Circadian Clock Genes in Diabetic Kidney Disease (DKD)

Olaoye, Olanrewaju A; Masten, Sarah; Mohandas, Rajesh; Gumz, Michelle L.

doi:10.1007/s11892-019-1156-z

Cited by 11 publications

(7 citation statements)

References 76 publications

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“…Of these genes, Cry1 have been reported to influence DKD by disrupting the circadian rhythm, which results in cellular instability. 36,37 The other mRNAs have not been reported to be associated with the development of DKD, but the roles of these mRNAs should be investigated in future studies. In contrast, overexpression of miRNA-125b-5p did not have any effects on DKD in vivo.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Profiling in Diabetic Kidney Disease

Ishii¹,

Kaneko²,

Yanai³

et al. 2021

Translational Research

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The microRNAs (miRNAs) that can regulate diabetic kidney disease (DKD) have not been fully characterized. The aim of this study was to identify the miRNAs that affect DKD and could be used as specific biomarkers or therapeutic agents. First, kidney tissues from two DKD mouse models and control mice were screened for differences in miRNA expression by microarray analysis followed by quantitative real-time reverse transcription-PCR. Six miRNAs were differentially expressed from controls in both DKD mouse models. Among them, miRNA-125b-5p and miRNA-181b-5p were exclusively downregulated in the DKD mouse model. Next, we administered miRNA-181b-5p-mimic to DKD mice, which reduced the albuminuria and abnormal mesangial expansion. Pathway analysis and database research revealed that overexpression of miRNA-181b-5p significantly altered the expression of seven mRNAs in six known signaling pathways in the kidneys of DKD mice. Furthermore, the serum level of miRNA-125b-5p was significantly higher in patients with DKD (1.89 §0.40-fold, P<0.05) compared with patients with other kidney diseases (0.94 § 0.13-fold) and healthy subjects (1.00 §0.19-fold). Serum levels of miRNA-181b-5p were lower in patients with DKD (0.30 §0.06-fold, P<0.05) compared with patients with other kidney diseases (1.06 §0.20-fold) and healthy subjects (1.00 §0.16-fold). These results suggest that miRNA-125b-5p and miRNA-181b-5p may represent novel diagnostic biomarkers and that miRNA-181b-5p may represent a therapeutic target for DKD. (Translational Research 2021; 000:1À22) Abbreviations: BMI = body mass index; DAPI = 4 0 ,6-diamidino-2-phenylindole; FITC = fluorescein isothiocyanate; DKD = diabetic kidney disease; eGFR = estimated glomerular filtration rate; HDL high-density lipoprotein; HIGA = high immunoglobulin A; IRI = ischemia-reperfusion injury; LDL = low-density lipoprotein; ns = not significant; PEI-NPs = polyethylenimine nanoparticles; RNU6 = U6 Small Nuclear 1; SAMP = senescence-accelerated mouse; SAMR = control for the senescence-accelerated mouse; UACR = urine albumin-to-creatinine ratio; UUO = unilateral ureteral obstruction

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Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Profiling in Diabetic Kidney Disease

Ishii¹,

Kaneko²,

Yanai³

et al. 2021

Translational Research

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“…Although circadian disruption is thought to contribute to kidney disease 3 , 4 , no predictive or diagnostic capacity of PER2 or HO1 expression could be found for AKI. However, this may be due to the limited amount of AKI cases in our patient cohort.…”

Section: Discussionmentioning

confidence: 99%

“…Trauma patients in the ICU often exhibit impaired sleep–wake-cycles 1 , impaired cognition and impaired organ function, which might become manifest clinically as delirium and acute kidney injury (AKI). Disruption in circadian rhythm is now believed to play a major role in development of delirium 2 and contribute to the pathogenesis of kidney disease 3 , 4 . Both delirium and AKI are independently associated with adverse patient outcome and mortality 5 , 6 .…”

Section: Introductionmentioning

confidence: 99%

Expression of HO1 and PER2 can predict the incidence of delirium in trauma patients with concomitant brain injury

Steimer

Kaiser

Ulbrich

et al. 2021

Sci Rep

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Intensive care unit (ICU)-acquired delirium is associated with adverse outcome in trauma patients with concomitant traumatic brain injury (TBI), but diagnosis remains challenging. Quantifying circadian disruption by analyzing expression of the circadian gene period circadian regulator 2 (PER2) and heme oxygenase 1 (HO1), which determines heme turnover, may prove to be potential diagnostic tools. Expression of PER2 and HO1 was quantified using qPCR from blood samples 1 day and 7 days after trauma. Association analysis was performed comparing mRNA expression levels with parameters of trauma (ISS—injury severity score), delirium, acute kidney injury (AKI) and length of ICU stay. 48 polytraumatized patients were included (equal distribution of TBI versus non-TBI) corrected for ISS, age and gender using a matched pairs approach. Expression levels of PER2 and HO1 were independent of age (PER2: P = 0.935; HO1: P = 0.988), while expression levels were significantly correlated with trauma severity (PER2: P = 0.009; HO1: P < 0.001) and longer ICU length of stay (PER2: P = 0.018; HO1: P < 0.001). High expression levels increased the odds of delirium occurrence (PER2: OR = 4.32 [1.14–13.87]; HO1: OR = 4.50 [1.23–14.42]). Patients with TBI showed a trend towards elevated PER2 (OR = 3.00 [0.84–9.33], P = 0.125), but not towards delirium occurrence (P = 0.556). TBI patients were less likely to develop AKI compared to non-TBI (P = 0.022). Expression levels of PER2 and HO1 correlate with the incidence of delirium in an age-independent manner and may potentially improve diagnostic algorithms when used as delirium biomarkers.Trial registration: German Clinical Trials Register (Trial-ID DRKS00008981; Universal Trial Number U1111-1172-6077; Jan. 18, 2018).

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“…Female rats have been shown to have higher expression levels of both Na ϩ /Cl Ϫ cotransporter and ENaC subunits as well as different urinary electrolyte excretion in response to a K ϩ -rich meal (48), which provides sufficient evidence to investigate the potential differences between male and female animals in renal insulin-mediated Na ϩ handling. Another avenue of investigation worth considering is the potential effect of circadian rhythms to influence these experiments, particularly given the circadian modulation of ␣ENaC expression (15) and the potential for disruption of normal circadian rhythm to contribute to the development of diabetic kidney disease (31). The experiments from this postprandial study were conducted after rats were fasted overnight, and the meal supplement was given early in the morning, roughly the human equivalent of fasting all day and then eating right before bedtime, which is the transition period between higher diurnal blood pressure and lower nocturnal blood pressure.…”

Section: Enac-mediated Na ؉ Retention In Nonpathological Insulin Signalingmentioning

confidence: 99%

Postprandial effects on electrolyte homeostasis in the kidney

Klemens

Brands

Staruschenko

2019

American Journal of Physiology-Renal Physiology

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Insulin is known to be an important regulator of a number of different channels and transporters in the kidney, but its role in the kidney to prevent Na+ and volume loss during the osmotic load after a meal has only recently been validated. With increasing numbers of people suffering from diabetes and hypertension, furthering our understanding of insulin signaling and renal Na+ handling in both normal and diseased states is essential for improving patient treatments and outcomes. The present review is focused on postprandial effects on Na+ reabsorption in the kidney and the role of the epithelial Na+ channels as an important channel contributing to insulin-mediated Na+ reclamation.

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Circadian Clock Genes in Diabetic Kidney Disease (DKD)

Cited by 11 publications

References 76 publications

MicroRNA Expression Profiling in Diabetic Kidney Disease

MicroRNA Expression Profiling in Diabetic Kidney Disease

Expression of HO1 and PER2 can predict the incidence of delirium in trauma patients with concomitant brain injury

Postprandial effects on electrolyte homeostasis in the kidney

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