SPAK plays a pathogenic role in IgA nephropathy through the activation of NF-κB/MAPKs signaling pathway

Lin, Tsai-Jung; Yang, Sung‐Sen; Hua, Kuo-Feng; Tsai, Yu‐Ling; Lin, Shih‐Hua; Ka, Shuk‐Man

doi:10.1016/j.freeradbiomed.2016.08.008

Cited by 22 publications

(36 citation statements)

References 56 publications

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“…NF‐κB pathway exerts the indispensable functions in the inflammation‐correlated ailments, which medicates the induction and resolution of inflammation . Activated NF‐κB pathway has been testified to be embroiled in aggravating the disease process of IgAN . One research explained that downregulation of lncRNA TUG1 accelerated the evolution of sepsis‐correlated acute kidney damage through modulating miR‐142‐3p and NF‐κB pathway .…”

Section: Discussionmentioning

confidence: 99%

Retracted: Long noncoding RNA Mirt2 prohibits lipopolysaccharide‐evoked HK‐2 cell injury via modulation of microRNA‐126

Bai

Nie

et al. 2019

BioFactors

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Long noncoding RNA myocardial infarction‐associated transcript 2 (lncRNA Mirt2) is a burgeoning lncRNA, its anti‐inflammatory capacity has been testified. Nonetheless, the functions of Mirt2 in immunoglobulin A nephropathy are unexplored. We tried to impart the influences of Mirt2 in lipopolysaccharide (LPS)‐evoked HK‐2 cells damage. HK‐2 cells were manipulated with 10 ng/ml LPS, next cell viability, apoptosis, reactive oxygen species (ROS) generation, pro‐inflammatory factors and Mirt2 expression were evaluated. After pc‐Mirt2 vector transfection, the aforementioned trials were performed. Meanwhile, real‐time quantitative polymerase chain reaction (PCR) experiment was used to detect miR‐126 expression. Subsequently, functions of miR‐126 in LPS‐treated HK‐2 cells were further delved after transfection with miR‐126 mimic. Western blot was used to evaluate NF‐κB pathway. The data showed that LPS invoked HK‐2 cells inflammatory damage via the suppression of cell viability and the acceleration of apoptosis, ROS level, and IL‐1β and IL‐6 secretion. LPS inhibited Mirt2 expression and overexpression of Mirt2 mitigated LPS‐caused inflammatory damage in HK‐2 cells. Additionally, overexpression of Mirt2 repressed miR‐126 expression in LPS‐stimulated cells. Meanwhile the anti‐inflammatory effect of Mirt2 was inverted by upregulating miR‐126 expression. Besides, overexpressed Mirt2 retarded LPS‐activated NF‐κB pathway via repressing miR‐126. The research certified the anti‐inflammatory impacts of Mirt2 on LPS‐impaired HK‐2 cells.

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Section: Discussionmentioning

confidence: 99%

Retracted: Long noncoding RNA Mirt2 prohibits lipopolysaccharide‐evoked HK‐2 cell injury via modulation of microRNA‐126

Bai

Nie

et al. 2019

BioFactors

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“…This finding might also imply that WNK kinases have other tumor-promoting effects including direct proliferative actions on tumors [11,32]. Similar to WNK1 downstream target-SPAK functions both downstream and also upstream of NF-κB signaling [33,34] forming a positive feedback loop to promote tumorigenesis. WNK1 might also play multiple roles in tumorigenesis through cross-talk with multiple signal pathways.…”

Section: Discussionmentioning

confidence: 96%

WNK1 Kinase Stimulates Angiogenesis to Promote Tumor Growth and Metastasis

Sie

Sampurna

et al. 2020

Cancers

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With-no-lysine (K)-1 (WNK1) is the founding member of family of four protein kinases with atypical placement of catalytic lysine that play important roles in regulating epithelial ion transport. Gain-of-function mutations of WNK1 and WNK4 cause a mendelian hypertension and hyperkalemic disease. WNK1 is ubiquitously expressed and essential for embryonic angiogenesis in mice. Increasing evidence indicates the role of WNK kinases in tumorigenesis at least partly by stimulating tumor cell proliferation. Here, we show that human hepatoma cells xenotransplanted into zebrafish produced high levels of vascular endothelial growth factor (VEGF) and WNK1, and induced expression of zebrafish wnk1. Knockdown of wnk1 in zebrafish decreased tumor-induced ectopic vessel formation and inhibited tumor proliferation. Inhibition of WNK1 or its downstream kinases OSR1 (oxidative stress responsive kinase 1)/SPAK (Ste20-related proline alanine rich kinase) using chemical inhibitors decreased ectopic vessel formation as well as proliferation of xenotransplanted hepatoma cells. The effect of WNK and OSR1 inhibitors is greater than that achieved by inhibitor of VEGF signaling cascade. These inhibitors also effectively inhibited tumorigenesis in two separate transgenic zebrafish models of intestinal and hepatocellular carcinomas. Endothelial-specific overexpression of wnk1 enhanced tumorigenesis in transgenic carcinogenic fish, supporting endothelial cell-autonomous effect of WNK1 in tumor promotion. Thus, WNK1 can promote tumorigenesis by multiple effects that include stimulating tumor angiogenesis. Inhibition of WNK1 may be a potent anti-cancer therapy.

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“…According to the predictor, the numerical density higher than 100,000/mm 3 indicated more rapid progression of CRF towards the end stage renal disease and simultaneous deterioration of the pathohistological findings through verified changes characteristic of fibrosis, which was proven in several studies 24 . Therefore, over the last few years, a considerable effort was made to discover appropriate inflammation inhibitors, primarily endogenous, which would decrease infiltration of the interstitium, modify the role of proximal tubular cells to infiltration and fibrosis and slow down the progression of CRF [25][26][27] .…”

Section: Discussionmentioning

confidence: 99%

Influence of infiltrate density in the interstitium on the prognosis of primary glomerulonephritis

Bozic

Knežević

Strazmester-Majstorovic

et al. 2019

VOJNOSANIT PREGL

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Background/Aim. Development of inflammatory changes, fibrosis and loss of morphological structures of the interstitium have an important role in pathogenesis of primary glomerulonephritis, affecting the development, course and prognosis of the disease. The aim of this study was to determine the influence of changes in the interstitium on the prognosis of primary glomerulonephritis. Methods. The research included 216 patients suffering from different types of primary glumeronephritis treated at the Clinic for Nephrology and Clinical Immunology of the Clinical Center of Vojvodina, Serbia who were being monitored on average for 77.5 months. After determining on pathohistological diagnosis of the type of glomerulonephritis, renal changes in the interstitium were quantified. Numerical density in the tissue volume unit and structure of infiltrates of the interstitium were established by using the Weibel system (M42) incorporated into light microscope. Routine analyses were performed by using standard laboratory procedure. Results. During the research period the highest numerical density of infiltrates was verified in extracapillary glomerulonephritis (147,869 × mm-3), slightly less in membranoproliferative siju bubrežne insuficijencije. Zaključak. Gustina infiltrata u intersticijumu kod primarnih glomerulonefritisa je važan, rani prognostički prediktor progresije bubrežne insuficijencije. Ključne reči: glomerulonefritis; bubreg, hronična insuficijencija; vezivno tkivo; prognoza; histološke tehnike.

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SPAK plays a pathogenic role in IgA nephropathy through the activation of NF-κB/MAPKs signaling pathway

Cited by 22 publications

References 56 publications

Retracted: Long noncoding RNA Mirt2 prohibits lipopolysaccharide‐evoked HK‐2 cell injury via modulation of microRNA‐126

Retracted: Long noncoding RNA Mirt2 prohibits lipopolysaccharide‐evoked HK‐2 cell injury via modulation of microRNA‐126

WNK1 Kinase Stimulates Angiogenesis to Promote Tumor Growth and Metastasis

Influence of infiltrate density in the interstitium on the prognosis of primary glomerulonephritis

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