Resveratrol inhibits adventitial fibroblast proliferation and induces cell apoptosis through the SIRT1 pathway

Lin, Ling; Gu, Shaohua; Cheng, Yan

doi:10.3892/mmr.2016.6098

Cited by 16 publications

(10 citation statements)

References 26 publications

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“…The atheroprotective effect of SIRT1 is also exerted through the fine modulation of EPC senescence and adventitial fibroblast migration (107,124). In particular, in EPCs, the nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD + biosynthetic pathway, attenuates oxLDL-induced senescence by upregulating SIRT1 expression through the PI3K/Akt/ERK pathway (124).…”

Section: Sirt1 and Atherosclerosismentioning

confidence: 99%

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

D’Onofrio¹,

Servillo²,

Balestrieri³

2018

Antioxidants & Redox Signaling

295

238

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Significance: Oxidative stress represents the common hallmark of pathological conditions associated with cardiovascular disease (CVD), including atherosclerosis, heart failure, hypertension, aging, diabetes, and other vascular system-related diseases. The sirtuin (SIRT) family, comprising seven proteins (SIRT1-SIRT7) sharing a highly conserved nicotinamide adenine dinucleotide (NAD + )-binding catalytic domain, attracted a great attention for the past few years as stress adaptor and epigenetic enzymes involved in the cellular events controlling aging-related disorder, cancer, and CVD. Recent Advances: Among sirtuins, SIRT1 and SIRT6 are the best characterized for their protective roles against inflammation, vascular aging, heart disease, and atherosclerotic plaque development. This latest role has been only recently unveiled for SIRT6. Of interest, in recent years, complex signaling networks controlled by SIRT1 and SIRT6 common to stress resistance, vascular aging, and CVD have emerged. Critical Issues: We provide a comprehensive overview of recent developments on the molecular signaling pathways controlled by SIRT1 and SIRT6, two post-translational modifiers proven to be valuable tools to dampen inflammation and oxidative stress at the cardiovascular level. Future Directions: A deeper understanding of the epigenetic mechanisms through which SIRT1 and SIRT6 act in the signalings responsible for onset and development CVD is a prime scientific endeavor of the upcoming years. Multiple ''omic'' technologies will have widespread implications in understanding such mechanisms, speeding up the achievement of selective and efficient pharmacological modulation of sirtuins for future applications in the prevention and treatment of CVD. Antioxid. Redox Signal. 28, 711-732.

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Section: Sirt1 and Atherosclerosismentioning

confidence: 99%

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

D’Onofrio¹,

Servillo²,

Balestrieri³

2018

Antioxidants & Redox Signaling

295

238

View full text Add to dashboard Cite

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“…Among SIRT family, SIRT1 has been validated to be most related in this family and function as deacetylating and regulating histones (Ling et al, 2018) as well as a wide range of non-histone substrates, such as NF-κB (Kauppinen et al, 2013), p53 (Nakamura et al, 2017), FOXO (Brunet et al, 2004), ERK (Han et al, 2017), peroxisome proliferator-activated receptor γ (PPARγ) and others (Kauppinen et al, 2013). With regulating this protein, SIRT1 plays a central role in regulating cellular processes, including apoptosis (Ling et al, 2017), cellular proliferation (Jablonska et al, 2016), and inflammation . In the nervous system, SIRT1 suppress the neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease via anti-apoptosis, anti-inflammation (Singh et al, 2017;Gomes et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Reduction of Silent Information Regulator 1 Activates Interleukin-33/ST2 Signaling and Contributes to Neuropathic Pain Induced by Spared Nerve Injury in Rats

Shi

Zhan

Liu

et al. 2020

Front. Mol. Neurosci.

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Emerging studies have demonstrated that interleukin (IL)-33 and its receptor ST2 act as key factors in inflammatory diseases. Moreover, accumulating evidence has suggested that cytokines, including tumor necrosis factor (TNF)-α and IL-1β, trigger an inflammatory cascade. SIRT1 has been shown to suppress the expression of inflammatory cytokines. However, the effects of SIRT1 on IL-33/ST2 signaling and initiation of the inflammatory cascade via modulation of TNF-α and IL-1β by IL-33 remain unclear. In the present study, we found that the dorsal root ganglion (DRG) IL-33 and ST2 were upregulated in a rat model of spared nerve injury (SNI) and intrathecal injection of either IL-33 or ST2 antibodies alleviated mechanical allodynia and downregulated TNF-α and IL-1β induced by SNI. In addition, activation of SIRT1 decreased enhanced DRG IL-33/ST2 signaling in SNI rats. Artificial inactivation of SIRT1 via intrathecal injection of an SIRT1 antagonist could induce mechanical allodynia and upregulate IL-33 and ST2. These results demonstrated that reduction in SIRT1 could induce upregulation of DRG IL-33 and ST2 and contribute to mechanical allodynia induced by SNI in rats.

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“…It can inhibit the proliferation of pathological scar fibroblasts via downregulating the expression of mammalian target of rapamycin (mTOR) /70S6K signaling pathway or TGF-β1, Smad-2, 3,4, and upregulating expression of Smad 7 [58,59]. It can also inhibited proliferation of hypertrophic scar-derived fibroblasts and adventitial fibroblast in vitro and led to a more organized and thinner collagen fibre in the mouse model of wound healing via up-regulating expression of Sirt1 [60][61][62]. Here, we showed that resveratrol could enhance viability of NIH3T3 cells via activating the Shh signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

Guo¹,

Liao²,

Liu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Injuries of the brain and spinal cord result in the formation of glial (reactive gliosis) and fibrotic (formed by fibroblasts) scars. Recent studies have shown that the fibrotic scar was much more important for hindering regeneration after brain or spinal cord injury than the astrocytic scar. However, it has been given much less attention for effects and mechanism of fibroblasts during formation of the fibrotic scar. Resveratrol may be a potential anti-scarring agent in burn-related scarring and keloid fibroblasts. However, it is unclear whether and how resveratrol affects formation of the fibrotic scar after brain or spinal cord injury. Earlier studies have shown that the activated Shh signaling has anti-apoptosis, anti-oxidation, anti-inflammation properties. Moreover, resveratrol can activate the Shh signaling. However, it is unclear how resveratrol activates the Shh signaling. Resveratrol is a activator of Sirt1. It is unknown whether resveratrol activates the Shh signaling via Sirt1. Methods: NIH3T3 cells, a fibroblast cell line, were used as model cells and treated with drugs. Cell viability was assessed by Cell Counting Kit 8. The expressions and activity of Shh signaling pathway proteins were evaluated by immunocytochemistry and Western blotting. Transcriptional activity of Gli-1 was detected with Dual-Luciferase Reporter Gene Assay Kit. Results: Resveratrol, Sirt1 agonist STR1720 and recombinant mouse Shh protein, an activator of hedgehog signaling, enhanced the viability of NIH3T3 cells, promoted Smo to translocated to the primary cilia and Gli-1 entered into the nuclei from cytoplasm, and upregulated expressions of Shh, Ptc-1, Smo, and Gli-1 proteins, which can be reversed by Smo antagonist cyclopamine and Sirt1 antagonist Sirtinol. Additionally, resveratrol increased transcriptional activity of Gli-1. Conclusion: We indicate in the first time that it may be mediated by Sirt1 for resveratrol activating the Shh signaling to enhance viability of NIH3T3 cells, and Sirt1 may be a regulator for upstream of the Shh signaling pathway.This study provides a basis for further investigating effects and mechanism of resveratrol during the formation of fibrous scar after brain or spinal cord injury.

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Resveratrol inhibits adventitial fibroblast proliferation and induces cell apoptosis through the SIRT1 pathway

Cited by 16 publications

References 26 publications

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

Reduction of Silent Information Regulator 1 Activates Interleukin-33/ST2 Signaling and Contributes to Neuropathic Pain Induced by Spared Nerve Injury in Rats

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

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