scholarly journals ACE2 Expression in Kidney and Testis May Cause Kidney and Testis Damage After 2019-nCoV Infection

2020 ◽  
Author(s):  
Caibin Fan ◽  
Kai Li ◽  
Yanhong Ding ◽  
Wei Lu ◽  
Jianqing Wang
Keyword(s):  
Renal Function ◽  
Young Patients ◽  
Clinical Work ◽  
Testicular Tissue ◽  
Kidney Damage ◽  
Function Evaluation ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Novel Coronavirus ◽  
Potential Pathogenicity

AbstractIn December 2019 and January 2020, novel coronavirus (2019-nCoV) - infected pneumonia (NCIP) occurred in Wuhan, and has already posed a serious threat to public health. ACE2 (Angiotensin Converting Enzyme 2) has been shown to be one of the major receptors that mediate the entry of 2019-nCoV into human cells, which also happens in severe acute respiratory syndrome coronavirus (SARS). Several researches have indicated that some patients have abnormal renal function or even kidney damage in addition to injury in respiratory system, and the related mechanism is unknown. This arouses our interest in whether coronavirus infection will affect the urinary and male reproductive systems. Here in this study, we used the online datasets to analyze ACE2 expression in different human organs. The results indicate that ACE2 highly expresses in renal tubular cells, Leydig cells and cells in seminiferous ducts in testis. Therefore, virus might directly bind to such ACE2 positive cells and damage the kidney and testicular tissue of patients. Our results indicate that renal function evaluation and special care should be performed in 2019-nCoV patients during clinical work, because of the kidney damage caused by virus and antiviral drugs with certain renal toxicity. In addition, due to the potential pathogenicity of the virus to testicular tissues, clinicians should pay attention to the risk of testicular lesions in patients during hospitalization and later clinical follow-up, especially the assessment and appropriate intervention in young patients’ fertility.

scholarly journals ACE2 Expression in Kidney and Testis May Cause Kidney and Testis Infection in COVID-19 Patients

2021 ◽  
Vol 7 ◽  
Author(s):  
Caibin Fan ◽  
Wei Lu ◽  
Kai Li ◽  
Yanhong Ding ◽  
Jianqing Wang
Keyword(s):  
Young Patients ◽  
Clinical Work ◽  
Function Evaluation ◽  
Binding Assays ◽  
Angiotensin Converting Enzyme 2 ◽  
Renal Tubular Cells ◽  
New Type ◽  
Testicular Lesions ◽  
Renal Tubular

In December 2019, a new type of pneumonia caused by SARS-Cov-2 (COVID-19) occurred in Wuhan and has been discovered in many countries around the world. ACE2 (angiotensin-converting enzyme 2) has been shown to be one of the major receptors that mediate the entry of SARS-Cov-2 into human cells. Here in this study, we used the online datasets to analyze ACE2 expression in different human organs. The results indicated that ACE2 highly expresses in renal tubular cells, Sertoli cells, Leydig cells, and cells in seminiferous ducts in testis. Recombinant SARS-CoV-2 spike protein (RBD) domain and ACE2 of RPTEC/SerC cell-binding assays confirmed that SARS-Cov-2 can bind to ACE2 on the surface of these cells. Our results suggest that ACE2 expression could contribute to kidney and testis infection after COVID-19 infection. Renal function evaluation and special care should be performed during clinical work. Clinicians should also pay attention to the risk of testicular lesions in patients during hospitalization and later clinical follow-up, especially the assessment and appropriate intervention in young patients' fertility.

Physiologic Variation Of Renal Function In Twins: Diuresis After Water Intake

1958 ◽  
Vol 7 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Bertha M. Aschner ◽  
Stanley M. Gartler
Keyword(s):  
Renal Function ◽  
Maximum Rate ◽  
Genetic Factors ◽  
Twin Pair ◽  
Urine Flow ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Diuretic Response ◽  
The Difference ◽  
Renal Tubular

SUMMARYIn six monozygotic and six dizygotic healthy twin pairs the urine elimination after rapid drinking of 1000 cc of water (Fishberg-Volhard test) was studied. Considerabbe variation wes observed in the diuretic response of these individuals, particularly in the maximum rate of the reactive diuresis. The minute volumes of urine during the half-hour period of the largest output were compared between the partners of each twin pair. It was found that the difference of the maximum rate of urine flow was significantly (0.01 level) smaller between one-egg than between two-egg twins under otherwise equal conditions. The concept of genetic factors controlling the function of the renal tubular cells is discussed.

scholarly journals Fibrinogen β–derived Bβ15-42 peptide protects against kidney ischemia/ reperfusion injury

Blood ◽  
2011 ◽  
Vol 118 (7) ◽  
pp. 1934-1942 ◽  
Author(s):  
Aparna Krishnamoorthy ◽  
Amrendra Kumar Ajay ◽  
Dana Hoffmann ◽  
Tae-Min Kim ◽  
Victoria Ramirez ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
High Sensitivity ◽  
Kidney Damage ◽  
Therapeutic Interventions ◽  
Mrna Levels ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Injury And Repair

AbstractIschemia/reperfusion (I/R) injury in the kidney is a major cause of acute kidney injury (AKI) in humans and is associated with significantly high mortality. To identify genes that modulate kidney injury and repair, we conducted genome-wide expression analysis in the rat kidneys after I/R and found that the mRNA levels of fibrinogen (Fg)α, Fgβ, and Fgγ chains significantly increase in the kidney and remain elevated throughout the regeneration process. Cellular characterization of Fgα and Fgγ chain immunoreactive proteins shows a predominant expression in renal tubular cells and the localization of immunoreactive Fgβ chain protein is primarily in the renal interstitium in healthy and regenerating kidney. We also show that urinary excretion of Fg is massively increased after kidney damage and is capable of distinguishing human patients with acute or chronic kidney injury (n = 25) from healthy volunteers (n = 25) with high sensitivity and specificity (area under the receiver operating characteristic of 0.98). Furthermore, we demonstrate that Fgβ-derived Bβ15-42 peptide administration protects mice from I/R-induced kidney injury by aiding in epithelial cell proliferation and tissue repair. Given that kidney regeneration is a major determinant of outcome for patients with kidney damage, these results provide new opportunities for the use of Fg in diagnosis, prevention, and therapeutic interventions in kidney disease.

scholarly journals Indirect effects of severe acute respiratory syndrome coronavirus 2 on the kidney in coronavirus disease patients

2020 ◽  
Vol 13 (3) ◽  
pp. 347-353 ◽  
Author(s):  
Aymeric Couturier ◽  
Sophie Ferlicot ◽  
Kévin Chevalier ◽  
Matthieu Guillet ◽  
Marie Essig ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Renal Tubular Cells ◽  
Collapsing Glomerulopathy ◽  
Tubulointerstitial Lesions ◽  
Polymerase Chain ◽  
Renal Tubular ◽  
Novel Coronavirus ◽  
Kidney Lesions

Abstract Among patients hospitalized for novel coronavirus disease (COVID-19), between 10 and 14% develop an acute kidney injury and around half display marked proteinuria and haematuria. Post-mortem analyses of COVID-19 kidney tissue suggest that renal tubular cells and podocytes are affected. Here we report two cases of collapsing glomerulopathy and tubulointerstitial lesions in living COVID-19 patients. Despite our use of sensitive reverse transcription polymerase chain reaction techniques in this study, we failed to detect the virus in blood, urine and kidney tissues. Our observations suggest that these kidney lesions are probably not due to direct infection of the kidney by severe acute respiratory syndrome coronavirus 2.

scholarly journals Inhibition of PDE4/PDE4B improves renal function and ameliorates inflammation in cisplatin-induced acute kidney injury

2020 ◽  
Vol 318 (3) ◽  
pp. F576-F588 ◽  
Author(s):  
Man Xu ◽  
Xiaowen Yu ◽  
Xia Meng ◽  
Songming Huang ◽  
Yue Zhang ◽  
...  
Keyword(s):  
Renal Function ◽  
Cell Survival ◽  
Tubular Cell ◽  
Pde4 Inhibitor ◽  
Renal Tubular Cell ◽  
Renal Tubules ◽  
Cisplatin Nephrotoxicity ◽  
Renal Tubular Cells ◽  
Phosphorylated Akt ◽  
Renal Tubular

Nephrotoxicity is a known clinical complication of cisplatin that limits the use of this potent antitumor drug. Cyclic nucleotide phosphodiesterases (PDEs) play complex roles in physiology and pathology. PDE4, which is a member of the PDE family, has four subtypes (PDE4A–PDE4D), and PDE4B plays an important role in inflammation. Thus, in the present study, we investigated the effect of PDE4/PDE4B inhibition on renal function and inflammation in a cisplatin nephrotoxicity model. In mice, cisplatin enhanced mRNA and protein expression of PDE4B in renal tubules. After treatment with the PDE4 inhibitor cilomilast, cisplatin-induced renal dysfunction, renal tubular injury, tubular cell apoptosis, and inflammation were all improved. Next, after silencing PDE4B in vivo, we observed a protective effect against cisplatin nephrotoxicity similar to that of the PDE4 inhibitor. In vitro, cisplatin-induced renal tubular cell death was strikingly ameliorated by the PDE4 inhibitor and PDE4B knockdown along with the blockade of the inflammatory response. Considering the known roles of some cell survival pathways in antagonizing insults, we examined levels of PDE4-associated proteins sirtuin 1, phosphatidylinositol 3-kinase, and phosphorylated AKT in cisplatin-treated renal tubular cells with or without cilomilast treatment. Strikingly, cisplatin treatment downregulated the expression of the above proteins, and this effect was largely abolished by the PDE4 inhibitor. Together, these findings indicate the beneficial role of PDE4/PDE4B inhibition in treating cisplatin nephrotoxicity, possibly through antagonizing inflammation and restoring cell survival signaling pathways.

Epigenetic mechanisms of nephroprotection in diabetic nephropathy: focus is on sirtuin-1

2021 ◽  
Vol 25 (6) ◽  
pp. 9-15
Author(s):  
K. A. Aitbaev ◽  
I. T. Murkamilov ◽  
V. V. Fomin ◽  
Zh. A. Murkamilova ◽  
F. A. Yusupov
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Diseases ◽  
Critical Role ◽  
Protective Role ◽  
Kidney Damage ◽  
Sirtuin 1 ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Nephroprotective Effect

Numerous studies have shown the critical role of sirtuin-1 deacetylase (SIRT1) in the protection of renal cells from endogenous and exogenous stresses. A protective role for SIRT1 has been established in both podocytes and renal tubular cells in many kidney diseases, including diabetic nephropathy (DN). SIRT1 has also been shown to have nephroprotective effects in DN, in part through the deacetylation of transcription factors involved in disease pathogenesis, such as p53, FOXO, RelA / p65NF-KB, STAT3, and PGC1a / PPARy. Recently, it was found that podocyte-specific overexpression of SIRT1 attenuates proteinuria and kidney damage in an experimental model of DN, suggesting the possibility of using SIRT1 as a potential target for the treatment of kidney disease. In addition, SIRT1 agonists such as resveratrol and BF175 have been shown to reduce diabetic kidney damage in several experimental animal models. It has also been shown that puerarin, a Chinese herbal medicine, activates SIRT1, providing nephroprotection in a mouse model of DN. In addition to SIRT1 agonists, inhibitors of bromodomain, in particular, MS417, also have a nephroprotective effect. These results suggest that SIRT1 agonists and bromodomain inhibitors may be new potential therapeutic agents that slow the progression of DN.

scholarly journals Pinocembrin attenuates gentamicin-induced nephrotoxicity in rats

2016 ◽  
Vol 94 (8) ◽  
pp. 808-818 ◽  
Author(s):  
Sasivimon Promsan ◽  
Krit Jaikumkao ◽  
Anchalee Pongchaidecha ◽  
Nipon Chattipakorn ◽  
Varanuj Chatsudthipong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Caspase 3 ◽  
Biological Activities ◽  
Ischemia Reperfusion ◽  
Renal Tubular Cells ◽  
Gentamicin Treatment ◽  
Renal Tubular ◽  
Apoptotic Effects ◽  
Antioxidant Effects

Oxidative stress mediated apoptosis of renal tubular cells is a major pathology of gentamicin-induced nephrotoxicity, which is one of the prevailing causes of acute renal failure. Pinocembrin is a major flavonoid found in rhizomes of fingerroot (Boesenbergia pandurata). It has pharmacological and biological activities including antimicrobial, anti-inflammatory, and antioxidant effects. Preclinical studies have suggested that pinocembrin protects rat brain and heart against oxidation and apoptosis induced by ischemia–reperfusion. The aim of the current study was to investigate the mechanisms of renoprotection elicited by pinocembrin in gentamicin-induced nephrotoxicity. Nephrotoxicity was induced in rats by intraperitoneal injection (i.p.) of gentamicin, and pinocembrin was administered via i.p. 30 min before gentamicin treatment for 10 days. Gentamicin-induced nephrotoxicity was indicated by the reduced renal function and renal Oat3 function and expression. Gentamicin treatment also stimulated Nrf2, HO-1, and NQO1, as well as the pro-apoptotic proteins Bax and caspase-3, concomitant with the attenuation of Bcl-XL expression in the renal cortical tissues. Pinocembrin pretreatment improved renal function and renal Oat3 function and reduced oxidative stress and apoptotic conditions. These findings indicate that pinocembrin has a protective effect against gentamicin-induced nephrotoxicity, which may be due in part to its antioxidant and anti-apoptotic effects, subsequently leading to improved renal function.

scholarly journals Taurine Antioxidant Effect in Decreasing Kidney Damage in Male Mice (Mus Musculus) due to Oxidative Stress Induced by Paraquat

2021 ◽  
Vol 10 (2) ◽  
pp. 51
Author(s):  
Ricki Pratama ◽  
Eka Pramyrtha Hestianah ◽  
Thomas Valentinus Widiyatno ◽  
Dewa Ketut Meles ◽  
Rochmah Kurnijasanti
Keyword(s):  
Oxidative Stress ◽  
Kidney Damage ◽  
Histopathological Changes ◽  
Male Adult ◽  
Treatment Groups ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Ability To Act ◽  
High Production ◽  
Renal Tubular

Paraquat toxicity occurs through the high production of reactive oxygen species (ROS) which cause damage due to oxidative stress. Antioxidants can reduce damage through prevention of oxidative stress. Taurine has shown the ability to act as an antioxidant. The aim of this research is to find a effect of antioxidant taurine to decrease kidney damage caused by oxidative stress due to paraquat by looking at the histopathology changes. 25 male adult mices from strain DDY were used and divided into five treatment groups; C(-) (Aquadest IP), C(+) (Paraquat 30mg/kg), P1 (Paraquat 30mg/kg + Taurine 250mg/kg), P2 (Paraquat 30mg/kg + Taurine 500mg/kg) and P3 (Paraquat 30mg/kg + Taurine 1000mg/kg). All groups were given treatment intraperitoneal for twenty one days. The mices were sacrificed where kidney were collected for histopathology preparation. The parameters measured were renal histopathological changes in form of degeneration and necrosis. The results show that taurine administration had an effect on decreased degrees of damage to kidney tubular cells, with a decrease in the mean degree of renal tubular degeneration and necrosis. Degeneration of renal tubular cells in groups (P2) reduced compared to the group (C+) there were significant differences (P <0.05). Necrosis of renal tubular cells in groups (P1, P2) reduced compared to the group (C+) there were significant differences (P <0.05).  In conclusion, this research proves that administration of paraquat causes renal histopathological changes which are characterized by degeneration and necrosis. It also proves that taurine dose of 500 mg/kgBB could provided optimal effect.

scholarly journals P0969PARKIN INHIBITS THE PROGRESSION OF DIABETIC NEPHROPATHY BY PROMOTING GATA4 DEGRADATION TO REDUCE THE SENESCENCE OF RENAL TUBULAR CELLS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Kehong Chen ◽  
Jia Chen ◽  
Yani He
Keyword(s):  
Renal Function ◽  
Diabetic Nephropathy ◽  
High Glucose ◽  
Specific Gene ◽  
Protective Mechanism ◽  
Premature Senescence ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Tgf Β1

Abstract Background and Aims Diabetic nephropathy (DN) can cause end-stage renal disease. During the progression of DN, hyperglycemia accelerates the senescence of renal tubular epithelial cells (RTECs), leading to the tubulointerstitial inflammation and fibrosis. E3-ubiquitin ligase Parkin can regulate several pathophysiological processes. This study explored the role and mechanisms of Parkin in the progression of diabetic nephropathy (DN). Method 149 cases of patients with DN diagnosed by renal biopsy were recruited in our study. 32 normal kidney samples were obtained from renal carcinoma as control. Renal Parkin expression was detected by immunohistochemistry. The correlation between Parkin expression and renal pathological injury scores, renal function injury parameters were analyzed. In vivo, we generated Parkin overexpressed streptozotocin-induced DN mice using ultrasound- mediated adenovirus transfection. In vitro, knockdown and overexpression experiments were performed by parkin siRNA or Parkin overexpressed adenovirus in high glucose (HG) stimulated mouse primary RTEC. Moreover, we used co-immunoprecipitation and pull down experiments to evaluate the interaction of GATA4 with parkin. Results We found that Parkin expression gradually decreased and was inversely associated with IL-6, TGF-β1 and GATA4 expression in the kidney during the progression of DN. Parkin over-expression (OE) reduced inflammation, fibrosis, premature senescence of RTECs and improved renal function while Parkin knockout (KO) had opposite effects in DN mice. Parkin-OE decreased GATA4 protein, but not its mRNA transcripts in the kidney of DN mice and high glucose (HG)-treated RTECs. Immunoprecipitation indicated that Parkin directly interacted with GATA4 in DN kidney. Parkin-OE enhanced GATA4 ubiquitination. Furthermore, Parkin-KO up-regulated growth arrest specific gene 1 (GAS1) expression in renal tubular tissues of DN mice and GATA4-OE enhanced the HG-up-regulated GAS1 expression in RTECs. Conversely, GAS1-OE mitigated the effect of Parkin-OE on HG-induced P21, IL-6 and TGF-β1 expression in RTECs. These results indicate that Parkin inhibits the progression of DN by promoting GATA4 ubiquitination and downregulating the GATA4/GAS1 signaling to inhibit premature senescence, inflammation and fibrosis in DN mice. Thus, these findings uncover new mechanisms underlying the action of Parkin during the process of DN. Conclusion Parkin inhibited the progression of DN by promoting GATA4 ubiquitination and downregulating the GATA4/GAS1 signaling to inhibit premature senescence, inflammation and fibrosis. Our findings uncover a novel endogenous protective mechanism by which Parkin regulates the senescence of RTECs, inflammation and fibrosis during the pathogenesis of DN.

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