Peroxiredoxin5 Controls Vertebrate Ciliogenesis by Modulating Mitochondrial Reactive Oxygen Species

Ji, Yurim; Chae, Soomin; Lee, Hyun Kyung; Park, Inji; Kim, Chowon; Ismail, Tayaba; Kim, Youni; Park, Jeen Woo; Kwon, Oh Nam; Kang, Beom Sik; Lee, Dong Seok; Bae, Jong Sup; Kim, Sang Hyun; Moon, Pyung Gon; Baek, Moon Chang; Park, Mae Ja; Kil, In Sup; Rhee, Sue Goo; Kim, Joon; Huh, Yang Hoon; Shin, Jong Yeon; Min, Kyoung Jin; Kwon, Taeg Kyu; Jang, Dong Gil; Woo, Hyun Ae; Kwon, Taejoon; Park, Tae Joo; Lee, Hyun Shik

doi:10.1089/ars.2018.7507

Cited by 16 publications

(13 citation statements)

References 37 publications

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“…Many studies have shown that Prx5 has antioxidant protective functions and can effectively remove oxidative stress [ 17 ] [ 23 ]. Thus, we investigated whether Prx5 is involved in the occurrence of cardiac hypertrophy and dysfunction by regulating oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, overexpression of Prx3 prevents cardiac hypertrophy and failure after myocardial infarction in mice [ 15 ]. As an important member of the Prx family, Prx5 has antioxidant protective functions and can effectively remove reactive oxygen species (ROS) [ 16 , 17 ]. However, the involvement of Prx5 in cardiac hypertrophy remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice

Dai

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown accelerated pressure overload-induced cardiac hypertrophy and dysfunction in mice by activating oxidative stress and cardiomyocyte apoptosis. Importantly, heart deterioration caused by Prx5 knockdown was related to mitogen-activated protein kinase (MAPK) pathway activation. These findings suggest that Prx5 could be a novel target for treating cardiac hypertrophy and heart failure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice

Dai

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Abnormal phenotypes, such as reduced glucose utilization and increased fatty acid consumption, lead to the accumulation of toxic intermediates in diabetic patients [70] . For example, excessive ROS can damage DNA, lipids, endoplasmic reticulum, peroxisomes, mitochondria and other cellular components and organelles [71] . Mitochondria not only participate in the synthesis of ATP, but also metabolize fatty acid, lactic acid and ketone body.…”

Section: Discussionmentioning

confidence: 99%

ICA treatment diabets induced bone loss via primary cilia/Gli2/Osteocalcin signaling pathway

Liu

Deng

et al. 2021

Preprint

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Diabetes mellitus, as a metabolic system disorder disease, aggravates the disease burden of patients and affects the quality of human life. Diabetes-associatedbone complications lead to decreased bone mechanical strength and osteoporosis.Evidencesshow that chronic hyperglycemia and metabolic intermediates , such as inflammatory factor, reactive oxygen species(ROS) and advanced glycation end products(AGEs), are regarded as dominanthazardous factors of primary cilia/Gli2 signal disorders.Case studies have demonstrated abnormal bone metabolism in diabetics, however, how diabetes damages primarycilia/Gli2 signal is largely unknown. Therefore, we studied the effects of diabetes on femoral primary cilia by establishing aStreptozocin (STZ)-induced diabetic (SpragueDawley) SD rat model and diabetic bone loss cell modelin vitro. Our results confirmed that diabetes impaired femur primary cilia,osteoblast differentiation and mineralization by inhibiting primary cilia/Gli2signaling pathway, additionally,Icariin(ICA) treatment could rescue the impairment of osteoblast differentiation causedby high glucose mediumin vitro. ICA activated primary cilia/Gli2/osteocalcinsignaling pathway of osteoblasts by protecting primary cilia from glucotoxicityimposed by diabetes, intactprimary cilia couldbe as anchoring sites, in which Gli2 was processed and modified,and matured Gli2 entered the nucleus to initiate downstream osteocalcingene transcription.Additionally,ICA inhibited ROS production of mitochondria, thus balanced mitochondrial energy metabolism and oxidative phosphorylation.All results suggest that ICA can protect the primary cilia and mitochondria of osteoblastby reducingintracellular ROS, thereby recover primary cilia/Gli2signaling pathway to facilitateosteoblast differentiation and mineralization, suggesting that ICA has potential as a novel typeof drugtreatingbone loss induced bydiabetes.

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“…The critical balance of ROS is indispensable for embryonic development, and the members of thiol peroxidases have been studied for their essential roles in early vertebrate embryogenesis, for example, Prdx1 plays a crucial role in pronephros development during embryogenesis [24], and Prdx5 has been found to control vertebrate ciliogenesis [25]. In addition to Prdxs, GPx3 is involved in posterior development during vertebrate embryonic development [26].…”

Section: Introductionmentioning

confidence: 99%

Physiological Functions of Thiol Peroxidases (Gpx1 and Prdx2) during Xenopus laevis Embryonic Development

Lee

Kim

et al. 2021

Antioxidants

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Glutathione peroxidase 1 (Gpx1) and peroxiredoxin 2 (Prdx2) belong to the thiol peroxidase family of antioxidants, and have been studied for their antioxidant functions and roles in cancers. However, the physiological significance of Gpx1 and Prdx2 during vertebrate embryogenesis are lacking. Currently, we investigated the functional roles of Gpx1 and Prdx2 during vertebrate embryogenesis using Xenopus laevis as a vertebrate model. Our investigations revealed the zygotic nature of gpx1 having its localization in the eye region of developing embryos, whereas prdx2 exhibited a maternal nature and were localized in embryonic ventral blood islands. Furthermore, the gpx1-morphants exhibited malformed eyes with incompletely detached lenses. However, the depletion of prdx2 has not established its involvement with embryogenesis. A molecular analysis of gpx1-depleted embryos revealed the perturbed expression of a cryba1-lens-specific marker and also exhibited reactive oxygen species (ROS) accumulation in the eye regions of gpx1-morphants. Additionally, transcriptomics analysis of gpx1-knockout embryos demonstrated the involvement of Wnt, cadherin, and integrin signaling pathways in the development of malformed eyes. Conclusively, our findings indicate the association of gpx1 with a complex network of embryonic developmental pathways and ROS responses, but detailed investigation is a prerequisite in order to pinpoint the mechanistic details of these interactions.

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Peroxiredoxin5 Controls Vertebrate Ciliogenesis by Modulating Mitochondrial Reactive Oxygen Species

Abstract: Prdx5 plays protective roles in mitochondria and is critical for normal cilia development by regulating the levels of ROS. The loss of Prdx5 is associated with excessive production of ROS, resulting in mitochondrial dysfunction and aberrant ciliogenesis.

Cited by 16 publications

References 37 publications

Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice

Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice

ICA treatment diabets induced bone loss via primary cilia/Gli2/Osteocalcin signaling pathway

Physiological Functions of Thiol Peroxidases (Gpx1 and Prdx2) during Xenopus laevis Embryonic Development

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