-α induces cardiac metabolic disorder and mitochondrial dysfunction. Hydrogen sulphide (H2S) contains anti-inflammatory and biological effects in cardiomyocytes. This study investigated whether H2S modulates TNF-α-dysregulated mitochondrial function and metabolism in cardiomyocytes. HL-1 cells were incubated with TNF-α (25 ng/mL) with or without sodium hydrosulphide (NaHS, 0.1 mmol/L) for 24 hours. Cardiac peroxisome proliferator-activated receptor (PPAR) isoforms, pro-inflammatory cytokines, receptor for advanced glycation end products (RAGE) and fatty acid metabolism were evaluated through Western blotting. The mitochondrial oxygen consumption rate and adenosine triphosphate (ATP) production were investigated using Seahorse XF24 extracellular flux analyzer and bioluminescence assay. Fluorescence intensity using 2′, 7′-dichlorodihydrofluorescein diacetate was used to evaluate mitochondrial oxidative stress. NaHS attenuated the impaired basal and maximal respiration, ATP production and ATP synthesis and enhanced mitochondrial oxidative stress in TNF-α-treated HL-1 cells. TNF-α-treated HL-1 cells exhibited lower expression of PPAR-α, PPAR-δ, phosphorylated 5′ adenosine monophosphate-activated protein kinase-α2, phosphorylated acetyl CoA carboxylase, carnitine palmitoyltransferase-1, PPAR-γ coactivator 1-α and diacylglycerol acyltransferase 1 protein, but higher expression of PPAR-γ, interleukin-6 and RAGE protein than control or combined NaHS and TNF-α-treated HL-1 cells. NaHS modulates the effects of TNF-α on mitochondria and the cardiometabolic system, suggesting its therapeutic potential for inflammation-induced cardiac dysfunction.",
keywords = "fatty acid metabolism, HL-1 cardiomyocytes, peroxisome proliferator-activated receptors, proinflammatory cytokines, receptor for advanced glycation end, sodium hydrosulphide",
author = "Lee, {Ting I.} and Kao, {Yu Hsun} and Lkhagva Baigalmaa and Lee, {Ting Wei} and Lu, {Yen Yu} and Chen, {Yao Chang} and Chao, {Tze Fan} and Chen, {Yi Jen}",
year = "2019",
month = "1",
day = "1",
doi = "10.1111/jcmm.14637",
language = "English",
journal = "Journal of Cellular and Molecular Medicine",
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T1 - Sodium hydrosulphide restores tumour necrosis factor-α-induced mitochondrial dysfunction and metabolic dysregulation in HL-1 cells

AU - Lee, Ting I.

AU - Kao, Yu Hsun

AU - Baigalmaa, Lkhagva

AU - Lee, Ting Wei

AU - Lu, Yen Yu

AU - Chen, Yao Chang

AU - Chao, Tze Fan

AU - Chen, Yi Jen

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Tumour necrosis factor (TNF)-α induces cardiac metabolic disorder and mitochondrial dysfunction. Hydrogen sulphide (H2S) contains anti-inflammatory and biological effects in cardiomyocytes. This study investigated whether H2S modulates TNF-α-dysregulated mitochondrial function and metabolism in cardiomyocytes. HL-1 cells were incubated with TNF-α (25 ng/mL) with or without sodium hydrosulphide (NaHS, 0.1 mmol/L) for 24 hours. Cardiac peroxisome proliferator-activated receptor (PPAR) isoforms, pro-inflammatory cytokines, receptor for advanced glycation end products (RAGE) and fatty acid metabolism were evaluated through Western blotting. The mitochondrial oxygen consumption rate and adenosine triphosphate (ATP) production were investigated using Seahorse XF24 extracellular flux analyzer and bioluminescence assay. Fluorescence intensity using 2′, 7′-dichlorodihydrofluorescein diacetate was used to evaluate mitochondrial oxidative stress. NaHS attenuated the impaired basal and maximal respiration, ATP production and ATP synthesis and enhanced mitochondrial oxidative stress in TNF-α-treated HL-1 cells. TNF-α-treated HL-1 cells exhibited lower expression of PPAR-α, PPAR-δ, phosphorylated 5′ adenosine monophosphate-activated protein kinase-α2, phosphorylated acetyl CoA carboxylase, carnitine palmitoyltransferase-1, PPAR-γ coactivator 1-α and diacylglycerol acyltransferase 1 protein, but higher expression of PPAR-γ, interleukin-6 and RAGE protein than control or combined NaHS and TNF-α-treated HL-1 cells. NaHS modulates the effects of TNF-α on mitochondria and the cardiometabolic system, suggesting its therapeutic potential for inflammation-induced cardiac dysfunction.

AB - Tumour necrosis factor (TNF)-α induces cardiac metabolic disorder and mitochondrial dysfunction. Hydrogen sulphide (H2S) contains anti-inflammatory and biological effects in cardiomyocytes. This study investigated whether H2S modulates TNF-α-dysregulated mitochondrial function and metabolism in cardiomyocytes. HL-1 cells were incubated with TNF-α (25 ng/mL) with or without sodium hydrosulphide (NaHS, 0.1 mmol/L) for 24 hours. Cardiac peroxisome proliferator-activated receptor (PPAR) isoforms, pro-inflammatory cytokines, receptor for advanced glycation end products (RAGE) and fatty acid metabolism were evaluated through Western blotting. The mitochondrial oxygen consumption rate and adenosine triphosphate (ATP) production were investigated using Seahorse XF24 extracellular flux analyzer and bioluminescence assay. Fluorescence intensity using 2′, 7′-dichlorodihydrofluorescein diacetate was used to evaluate mitochondrial oxidative stress. NaHS attenuated the impaired basal and maximal respiration, ATP production and ATP synthesis and enhanced mitochondrial oxidative stress in TNF-α-treated HL-1 cells. TNF-α-treated HL-1 cells exhibited lower expression of PPAR-α, PPAR-δ, phosphorylated 5′ adenosine monophosphate-activated protein kinase-α2, phosphorylated acetyl CoA carboxylase, carnitine palmitoyltransferase-1, PPAR-γ coactivator 1-α and diacylglycerol acyltransferase 1 protein, but higher expression of PPAR-γ, interleukin-6 and RAGE protein than control or combined NaHS and TNF-α-treated HL-1 cells. NaHS modulates the effects of TNF-α on mitochondria and the cardiometabolic system, suggesting its therapeutic potential for inflammation-induced cardiac dysfunction.

KW - fatty acid metabolism

KW - HL-1 cardiomyocytes

KW - peroxisome proliferator-activated receptors

KW - proinflammatory cytokines

KW - receptor for advanced glycation end

KW - sodium hydrosulphide

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U2 - 10.1111/jcmm.14637

DO - 10.1111/jcmm.14637

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