Transcription Factor Trps1 Promotes Tubular Cell Proliferation after Ischemia-Reperfusion Injury through cAMP–Specific 3′,5′-Cyclic Phosphodiesterase 4D and AKT

Yang, Jing; Chen, Kehong; Huang, Kun; Fu, Bi-Qiong; Li, Lin; Zhang, Jianguo; Li, Kailong; He, Yong

doi:10.1681/asn.2016010009

Cited by 18 publications

(14 citation statements)

References 46 publications

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“…To investigate the role of DcR2 in renal fibrosis, green fluorescent protein (GFP)-DcR2 small interfering RNA (siRNA) or overexpression plasmids were injected into the kidney via tail vein under ultrasonography guidance as per the established procedures. 26 As shown in Supplementary Figure S1A and B, GFP was expressed in tubules after control vectorand DcR2-related plasmid transfection, and GFP was coexpressed with DcR2 in mice treated with DcR2-overexpression plasmid. DcR2 mRNA and protein levels were decreased by 74.7% and 69.0% after DcR2-siRNA transfection, respectively, whereas they were increased by 215% and 192% after DcR2-overexpression transfection, respectively (Supplementary Figure S1C-E).…”

Section: Role Of Dcr2 In Renal Fibrosis In Dnmentioning

confidence: 82%

“…Ultrasonography-mediated gene transfer of DcR2-siRNA or DcR2-overexpression plasmid in vivo DcR2-siRNA or DcR2-overexpression plasmid (OBiO Technology, Shanghai, China) was transferred into the kidney of mice using the ultrasonography microbubble-mediated gene transfer technique as per our previously published research. 26 Briefly, the DcR2 expression plasmids were mixed with Sonovue (Bracco, Milan, Italy) at a ratio of 1:1 (vol/vol). For the control vector group, the same amount of empty control plasmids was used.…”

Section: Animal Modelsmentioning

confidence: 99%

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Decoy receptor 2 mediation of the senescent phenotype of tubular cells by interacting with peroxiredoxin 1 presents a novel mechanism of renal fibrosis in diabetic nephropathy

Chen

Xiao

et al. 2020

Kidney International

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Premature senescence of renal tubular epithelial cell (RTEC), which is involved in kidney fibrosis, is a key event in the progression of diabetic nephropathy. However, the underlying mechanism remains unclear. Here we investigated the role and mechanism of decoy receptor 2 (DcR2) in kidney fibrosis and the senescent phenotype of RTEC. DcR2 was specifically expressed in senescent RTEC and associated with kidney fibrosis in patients with diabetic nephropathy and mice with streptozotocin-induced with diabetic nephropathy. Knockdown of DcR2 decreased the expression of a-smooth muscle actin, collagen I, fibronectin and serum creatinine levels in streptozotocin-induced mice. DcR2 knockdown also inhibited the expression of senescent markers p16, p21, senescence-associated betagalactosidase and senescence-associated heterochromatic foci and promoted the secretion of a senescence-associated secretory phenotype including IL-6, TGF-b1, and matrix metalloproteinase 2 in vitro and in vivo. However, DcR2 overexpression showed the opposite effects. Quantitative proteomics and validation studies revealed that DcR2 interacted with peroxiredoxin 1 (PRDX1), which regulated the cell cycle and senescence. Knockdown of PRDX1 upregulated p16 and cyclin D1 while downregulating cyclin-dependent kinase 6 expression in vitro, resulting in RTEC senescence. Furthermore, PRDX1 knockdown promoted DcR2-induced p16, cyclin D1, IL-6, and TGF-b1 expression, whereas PRDX1 overexpression led to the opposite results. Subsequently, DcR2 regulated PRDX1 phosphorylation, which could be inhibited by the specific tyrosine kinase inhibitor genistein. Thus, DcR2 mediated the senescent phenotype of RTEC and kidney fibrosis by interacting with PRDX1. Hence, DcR2 may act as a potential therapeutic target for the amelioration of diabetic nephropathy progression.

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Section: Role Of Dcr2 In Renal Fibrosis In Dnmentioning

confidence: 82%

Section: Animal Modelsmentioning

confidence: 99%

Decoy receptor 2 mediation of the senescent phenotype of tubular cells by interacting with peroxiredoxin 1 presents a novel mechanism of renal fibrosis in diabetic nephropathy

Chen

Xiao

et al. 2020

Kidney International

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“…C1orf54 was reported to potentially function in the pathophysiology of diffuse congenital hyperinsulinism through the IGF-1/mTOR/AKT pathway, 19 and the PI3K/AKT pathway is known to play a critical role in cell proliferation. 20,21 Here, we demonstrated that AKT phosphorylation was inhibited in C1orf54-deficient mice after kidney IRI and that this could be reproduced in HK-2 cells subject to hypoxia/reoxygenation.…”

Section: C1orf54 Overexpression Alleviated Post-iri Renal Dysfunctionmentioning

confidence: 79%

Tubular epithelial C1orf54 mediates protection and recovery from acute kidney injury

Xie

Wang

Zhang

et al. 2018

J Cellular Molecular Medi

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Acute kidney injury (AKI) incidence among hospitalized patients is increasing steadily. Despite progress in prevention strategies and support measures, AKI remains correlated with high mortality, particularly among ICU patients, and no effective AKI therapy exists. Here, we investigated the function in kidney ischaemia‐reperfusion injury (IRI) of C1orf54, a newly identified protein encoded by an open reading frame on chromosome 1. C1orf54 expression was high in kidney and low in heart, liver, spleen, lung and skeletal muscle in healthy mice, and in the kidney, C1orf54 was expressed in tubular epithelial cells (TECs), but not in glomeruli. C1orf54 expression was markedly decreased on Day 1 after kidney IRI and then gradually recovered to baseline levels by Day 7. Notably, relative to wild‐type mice, C1orf54‐knockout mice exhibited impaired TEC proliferation and delayed recovery after kidney IRI, which led to deteriorated renal function and increased mortality. Conversely, adenovirus‐mediated C1orf54 overexpression promoted TEC proliferation and ameliorated kidney pathology, which resulted in accelerated renal repair and improved renal function. Mechanistically, C1orf54 was found to promote TEC proliferation through PI3K/AKT signalling. Thus, C1orf54 holds considerable potential as a therapeutic target in kidney IRI.

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“…Suppressed cell proliferation has been frequently observed during renal iri and the promotion of tubular cell proliferation is the natural response during recovery from renal dysfunction (52,53); for example, the transcription factor transcriptional repressor GaTa-binding 1, which was initially characterized as an essential regulator of cell morphogenesis during kidney development, promoted tubular cell proliferation following iri through regulating cyclic AMP-specific 3' ,5'-cyclic phosphodiesterase activity and aKT signaling, and it is thus viewed as a potential target for treating kidney iri (53). in the present study, it was demonstrated that PHC treatment significantly promoted renal cell proliferation, alongside increasing Bcl-2 expression levels ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation

Kang

Wen

et al. 2020

Mol Med Report

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Penehyclidine hydrochloride (PHc) suppresses renal ischemia and reperfusion (i/r) injury (iri); however, the underlying mechanism of action that achieves this function remains largely unknown. The present study aimed to investigate the potential role of autophagy in PHc-induced suppression of renal iri, as well as the involvement of cell proliferation and apoptosis. a rat iri model and a cellular hypoxia/oxygenation (H/r) model were established; PHc, 3-methyladenine (3-Ma) and rapamycin (rapa) were administered to the iri model rats prior to i/r induction and to H/r cells following reperfusion. Serum creatinine was measured using a biochemistry analyzer, whereas aspartate aminotransferase (aSaT) and alanine aminotransferase (alaT) expression levels were detected using eliSa kits. renal tissue injury was evaluated by histological examination. in addition, microtubule-associated protein light chain 3B (lc3B) expression, autophagosome formation, cell proliferation and apoptosis were detected in the cellular H/r model. The results demonstrated that i/r induced renal injury in iri model rats, upregulated serum creatinine, alaT and aSaT expression levels, and increased autophagic processes. in contrast, pretreatment with PHC or Rapa significantly prevented these i/r-induced changes, whereas the administration of 3-Ma enhanced i/r-induced injuries through suppressing autophagy. PHc and rapa increased lc3B and Beclin-1 expression levels, but decreased sequestome 1 (p62) expression in the cellular H/r model, whereas 3-Ma prevented these PHc-induced changes. PHc and rapa promoted proliferation and autophagy in the cellular H/r model; these effects were accompanied by increased expression levels of lc3B and Beclin-1, and reduced p62 expression levels, whereas these levels were inhibited by 3-Ma. Furthermore, PHc and rapa inhibited apoptosis in the cellular H/r model through increasing Bcl-2 expression levels, and suppressing Bax and caspase-3 expression levels; the opposite effect was induced by 3-Ma. in conclusion, PHc suppressed renal iri through the induction of autophagy, which in turn promoted proliferation and suppressed apoptosis in renal cells.

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Transcription Factor Trps1 Promotes Tubular Cell Proliferation after Ischemia-Reperfusion Injury through cAMP–Specific 3′,5′-Cyclic Phosphodiesterase 4D and AKT

Cited by 18 publications

References 46 publications

Decoy receptor 2 mediation of the senescent phenotype of tubular cells by interacting with peroxiredoxin 1 presents a novel mechanism of renal fibrosis in diabetic nephropathy

Decoy receptor 2 mediation of the senescent phenotype of tubular cells by interacting with peroxiredoxin 1 presents a novel mechanism of renal fibrosis in diabetic nephropathy

Tubular epithelial C1orf54 mediates protection and recovery from acute kidney injury

Prevention of renal ischemia and reperfusion injury by penehyclidine hydrochloride through autophagy activation

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