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CRIF1 deficiency induced mitophagy via p66shc-regulated ROS in endothelial cells
Piao, Shuyu,Nagar, Harsha,Kim, Seonhee,Lee, Ikjun,Choi, Su-jeong,Kim, Taehee,Jeon, Byeong Hwa,Kim, Cuk-Seong Elsevier 2020 Biochemical and biophysical research communication Vol.522 No.4
<P><B>Abstract</B></P> <P>Inhibition of mitochondrial protein CR6 interacting factor 1 (CRIF1) disturbs mitochondrial function, depolarizes membrane potential, and increases reactive oxygen species (ROS) levels in endothelial cells. Impaired mitochondrial function accompanied by oxidative damage is a major contributor to the initiation of mitophagy. We hypothesized that CRIF1 deficiency-induced harmful effects may promote mitophagy, and explored the mechanism underlying this effect in human umbilical vein endothelial cells (HUVECs). Our results showed that CRIF1 downregulation not only induced the mitophagy-related markers LC3 (LC3-II/Ⅰ), PTEN-induced putative kinase 1 (PINK1) and parkin, but also stimulated redox enzyme p66shc expression. Scavenging mitochondrial ROS markedly blunted the CRIF1 deficiency-induced increase in p66shc expression. In addition, knockdown of p66shc inhibited the CRIF1 deletion-triggered mitochondrial ROS increase, membrane potential depolarization, and mitochondrial fusion. The restoration of mitochondrial dysfunction by p66shc downregulation also decreased CRIF1 deficiency-induced mitophagy, by elevating the levels of LC3-II/Ⅰ, PINK1 and parkin. These findings suggest that CRIF1 deficiency induces mitophagy via p66shc-regulated ROS in endothelial cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CRIF1 deficiency induces significant mitophagy in HUVECs. </LI> <LI> CRIF1 deficiency induces p66shc expression in a ROS-dependent manner in HUVECs. </LI> <LI> p66Shc knockdown rescues CRIF1 deficiency-induced mitochondrial dysfunction and mitophagy in HUVECs. </LI> </UL> </P>
Piao, Shuyu,Cha, Young-Nam,Kim, Chaekyun the Society for Free Radical Research Japan 2011 Journal of clinical biochemistry and nutrition Vol.49 No.1
<P>Taurine chloramine is the major chloramine generated in activated neutrophils via the reaction between the overproduced hypochlorous acid and the stored taurine. Taurine chloramine has anti-inflammatory and cytoprotective effects in inflamed tissues by inhibiting the production of inflammatory mediators. Taurine chloramine increases heme oxygenase activity and also protects against hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>)-derived necrosis in macrophages. In this study, we examined further whether taurine chloramine could protect RAW 264.7 macrophages from apoptosis caused by H<SUB>2</SUB>O<SUB>2</SUB>. Macrophages treated with 0.4 mM H<SUB>2</SUB>O<SUB>2</SUB> underwent apoptosis without showing immediate signs of necrosis, and the cells pretreated with taurine chloramine were protected from the H<SUB>2</SUB>O<SUB>2</SUB>-derived apoptosis. Taurine chloramine increased heme oxygenase-1 expression and heme oxygenase activity. The taurine chloramine-derived upregulation of heme oxygenase-1 expression was blocked by inhibition of ERK phosphorylation. Taurine chloramine decreased cellular glutathione (GSH) levels initially, but the GSH level increased above the control level by 10 h. Taurine chloramine also increased catalase expression and protected macrophages from the apoptotic effect of H<SUB>2</SUB>O<SUB>2</SUB>. Combined, these results indicate that the taurine chloramine, produced and released endogenously by the activated neutrophils, can protect the macrophages in inflamed tissues from the H<SUB>2</SUB>O<SUB>2</SUB>-derived apoptosis not only by increasing the expression of cytoprotective enzymes like heme oxygenase-1 and catalase, but also by increasing the intracellular antioxidant GSH level.</P>
Piao, Shuyu,Kim, In Gul,Lee, Ji Young,Hong, Sung Hoo,Kim, Sae Woong,Hwang, Tae-Kon,Oh, Se Heang,Lee, Jin Ho,Ra, Jeong Chan,Lee, Ji Youl Blackwell Pub 2012 JOURNAL OF SEXUAL MEDICINE Vol.9 No.8
<P>Cavernous nerve injury is the main reason for post-prostatectomy erectile dysfunction (ED). Stem cell and neuroprotection therapy are promising therapeutic strategy for ED.</P>
Piao Shuyu,Seonhee Kim,Youngduk Seo,Jinsun Lee,Sunhee Jeon,Giang-Huong Vu,Yeo Min-Kyung,Cuk-Seong Kim 대한종양외과학회 2023 Korean Journal of Clinical Oncology Vol.19 No.2
Purpose: The isocitrate dehydrogenase (IDH) family plays an essential role in metabolism and energy production. The relative expression levels of IDH isoforms (IDH1, IDH2, and IDH3) have prognostic significance in several malignancies, including breast carcinoma. However, the IDH isozyme expression levels in different cancer stages and types have not been determined in breast carcinoma tissues.Methods: We analyzed the messenger RNA (mRNA) and protein levels of IDH (IDH1, IDH2, and IDH3A) and α-ketoglutarate (α-KG) in 59 breast carcinoma tissues.Results: The mRNA level of IDH2 was significantly increased at stages 2 and 3 in triple-negative and (ER-/PR-/HER+) breast cancers. However, the elevated α-KG level was only observed in stages 2 and 3, with no differences in the various breast carcinoma types. Western blotting analysis showed that IDH2 protein expression increased in the patient tissues and cell lines. An <i>in vitro</i> study showed IDH2 downregulation in the triple-negative breast cancer cell line MDA-MB-231 that inhibited cell proliferation and migration and induced cell cycle arrest in the G0/G1 phase.Conclusion: These findings suggest that different from IDH1 and IDH3, IDH2 is more highly expressed in stages 2 and 3 breast cancer tissues, especially in triple-negative breast cancer. IDH2 potentially serves as a target to detect unknown mechanisms in breast cancer.
Role of Mitochondrial Oxidative Stress in Sepsis
Harsha Nagar,Shuyu Piao,Cuk-Seong Kim 대한중환자의학회 2018 Acute and Critical Care Vol.33 No.2
Mitochondria are considered the power house of the cell and are an essential part of the cellular infrastructure, serving as the primary site for adenosine triphosphate production via oxidative phosphorylation. These organelles also release reactive oxygen species (ROS), which are normal byproducts of metabolism at physiological levels; however, overproduction of ROS under pathophysiological conditions is considered part of a disease process, as in sepsis. The inflammatory response inherent in sepsis initiates changes in normal mitochondrial functions that may result in organ damage. There is a complex system of interacting antioxidant defenses that normally function to combat oxidative stress and prevent damage to the mitochondria. It is widely accepted that oxidative stress-mediated injury plays an important role in the development of organ failure; however, conclusive evidence of any beneficial effect of systemic antioxidant supplementation in patients with sepsis and organ dysfunction is lacking. Nevertheless, it has been suggested that antioxidant therapy delivered specifically to the mitochondria may be useful.
Choi, Su-jeong,Piao, Shuyu,Nagar, Harsha,Jung, Saet-byel,Kim, Seonhee,Lee, Ikjun,Kim, Sung-min,Song, Hee-Jung,Shin, Nara,Kim, Dong Woon,Irani, Kaikobad,Jeon, Byeong Hwa,Park, Jeen-Woo,Kim, Cuk-Seong Elsevier 2018 Biochemical and biophysical research communication Vol.503 No.3
<P><B>Abstract</B></P> <P>Isocitrate dehydrogenase 2 (IDH2) is an essential enzyme in the mitochondrial antioxidant system, which produces nicotinamide adenine dinucleotide phosphate, and thereby defends against oxidative stress. We have shown that IDH2 downregulation results in mitochondrial dysfunction and reactive oxygen species (ROS) generation in mouse endothelial cells. The redox enzyme p66shc is a key factor in regulating the level of ROS in endothelial cells. In this study, we hypothesized that IDH2 knockdown-induced mitochondrial dysfunction stimulates endothelial inflammation, which might be regulated by p66shc-mediated oxidative stress. Our results showed that IDH2 downregulation led to mitochondrial dysfunction by decreasing the expression of mitochondrial oxidative phosphorylation complexes I, II, and IV, reducing oxygen consumption, and depolarizing mitochondrial membrane potential in human umbilical vein endothelial cells (HUVECs). The dysfunction not only increased mitochondrial ROS levels but also activated p66shc expression in HUVECs and IDH2 knockout mice. IDH2 deficiency increased intercellular adhesion molecule (ICAM)-1 expression and mRNA levels of pro-inflammatory cytokines (tumor necrosis factor [TNF]-α, and interleukin [IL]-1β) in HUVECs. The mRNA expression of ICAM-1 in endothelial cells and plasma levels of TNF-α and IL-1β were also markedly elevated in IDH2 knockout mice. However, p66shc knockdown rescued IDH2 deficiency-induced mitochondrial ROS levels, monocyte adhesion, ICAM-1, TNF-α, and IL-1β expression in HUVECs. These findings suggest that IDH2 deficiency induced endothelial inflammation via p66shc-mediated mitochondrial oxidative stress.</P> <P><B>Highlights</B></P> <P> <UL> <LI> IDH2 deficiency triggers severe mitochondrial dysfunction in HUVECs. </LI> <LI> IDH2 deficiency induces endothelial inflammation by the increased mitochondrial ROS and p66shc expression. </LI> <LI> p66shc mediated IDH2 deficiency-induced inflammatory molecule expression in HUVECs. </LI> </UL> </P>
The effect of a bioactive tissue‐engineered sling in a rat of stress incontinence model
Kim, In Gul,Piao, Shuyu,Hong, Sung Hoo,Kim, Sae Woong,Hwang, Tae Kon,Oh, Se Heang,Lee, Jin Ho,Lee, Ji Youl Wiley Subscription Services, Inc., A Wiley Company 2012 Journal of biomedical materials research. Part A Vol.a100 No.2
<P><B>Abstract</B></P><P>In this study, we attempt to examine the feasibility of the bioactive tissue‐engineered sling by using muscle precursor cells (MPCs)‐seeded Poly(ε‐caprolactone) (PCL) nanofiber sheet in a rat model of stress urinary incontinence (SUI). <I>In vitro</I>, MPCs were cultured on a PCL nanofiber sheet for one week, where the MPCs‐seeded PCL nanofiber sheet showed constant twitching contraction by electrical field stimulation in an organ bath. <I>In vivo</I>, MPCs‐seeded PCL nanofiber sheet was placed under the female rat's urethra after pudendal nerve denervation (animal model of SUI). The leak point pressure (LPP) was evaluated with the vertical tilt table after the operation for four weeks. The resulting LPP of MPCs‐seeded PCL nanofiber sheet group was observed to be significantly higher than the denervation‐only group's. Furthermore, PKH‐26‐labeled MPCs were observed under the urethral sphincter by immunohistochemistry. These results indicated that, the MPCs‐seeded PCL nanofiber sheet have not only provided support for the deficient sphincter, but also actively improved the sphincter's function overall. In conclusion, this bioactive tissue‐engineered sling could be used as an ideal material for the treatment of SUI. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2012.</P>
Kshitiz Raj Shrestha,박용현,최용선,김인걸,Shuyu Piao,정아량,정승환,오세행,이진호,이지열 한국조직공학과 재생의학회 2015 조직공학과 재생의학 Vol.12 No.6
Recently, studies have focused more towards using biocompatible scaffolds and stem cells to augment or replace the abnormal bladder. But, due to the lack of biomaterials with appropriate thickness as a suitable scaffold for smooth muscle regeneration, several structural, mechanical, and biocompatibility problems are encountered. Therefore, we aimed to demonstrate whether human muscle-derived stem cells (h-MDSCs) seeded on multilayered polycaprolactone (PCL) nanofiber is an appropriate scaffold for bladder smooth muscle regeneration. h-MDSCs were seeded on a multilayered PCL/collagen nanofiber sheet and implanted in the bladder of a mucosa preserving partial cystectomy rat. From our findings, h-MDSCs seeded on multilayered PCL showed efficient cell seeding and proliferation. In addition, the histological and immunohistochemical analysis showed cell survival in between the multilayered nanofiber sheet, which led to smooth muscle cell regeneration with improved pro-angiogenesis in the regenerated region of the bladder. Therefore, h-MDSCs seeded nanofibers could be a promising tool in treating neurogenic bladder and related diseases.
Nagar, Harsha,Jung, Saet-byel,Ryu, Min Jeong,Choi, Su-Jung,Piao, Shuyu,Song, Hee-Jung,Kang, Shin Kwang,Shin, Nara,Kim, Dong Woon,Jin, Seon-Ah,Jeong, Jin-Ok,Irani, Kaikobad,Jeon, Byeong Hwa,Shong, Minh Mary Ann Liebert, Inc. Publishers 2017 Antioxidants & Redox Signaling Vol. No.
<P>Conclusion: These findings indicate that CRIF1 plays an important role in maintaining mitochondrial and endothelial function through its effects on the SIRT1-eNOS pathway.</P>