PEP-1-SIRT2 causes dedifferentiation and COX-2 expression via the MAPK pathways in rabbit articular chondrocytes

Eo, Seong‐Hui; Kim, Dae Won; Choi, Soo Young; Kim, Hyun Ah; Kim, Song Ja

doi:10.1016/j.yexcr.2015.09.001

Cited by 12 publications

(14 citation statements)

References 48 publications

(59 reference statements)

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“…Kim and colleagues also performed a series of in vitro studies in this area. They investigated the effects of thymoquinone (TQ) and PEP-1-SIRT2 on the dedifferentiation and inflammation of rabbit chondrocytes 13,77 . TQ or PEP-1-SIRT2 induce the expression of cyclooxygenase-2 (COX-2), causing the dedifferentiation of rabbit articular chondrocytes 78 and subsequently leading to the dedifferentiation of chondrocytes through the ERK pathways.…”

Section: Dedifferentiation In Diseases (As a Pathological Factor)mentioning

confidence: 99%

“…Activation of the Wnt/β-catenin signaling pathway induces the dedifferentiation of epidermal cells 9 , articular chondrocytes 10 , or endothelial cells 11 for regeneration. In addition, some specific biomolecules trigger the dedifferentiation of vascular smooth muscle cells 12 or chondrocytes 13 via the mitogen-activated protein kinase (MAPK) pathways. Also, innovative biomaterials are designing and creating to regulate dedifferentiation 14 , 15 .…”

Section: Introductionmentioning

confidence: 99%

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Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Yao

Wang

2020

npj Regen Med

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Cell dedifferentiation is the process by which cells grow reversely from a partially or terminally differentiated stage to a less differentiated stage within their own lineage. This extraordinary phenomenon, observed in many physiological processes, inspires the possibility of developing new therapeutic approaches to regenerate damaged tissue and organs. Meanwhile, studies also indicate that dedifferentiation can cause pathological changes. In this review, we compile the literature describing recent advances in research on dedifferentiation, with an emphasis on tissue-specific findings, cellular mechanisms, and potential therapeutic applications from an engineering perspective. A critical understanding of such knowledge may provide fresh insights for designing new therapeutic strategies for regenerative medicine based on the principle of cell dedifferentiation.

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Section: Dedifferentiation In Diseases (As a Pathological Factor)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Yao

Wang

2020

npj Regen Med

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“…As one of the most crucial pathological processes in AIS, inflammation and its correlation with SIRT2 expression was also assessed in our study, which displayed that, SIRT2 expression was positively associated with pro-inflammatory cytokines expres- [27][28][29] As for possible explanations to our results, we presumed that it was possible that SIRT2 promoted the pro-inflammatory cytokines via interacting with various factors as described in the previous studies, such as COX-2 and PGE2. 25,26 There were some limitations in the present study. The first limitation was that the other types of stoke (such as hemorrhagic stroke) were not included in this study to exclude their possible interference to the results.…”

Section: Discussionmentioning

confidence: 89%

“…25 And a previous study reveals that the cellpermeative protein of SIRT2, PEP-1-SIRT2, results in an elevated inflammation in rabbit articular chondrocytes by enhancing the cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) expressions. 26 These data indicate that SIRT2 is a promoter in inflammation. As one of the most crucial pathological processes in AIS, inflammation and its correlation with SIRT2 expression was also assessed in our study, which displayed that, SIRT2 expression was positively associated with pro-inflammatory cytokines expres- [27][28][29] As for possible explanations to our results, we presumed that it was possible that SIRT2 promoted the pro-inflammatory cytokines via interacting with various factors as described in the previous studies, such as COX-2 and PGE2.…”

Section: Discussionmentioning

confidence: 91%

“…A study elucidates that SIRT2 aggravates inflammation in allergic asthma presented as positively modulating cellular recruitment, CC chemokine ligand 17 (CCL17), production, and goblet cell hyperplasia after Aspergillus fumigatus (DRA) challenge in cellular and mouse models 25 . And a previous study reveals that the cell‐permeative protein of SIRT2, PEP‐1‐SIRT2, results in an elevated inflammation in rabbit articular chondrocytes by enhancing the cyclooxygenase‐2 (COX‐2) and prostaglandin E2 (PGE2) expressions 26 . These data indicate that SIRT2 is a promoter in inflammation.…”

Section: Discussionmentioning

confidence: 99%

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Overexpression of sirtuin 2 and its association with prognosis in acute ischemic stroke patients

Zhang

Yan

Zhang

2021

Clinical Laboratory Analysis

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Cysteine thiol oxidation on SIRT2 regulates inflammation in obese mice with sepsis

et al. 2018

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Obesity increases morbidity and mortality in acute illnesses such as sepsis and septic shock. We showed previously that the early/hyper-inflammatory phase of sepsis is exaggerated in obese mice with sepsis; sirtuin 2 (SIRT2) modulates sepsis inflammation in obesity. Evidence suggests that obesity with sepsis is associated with increased oxidative stress. It is unknown whether exaggerated hyper-inflammation of obesity with sepsis modulates the SIRT2 function in return. We showed recently that SIRT6 oxidation during hyper-inflammation of sepsis modulates its glycolytic function. This study tested the hypothesis that increased oxidative stress and direct SIRT2 oxidation exaggerate hyper-inflammation in obesity with sepsis. Using spleen and liver tissue from mice with diet-induced obesity (DIO) we studied oxidized vs. total SIRT2 expression during hyper- and hypo-inflammation of sepsis. To elucidate the mechanism of SIRT2 oxidation (specific modifications of redox-sensitive cysteines) and its effect on inflammation, we performed site-directed mutations of redox-sensitive cysteines Cys221 and Cys224 on SIRT2 to serine (C221S and C224S), transfected HEK293 cells with mutants or WT SIRT2, and studied SIRT2 enzymatic activity and NFĸBp65 deacetylation. Finally, we studied the effect of SIRT2 mutation on LPS-induced inflammation using RAW 264.7 macrophages. In an inverse relationship, total SIRT2 decreased while oxidized SIRT2 expression increased during hyper-inflammation and SIRT2 was unable to deacetylate NFĸBp65 with increased oxidative stress of obesity with sepsis. Mechanistically, both the mutants (C221S and C224S) show decreased (1) SIRT2 enzymatic activity, (2) deacetylation of NFĸBp65, and (3) anti-inflammatory activity in response to LPS vs. WT SIRT2. Direct oxidation modulates SIRT2 function during hyper-inflammatory phase of obesity with sepsis via redox sensitive cysteines.

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PEP-1-SIRT2 causes dedifferentiation and COX-2 expression via the MAPK pathways in rabbit articular chondrocytes

Cited by 12 publications

References 48 publications

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Overexpression of sirtuin 2 and its association with prognosis in acute ischemic stroke patients

Cysteine thiol oxidation on SIRT2 regulates inflammation in obese mice with sepsis

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