Role of PIN1 on <i>in vivo</i> periodontal tissue and <i>in vitro</i> cells

Park, K.-H.; Cho, E.-H.; Bae, Won Kyung; Kim, H.-S.; Lim, Hyun Chang; Park, Young-Doo; Lee, M.-O.; Cho, E.-S.; Kim, E.-C.

doi:10.1111/jre.12430

Cited by 2 publications

(2 citation statements)

References 50 publications

(88 reference statements)

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“…In multiple cancer types, many studies have shown that the expression levels of PIN1 and levels of Akt phosphorylation are strongly correlated. However, experiments have shown that in mouse periodontal tissues, PIN1 siRNA enhanced mTOR and Akt activation, which was attenuated by PIN1 overexpression [ 52 ]. In the present study, PIN1 overexpression caused a reduction in the expression of p-Akt.…”

Section: Discussionmentioning

confidence: 99%

PIN1 Protects Hair Cells and Auditory HEI‐OC1 Cells against Senescence by Inhibiting the PI3K/Akt/mTOR Pathway

Zhang

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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A growing amount of evidence has confirmed the crucial role of the prolyl isomerase PIN1 in aging and age-related diseases. However, the mechanism of PIN1 in age-related hearing loss (ARHL) remains unclear. Pathologically, ARHL is primarily due to the loss and dysfunction of hair cells (HCs) and spiral ganglion cells (SGCs) in the cochlea. Therefore, in this study, we aimed to investigate the role of PIN1 in protecting hair cells and auditory HEI-OC1 cells from senescence. Enzyme-linked immunosorbent assays, immunohistochemistry, and immunofluorescence were used to detect the PIN1 protein level in the serum of ARHL patients and C57BL/6 mice in different groups, and in the SGCs and HCs of young and aged C57BL/6 mice. In addition, a model of HEI-OC1 cell senescence induced by H2O2 was used. Adult C57BL/6 mice were treated with juglone, or juglone and NAC, for 4 weeks. Interestingly, we found that the PIN1 protein expression decreased in the serum of patients with ARHL, in senescent HEI-OC1 cells, and in the cochlea of aged mice. Moreover, under H2O2 and juglone treatment, a large amount of ROS was produced, and phosphorylation of p53 was induced. Importantly, PIN1 expression was significantly increased by treatment with the p53 inhibitor pifithrin-α. Overexpression of PIN1 reversed the increased level of p-p53 and rescued HEI-OC1 cells from senescence. Furthermore, PIN1 mediated cellular senescence by the PI3K/Akt/mTOR signaling pathway. In vivo data from C57BL/6 mice showed that treatment with juglone led to hearing loss. Taken together, these findings demonstrated that PIN1 may act as a vital modulator in hair cell and HEI-OC1 cell senescence.

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Section: Discussionmentioning

confidence: 99%

PIN1 Protects Hair Cells and Auditory HEI‐OC1 Cells against Senescence by Inhibiting the PI3K/Akt/mTOR Pathway

Zhang

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Conversely, PIN1 inhibition and silencing promoted anti‐inflammatory effects and blocked osteoclastic differentiation in LPS‐ and nicotine‐treated PDLCs 286 . PIN1 inhibition may also support periodontal tissue regeneration because it promotes osteoblast differentiation, although the underlying molecular mechanism remains poorly studied 287 . Inhibition of PIN1 reportedly stimulates odontogenic differentiation of human dental pulp cells by activating the bone morphogenetic protein/Wnt signalling pathway/B‐catenin/extracellular ERKs and c‐jun N‐terminal kinase/NFκB pathway 288 .…”

Section: Periodontitis and Periopathogens Interaction That Conditions...mentioning

confidence: 99%

SARS‐CoV‐2, periodontal pathogens, and host factors: The trinity of oral post‐acute sequelae of COVID‐19

Schwartz,

Capistrano,

Gluck

et al. 2024

Reviews in Medical Virology

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COVID‐19 as a pan‐epidemic is waning but there it is imperative to understand virus interaction with oral tissues and oral inflammatory diseases. We review periodontal disease (PD), a common inflammatory oral disease, as a driver of COVID‐19 and oral post‐acute‐sequelae conditions (PASC). Oral PASC identifies with PD, loss of teeth, dysgeusia, xerostomia, sialolitis‐sialolith, and mucositis. We contend that PD‐associated oral microbial dysbiosis involving higher burden of periodontopathic bacteria provide an optimal microenvironment for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection. These pathogens interact with oral epithelial cells activate molecular or biochemical pathways that promote viral adherence, entry, and persistence in the oral cavity. A repertoire of diverse molecules identifies this relationship including lipids, carbohydrates and enzymes. The S protein of SARS‐CoV‐2 binds to the ACE2 receptor and is activated by protease activity of host furin or TRMPSS2 that cleave S protein subunits to promote viral entry. However, PD pathogens provide additional enzymatic assistance mimicking furin and augment SARS‐CoV‐2 adherence by inducing viral entry receptors ACE2/TRMPSS, which are poorly expressed on oral epithelial cells. We discuss the mechanisms involving periodontopathogens and host factors that facilitate SARS‐CoV‐2 infection and immune resistance resulting in incomplete clearance and risk for ‘long‐haul’ oral health issues characterising PASC. Finally, we suggest potential diagnostic markers and treatment avenues to mitigate oral PASC.

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Role of PIN1 on in vivo periodontal tissue and in vitro cells

Abstract: In summary, this study is the first to demonstrate that PIN1 is expressed in developing periodontal tissue, and in vitro PDLCs and cementoblasts. PIN1 inhibition stimulates osteoblast differentiation, and thus may play an important role in periodontal regeneration.

Cited by 2 publications

References 50 publications

PIN1 Protects Hair Cells and Auditory HEI‐OC1 Cells against Senescence by Inhibiting the PI3K/Akt/mTOR Pathway

PIN1 Protects Hair Cells and Auditory HEI‐OC1 Cells against Senescence by Inhibiting the PI3K/Akt/mTOR Pathway

SARS‐CoV‐2, periodontal pathogens, and host factors: The trinity of oral post‐acute sequelae of COVID‐19

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