Sirtuin 1 in Host Defense during Infection

Kim, Jin‐Kyung; Silwal, Prashanta; Jo, Eun‐Kyeong

doi:10.3390/cells11182921

Cited by 10 publications

(3 citation statements)

References 87 publications

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“…In fact, at the postmortem interval, an over-expression of some genes associated with autophagy as LC3, ATG7 or ATG12 has been found ( Martínez et al, 2019 ). Also, SIRT1 regulates pro-inflamatory response through modulation of NF-κB signaling ( Kim, Silwal & Jo, 2022 ). Although downregulation of SIRT1 is important in the autolysis process at postmortem interval, its post-transcriptional regulation could be due to other mechanisms rather than microRNAs ( Cao et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

A miRNome analysis at the early postmortem interval

Guardado-Estrada

Cárdenas-Monroy

Martínez-Rivera

et al. 2023

PeerJ

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The postmortem interval (PMI) is the time elapsing since the death of an individual until the body is examined. Different molecules have been analyzed to better estimate the PMI with variable results. The miRNAs draw attention in the forensic field to estimate the PMI as they can better support degradation. In the present work, we analyzed the miRNome at early PMI in rats’ skeletal muscle using the Affymetrix GeneChip™ miRNA 4.0 microarrays. We found 156 dysregulated miRNAs in rats’ skeletal muscle at 24 h of PMI, out of which 84 were downregulated, and 72 upregulated. The miRNA most significantly downregulated was miR-139-5p (FC = −160, p = 9.97 × 10−11), while the most upregulated was rno-miR-92b-5p (FC = 241.18, p = 2.39 × 10−6). Regarding the targets of these dysregulated miRNAs, the rno-miR-125b-5p and rno-miR-138-5p were the miRNAs with more mRNA targets. The mRNA targets that we found in the present study participate in several biological processes such as interleukin secretion regulation, translation regulation, cell growth, or low oxygen response. In addition, we found a downregulation of SIRT1 mRNA and an upregulation of TGFBR2 mRNA at 24 h of PMI. These results suggest there is an active participation of miRNAs at early PMI which could be further explored to identify potential biomarkers for PMI estimation.

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Section: Discussionmentioning

confidence: 99%

A miRNome analysis at the early postmortem interval

Guardado-Estrada

Cárdenas-Monroy

Martínez-Rivera

et al. 2023

PeerJ

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“…Among the best studied member of sirtuin family is SIRT1 [ 98 ]. As a metabolic/nutrient sensor, SIRT1 is localized in the nucleus but can shuttle between the nucleus and cytoplasm under specific conditions [ 99 ].…”

Section: Signaling Molecules/pathwaysmentioning

confidence: 99%

Cellular Senescence in Intervertebral Disc Aging and Degeneration: Molecular Mechanisms and Potential Therapeutic Opportunities

et al. 2023

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Closely associated with aging and age-related disorders, cellular senescence (CS) is the inability of cells to proliferate due to accumulated unrepaired cellular damage and irreversible cell cycle arrest. Senescent cells are characterized by their senescence-associated secretory phenotype that overproduces inflammatory and catabolic factors that hamper normal tissue homeostasis. Chronic accumulation of senescent cells is thought to be associated with intervertebral disc degeneration (IDD) in an aging population. This IDD is one of the largest age-dependent chronic disorders, often associated with neurological dysfunctions such as, low back pain, radiculopathy, and myelopathy. Senescent cells (SnCs) increase in number in the aged, degenerated discs, and have a causative role in driving age-related IDD. This review summarizes current evidence supporting the role of CS on onset and progression of age-related IDD. The discussion includes molecular pathways involved in CS such as p53-p21CIP1, p16INK4a, NF-κB, and MAPK, and the potential therapeutic value of targeting these pathways. We propose several mechanisms of CS in IDD including mechanical stress, oxidative stress, genotoxic stress, nutritional deprivation, and inflammatory stress. There are still large knowledge gaps in disc CS research, an understanding of which will provide opportunities to develop therapeutic interventions to treat age-related IDD.

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“…31 SIRT1 has a role on regulatory mechanisms of bacterial, viral, and parasitic infections. 32 However, whether SIRT1 is implicated in infantile pneumonia needs consideration. Herein, SIRT1 protein level was lowered with the induction of LPS, but was reversed by DHK treatment.…”

Section: Dhk Modulated Infantile Pneumonia Via Sirt1/ Nf-κb Pathwaymentioning

confidence: 99%

Dihydrokaempferol attenuates LPS-induced inflammation and apoptosis in WI-38 cells

Wang,

Zhang,

Pang

2023

Allergol Immunopathol

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Background: Globally, pneumonia has been associated as a primary cause of mortality in children aged less than 5 years. Dihydrokaempferol (DHK) has been proposed for being correlated with the process of various diseases. Nevertheless, whether DHK has a role in the progression of infantile pneumonia remains unclear. This study aimed at exploring whether DHK was involved in the progression of infantile pneumonia. Methods: Human fibroblast cells WI-38 were treated with lipopolysaccharide (LPS). The viability of WI-38 cells was measured via Cell counting kit-8. Reverse transcription-quantitative polymerase chain reaction was used to evaluate the levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). Western blot analysis revealed the protein levels of IL-1β, IL-6, TNF-α, Bax, and cleaved-caspase 3. Flow cytometry was applied for exploring the apoptosis of WI-38 cells. The concentrations of IL-1β, IL-6, and TNF-α were assessed via enzyme-linked-immunosorbent serologic assay. Results: DHK modulated the viability of WI-38 cells in infantile pneumonia. Furthermore, we identified that DHK treatment inversely changed LPS induction-mediated elevation on the levels of inflammation biomarkers. Besides, DHK counteracted LPS-induced production of reactive oxygen species (ROS) in WI-38 cells. DHK also decreased LPS-induced elevation of WI-38 cells apoptosis and mediated the levels of apoptosis-associated indexes. Moreover, modulating sirtuin-1 (SIRT1) protein level was lowered by the induction of LPS, and was reversed by DHK treatment. In addition, DHK counteracted LPS induction-mediated elevation of p-p65 and phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha (p-IκBα) protein levels. Conclusion: DHK alleviated LPS-induced WI-38 cells inflammation injury in infantile pneumonia through SIRT1/NF-κB pathway. The results shed light on the implications of DHK on the prevention and treatment of infantile pneumonia.

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Sirtuin 1 in Host Defense during Infection

Cited by 10 publications

References 87 publications

A miRNome analysis at the early postmortem interval

A miRNome analysis at the early postmortem interval

Cellular Senescence in Intervertebral Disc Aging and Degeneration: Molecular Mechanisms and Potential Therapeutic Opportunities

Dihydrokaempferol attenuates LPS-induced inflammation and apoptosis in WI-38 cells

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