scholarly journals Sprr2f protects against renal injury by decreasing the level of reactive oxygen species in female mice

2020 ◽  
Vol 319 (5) ◽  
pp. F876-F884
Author(s):  
Kieu My Huynh ◽  
Anny Chuu-Yun Wong ◽  
Bo Wu ◽  
Marc Horschman ◽  
Hongjuan Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Renal Injury ◽  
Renal Damage ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Rich Region ◽  
Female Mice ◽  
Proline Rich Region

Renal injury leads to chronic kidney disease, with which women are not only more likely to be diagnosed than men but have poorer outcomes as well. We have previously shown that expression of small proline-rich region 2f ( Sprr2f), a member of the small proline-rich region ( Sprr) gene family, is increased several hundredfold after renal injury using a unilateral ureteral obstruction (UUO) mouse model. To better understand the role of Sprr2f in renal injury, we generated a Sprr2f knockout ( Sprr2f-KO) mouse model using CRISPR-Cas9 technology. Sprr2f-KO female mice showed greater renal damage after UUO compared with wild-type ( Sprr2f-WT) animals, as evidenced by higher hydroxyproline levels and denser collagen staining, indicating a protective role of Sprr2f during renal injury. Gene expression profiling by RNA sequencing identified 162 genes whose expression levels were significantly different between day 0 and day 5 after UUO in Sprr2f-KO mice. Of the 162 genes, 121 genes were upregulated after UUO and enriched with those involved in oxidation-reduction, a phenomenon not observed in Sprr2f-WT animals, suggesting a protective role of Sprr2f in UUO through defense against oxidative damage. Consistently, bilateral ischemia-reperfusion injury resulted in higher serum blood urea nitrogen levels and higher tissue reactive oxygen species in Sprr2f-KO compared with Sprr2f-WT female mice. Moreover, cultured renal epithelial cells from Sprr2f-KO female mice showed lower viability after oxidative damage induced by menadione compared with Sprr2f-WT cells that could be rescued by supplementation with reduced glutathione, suggesting that Sprr2f induction after renal damage acts as a defense against reactive oxygen species.

Protective role of carbon dioxide (CO2) in generation of reactive oxygen species

2015 ◽  
Vol 411 (1-2) ◽  
pp. 317-330 ◽  
Author(s):  
Sergey Bolevich ◽  
Alekandr Haritonovic Kogan ◽  
Vladimir Zivkovic ◽  
Dusan Djuric ◽  
Aleksey Aleksejevic Novikov ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Carbon Dioxide Co2

scholarly journals Role of reactive oxygen species in renal damage in experimental leprosy

1995 ◽  
Vol 66 (3) ◽  
Author(s):  
N. AGNIHOTRI ◽  
N. K. GANGULY ◽  
S. KAUR ◽  
M. KHULLAR ◽  
S. C. SHARMA ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Renal Damage ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Experimental Leprosy

scholarly journals Protective Role of Reactive Oxygen Species in Endotoxin-Induced Lung Inflammation through Modulation of IL-10 Expression

2012 ◽  
Vol 188 (11) ◽  
pp. 5734-5740 ◽  
Author(s):  
Jing Deng ◽  
Xuerong Wang ◽  
Feng Qian ◽  
Stephen Vogel ◽  
Lei Xiao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lung Inflammation ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species

scholarly journals Protective Role of Peroxiredoxins against Reactive Oxygen Species in Neonatal Rat Testicular Gonocytes

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 32 ◽  
Author(s):  
Cristian O’Flaherty ◽  
Annie Boisvert ◽  
Gurpreet Manku ◽  
Martine Culty
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Gene Array ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Protective Role ◽  
Neonatal Rat ◽  
Oxygen Species ◽  
Antioxidant Genes

Peroxiredoxins (PRDXs) are antioxidant enzymes that protect cells from oxidative stress and play a role in reactive oxygen species (ROS)-mediated signaling. We reported that PRDXs are critical for human fertility by maintaining sperm viability and regulating ROS levels during capacitation. Moreover, studies on Prdx6−/− mice revealed the essential role of PRDX6 in the viability, motility, and fertility competence of spermatozoa. Although PRDXs are abundant in the testis and spermatozoa, their potential role at different phases of spermatogenesis and in perinatal germ cells is unknown. Here, we examined the expression and role of PRDXs in isolated rat neonatal gonocytes, the precursors of spermatogonia, including spermatogonial stem cells. Gene array, qPCR analyses showed that PRDX1, 2, 3, 5, and 6 transcripts are among the most abundant antioxidant genes in postnatal day (PND) 3 gonocytes, while immunofluorescence confirmed the expression of PRDX1, 2, and 6 proteins. The role of PRDXs in gonocyte viability was examined using PRDX inhibitors, revealing that the 2-Cys PRDXs and PRDX6 peroxidases activities are critical for gonocytes viability in basal condition, likely preventing an excessive accumulation of endogenous ROS in the cells. In contrast to its crucial role in spermatozoa, PRDX6 independent phospholipase A2 (iPLA2) activity was not critical in gonocytes in basal conditions. However, under conditions of H2O2-induced oxidative stress, all these enzymatic activities were critical to maintain gonocyte viability. The inhibition of PRDXs promoted a two-fold increase in lipid peroxidation and prevented gonocyte differentiation. These results suggest that ROS are produced in neonatal gonocytes, where they are maintained by PRDXs at levels that are non-toxic and permissive for cell differentiation. These findings show that PRDXs play a major role in the antioxidant machinery of gonocytes, to maintain cell viability and allow for differentiation.

scholarly journals Diabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-30 ◽  
Author(s):  
Selim Fakhruddin ◽  
Wael Alanazi ◽  
Keith E. Jackson
Keyword(s):  
Reactive Oxygen Species ◽  
Glomerular Filtration ◽  
Renal Injury ◽  
Renal Damage ◽  
Structural Changes ◽  
Reactive Oxygen ◽  
Signaling Molecules ◽  
Oxygen Species ◽  
Filtration Barrier ◽  
Chronic Hyperglycemia

Diabetes induces the onset and progression of renal injury through causing hemodynamic dysregulation along with abnormal morphological and functional nephron changes. The most important event that precedes renal injury is an increase in permeability of plasma proteins such as albumin through a damaged glomerular filtration barrier resulting in excessive urinary albumin excretion (UAE). Moreover, once enhanced UAE begins, it may advance renal injury from progression of abnormal renal hemodynamics, increased glomerular basement membrane (GBM) thickness, mesangial expansion, extracellular matrix accumulation, and glomerulosclerosis to eventual end-stage renal damage. Interestingly, all these pathological changes are predominantly driven by diabetes-induced reactive oxygen species (ROS) and abnormal downstream signaling molecules. In diabetic kidney, NADPH oxidase (enzymatic) and mitochondrial electron transport chain (nonenzymatic) are the prominent sources of ROS, which are believed to cause the onset of albuminuria followed by progression to renal damage through podocyte depletion. Chronic hyperglycemia and consequent ROS production can trigger abnormal signaling pathways involving diverse signaling mediators such as transcription factors, inflammatory cytokines, chemokines, and vasoactive substances. Persistently, increased expression and activation of these signaling molecules contribute to the irreversible functional and structural changes in the kidney resulting in critically decreased glomerular filtration rate leading to eventual renal failure.

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