Expression of <scp>PINK1</scp> and Parkin in human apical periodontitis

Liu, B; Zhang, J; Liu, G; Zhu, Lingxin; Peng, Bin

doi:10.1111/iej.13760

Cited by 9 publications

(5 citation statements)

References 47 publications

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“…S1P/SK1/S1PR1 signaling might be involved in M2 macrophage polarization induced by ADSC-derived exosomes to improve cardiac damage [35], and pknox1 might participate in M2 macrophage polarization by BMSC-Exos and enhance cutaneous wound healing [36]. PINK1/Parkin signaling is important for macrophage polarization [37]. The activation/phosphorylation of Akt plays a negative role in the PINK1/Parkin signal pathway [38].…”

Section: Discussionmentioning

confidence: 99%

BMSC-derived Exosomes Attenuate Rat Osteoarthritis by Regulating Macrophage Polarization, and PINK1/Parkin Signaling May Be Involved

Shen

et al. 2023

Preprint

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Exosomes derived from bone marrow mesenchymal stem cells (BMSC-Exos) may modulate the M1/M2 polarization of macrophages during osteoarthritis (OA). However, the underlying mechanisms of BMSC-Exos in this process still need to be elucidated. In this study, the effects of BMSC-Exos on macrophages after induction of lipopolysaccharide (LPS) were determined. The protein expression of Akt, PINK1, and Parkin in macrophages were tested. We prepared an OA model by resecting the anterior cruciate ligament and medial meniscus of SD rats. BMSC-Exos could reduce M1 and promote M2 macrophage polarization, inhibit mitochondrial membrane damage and reactive oxygen species (ROS) production. Akt phosphorylation was downregulated but significantly recovered after treatment with BMSC-Exos (P<0.01). PINK1/Parkin signaling was crucial in mitochondrial damage and subsequent M1 macrophage polarization. The protein expression of PINK1 and Parkin was significantly inhibited by BMSC-Exos (P<0.01). Histological analyses revealed that BMSC-Exos alleviated cartilage damage, inhibited M1 polarization, and promoted M2 polarization in the synovium. The expression of PINK1 and Parkin in the synovium was decreased when BMSC-Exos were used. ELISA results revealed that BMSC-Exos also changed the systematic inflammatory state. These data suggest that BMSC-Exos ameliorate OA development by regulating synovial macrophage polarization, and one of the underlying mechanisms may be through inhibiting PINK1/Parkin signaling. Therefore, BMSC-Exos are a potential useful therapeutic approach for OA.

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Section: Discussionmentioning

confidence: 99%

BMSC-derived Exosomes Attenuate Rat Osteoarthritis by Regulating Macrophage Polarization, and PINK1/Parkin Signaling May Be Involved

Shen

et al. 2023

Preprint

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“…Apical periodontitis is primarily derived from complex microbial infections and has identified as a host–immune response against the invasion of microbes in the root canal (Azuma et al, 2018; Liu et al, 2022). Recent studies have suggested that the activation of a glycolytic phenotype is linked to immune responses (Song et al, 2022; Wang, Yu et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

Targeting hexokinase 1 alleviates NLRP3‐mediated inflammation in apical periodontitis: A laboratory investigation

et al. 2023

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Aim The aim of the study was to explore whether hexokinase 1 (HK1) is involved in the inhibition of inflammation mediated by nucleotide‐binding oligomerization domain‐like receptor protein 3 (NLRP3) signalling pathway in the development of apical periodontitis (AP). Methodology Human AP tissues and normal control tissues were collected in the clinic. First, the levels of glucose, pyruvate, lactate and hexokinase activity were examined in human AP tissues. ECAR and OCR were further measured to detect the level of glycolysis in vitro model of inflammation, which established with lipopolysaccharide (LPS)‐stimulated RAW264.7 cell line. Secondly, the expression of HK1, NLRP3, caspase‐1 and interleukin (IL)‐1β were measured by Western blot, immunohistochemistry or RT–qPCR. Finally, lentiviral short hairpin RNA (shRNA) silencing technique or the inhibitor 2‐deoxy‐d‐glucose (2‐DG) were used to further detect the relationship between HK1‐mediated glycolysis and NLRP3‐mediated inflammation in the development of AP in vitro. Results Initially, the level of glycolysis was significantly increased in human AP tissues. Subsequently, the expression of HK1, NLRP3, caspase‐1 and IL‐1β were upregulated significantly in human AP tissues. Furthermore, in the model of AP in vitro, a high level of glycolysis and the high expression of HK1, NLRP3, caspase‐1 and IL‐1β was observed. Finally, the expression of NLRP3, caspase‐1 and IL‐1β mediated by LPS stimulation was significantly reduced via HK1 knockdown or 2‐DG treatment in vitro. Conclusions Our data support that HK1‐mediated glycolysis plays a crucial role in the development of AP via upregulating the NLRP3 signalling pathway. Moreover, targeting HK1 may contribute to prevent the progression of AP, which has a potential clinical translation.

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“…The inhibition of AMPK abolished the effects of FSH on mitophagy, which was reflected in the reduction in TOMM20 expression, the LC3-II/LC3-I ratio, and cellular ATP levels, indicating that AMPK may be a central regulator connecting FSH and mitophagy. LC3 and TOMM20 are typically used as an indicator of autophagic or mitophagic flux, respectively, and the LC3 mitochondrial translocation (LC3 co-localization with TOMM20) represents the formation of mitophagosomes [ 41 ]. AMPK is essential for LC3 lipidation (LC3-I to LC3-II) to induce autophagosome formation, which is consistent with our findings [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Follicle-Stimulating Hormone Alleviates Ovarian Aging by Modulating Mitophagy- and Glycophagy-Based Energy Metabolism in Hens

Dong

Guo

Yang

et al. 2022

Cells

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As a predominant hormone in the reproductive axis, follicle-stimulating hormone (FSH) is known as the primary surviving factor for follicular growth. In this study, the alleviating effect of FSH on aging chicken granulosa cells (GCs) was investigated. Results showed that FSH activated mitophagy and relieved mitochondrial edema in D-gal-induced senescent GCs, which was evidenced by an increased number of mitophagosomes as well as increased mitochondria-light chain 3 (LC3) colocalization. Mitophagy activation was accompanied by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. Furthermore, upregulated glycophagy was demonstrated by an increased interaction of starch-binding domain protein 1 (STBD1) with GABA type A receptor-associated protein-like 1 (GABARAPL1) in D-gal-induced senescent GCs. FSH treatment further promoted glycophagy, accompanied by PI3K/AKT activation. PI3K inhibitor LY294002 and AKT inhibitor GSK690693 attenuated the effect of FSH on glycophagy and glycolysis. The inhibition of FSH-mediated autophagy attenuated the protective effect of FSH on naturally aging GC proliferation and glycolysis. The simultaneous blockage of PI3K/AKT and AMPK signaling also abolished the positive effect of FSH on naturally senescent ovarian energy regulation. These data reveal that FSH prevents chicken ovarian aging by modulating glycophagy- and mitophagy-based energy metabolism through the PI3K/AKT and AMPK pathways.

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Expression of PINK1 and Parkin in human apical periodontitis

Cited by 9 publications

References 47 publications

BMSC-derived Exosomes Attenuate Rat Osteoarthritis by Regulating Macrophage Polarization, and PINK1/Parkin Signaling May Be Involved

BMSC-derived Exosomes Attenuate Rat Osteoarthritis by Regulating Macrophage Polarization, and PINK1/Parkin Signaling May Be Involved

Targeting hexokinase 1 alleviates NLRP3‐mediated inflammation in apical periodontitis: A laboratory investigation

Follicle-Stimulating Hormone Alleviates Ovarian Aging by Modulating Mitophagy- and Glycophagy-Based Energy Metabolism in Hens

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