Mitochondrial dynamic remodeling in strenuous exercise-induced muscle and mitochondrial dysfunction: Regulatory effects of hydroxytyrosol

Feng, Zhihui; Bai, Li‐Yuan; Yan, Jingbo; Li, Yuan; Shen, Weili; Wang, Ying; Wertz, Karin; Weber, Peter; Zhang, Yong; Chen, Yan; Liu, Jiankang

doi:10.1016/j.freeradbiomed.2011.03.001

Cited by 99 publications

(87 citation statements)

References 56 publications

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“…In vitro, hydroxytyrosol (1-10 mM) activates PGC-1a through SIRT1 deacetylation and induces mitochondrial biogenesis in 3T3-L1 murine adipocytes and in ARPE-19 human retinal pigment epithelial cells (Zhu et al, 2010). The administration of hydroxytyrosol to rats (25 mg/kg daily during 8 weeks) by the same investigators stimulated PGC-1a activity and the expression of mitochondrial biogenesis markers in skeletal muscle of both treadmill-exercised and sedentary animals, and increased their endurance (Feng et al, 2011). The authors noted that in contrast to the mitochondrial biogenesis-inducing effect of moderate exercise, extreme exercise was associated with lower PGC-1a levels.…”

Section: Polyphenols and Other Natural Productsmentioning

confidence: 95%

Mitochondrial Quality Control as a Therapeutic Target

2015

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Section: Polyphenols and Other Natural Productsmentioning

confidence: 95%

Mitochondrial Quality Control as a Therapeutic Target

2015

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“…Mitochondrial complex activity assays Mitochondria isolation from cultured mouse C2C12 myoblasts, myotubes and skeletal muscle tissues were performed as previously described [27,28]. Mitochondrial complex activities were measured by spectrophotometer as described in previous reports [29,30].…”

Section: Methodsmentioning

confidence: 99%

O-GlcNAcase deficiency suppresses skeletal myogenesis and insulin sensitivity in mice through the modulation of mitochondrial homeostasis

et al. 2016

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Aims/hypothesis O-GlcNAcylation is implicated in modulating mitochondrial function, which is closely involved in regulating muscle metabolism. The presence of O-GlcNAcase (OGA), the enzyme involved in the removal of O-GlcNAc, in mitochondria was recently confirmed in rats. In the present study, we investigated the regulation of myogenesis and muscle insulin sensitivity to OGA in mice, with a focus on mitochondria. Methods C57BL/6J mice fed a high-fat diet for 4 months were used to observe mitochondrial density, activity and O-GlcNAcylation in muscle. Small interfering RNA and overexpression vectors were used to modulate protein content in vitro. Results High-fat feeding decreased the OGA level and largely increased mitochondrial O-GlcNAcylation in mouse skeletal muscle that was accompanied by decreased levels of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), decreased mitochondrial density and disrupted mitochondrial complex activities. Knockdown of OGA in C2C12 myoblasts promoted PGC-1α degradation, resulting in the suppression of mitochondrial biogenesis and myogenesis, whereas neither knockdown of O-GlcNAc transferase nor overexpression of OGA had significant effects on myogenesis. Mitochondrial dysfunction as evidenced by decreased ATP content and increased reactive oxygen species production, and increased lipid and protein oxidation was observed in both myoblasts and myotubes after OGA knockdown. Meanwhile, elevated O-GlcNAcylation through either OGA knockdown or treatment with the OGA inhibitor PUGNAc and the O-GlcNAc transferase substrate D-GlcNAc suppressed myotube insulin signalling transduction and glucose uptake. OGA overexpression had no significant effect on insulin sensitivity but sufficiently improved the insulin resistance induced by D-GlcNAc treatment. Conclusions/interpretation These data suggest that OGA can modulate mitochondrial density via PGC-1α and mitochondrial function via protein O-GlcNAcylation. In this manner, OGA appears to play a key role in myogenesis and the development of muscle insulin resistance.

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“…« was assessed as previously described (Feng et al, 2011). Briefly, cells were incubated with 5 mol/L 5,5 ,6,6 -tetrachloro-1,1 ,3,3 -tetraethylbenzimidazolyl-carbocyanine iodide (JC-1) (Invitrogen) at 37 • C for 60 min.…”

Section: Jc-1 Assay For Mitochondrial Membrane Potential ( « )mentioning

confidence: 99%

“…Western blots were performed as previously described (Feng et al, 2011). Briefly, blocked membranes were incubated with anti-PGC-1␣, anti-Mfn1, anti-Mfn2, anti-DRP1, anti-␤-actin, or anti-␣-tubulin (Santa Cruz); anti-OPA1 (BD Biosciences, San Jose, CA); anti-OxPhos Complex I, anti-OxPhos Complex II, anti-OxPhos Complex III or anti-Complex V (Invitrogen); anti-LL-37 (Abgent, San Diego, CA); or anti-Beclin1, anti-LC3B, anti-Atg 7, anti-mTOR, antip-mTOR (Ser2448), anti-p-ERK1/2 (Thr202/Tyr204) or anti-ERK2 (Cell Signaling Technology, Beverly, MA) at a dilution of 1:1000 or 1:2000 followed by chemiluminescent ECL detection (Pierce, Rockford, IL).…”

Section: Western Blot Assaysmentioning

confidence: 99%

LL-37 attenuates inflammatory impairment via mTOR signaling-dependent mitochondrial protection

Sun

Zheng

et al. 2014

The International Journal of Biochemistry & Cell Biology

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a b s t r a c tThe human cationic antimicrobial protein LL-37 is a multifunctional host defense peptide with a wide range of immunomodulatory activities. Previous work has shown that LL-37 exerts both pro-and antiinflammatory effects. The role of mitochondria in the skin inflammatory effects of LL-37 has not been well studied. Therefore, our aim was to investigate the immunomodulatory effect of LL-37 in HaCaT cells and to delineate the underlying mechanisms related to mitochondrial function. Immunohistochemistry results from tissue microarrays showed strong cytoplasmic LL-37 staining in inflammatory cells in chronic dermatic inflammation. Using exogenous LL-37 stimulation and LL-37 knockdown and overexpression, LL-37 was demonstrated to dramatically reduce the mRNA levels and protein secretion of inflammatory cytokines including IL-6, IL-8, IL-1␣ and tumor necrosis factor-␣ (TNF-␣), which are induced by lipopolysaccharides (LPS). The anti-inflammatory effects of LL-37 are dependent upon its ability to increase mitochondrial biogenesis and to maintain mitochondrial homeostasis. Furthermore, we observed that LL-37 enhances the LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and mammalian target of rapamycin (mTOR). The mTOR inhibitor rapamycin can neutralize the protective effects of LL-37 on mitochondria. In conclusion, these results suggest that high LL-37 expression levels correlate with chronic skin inflammation; mitochondrial dysfunction occurs in HaCaT cells during inflammation; and LL-37 attenuates inflammatory impairment by stimulating mitochondrial biogenesis and protecting mitochondrial function, which are dependent upon mTOR signaling. These findings provide new insights into targeting mitochondria with LL-37 to prevent skin inflammatory reactions.

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Mitochondrial dynamic remodeling in strenuous exercise-induced muscle and mitochondrial dysfunction: Regulatory effects of hydroxytyrosol

Cited by 99 publications

References 56 publications

Mitochondrial Quality Control as a Therapeutic Target

Mitochondrial Quality Control as a Therapeutic Target

O-GlcNAcase deficiency suppresses skeletal myogenesis and insulin sensitivity in mice through the modulation of mitochondrial homeostasis

LL-37 attenuates inflammatory impairment via mTOR signaling-dependent mitochondrial protection

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