Urinary Enzymes (a-Glucosidase and Lysozyme), Protein Pattern and �2-Microglobulin as Indexes of Tubular Damage

2015 ◽  
pp. 186-192
Author(s):  
G. F. Guarnieri ◽  
L. Faccini ◽  
E. Beltram ◽  
M. Chersicla ◽  
G. Battilana ◽  
...  
Keyword(s):  
Protein Pattern ◽  
Tubular Damage ◽  
Urinary Enzymes

Urinary Enzymes (a-Glucosidase and Lysozyme), Protein Pattern and �2-Microglobulin as Indexes of Tubular Damage

2015 ◽  
pp. 193-200 ◽  
Author(s):  
G. F. Guarnieri ◽  
L. Faccini ◽  
M. Chersicla ◽  
E. Beltram ◽  
G. Battilana ◽  
...  
Keyword(s):  
Protein Pattern ◽  
Tubular Damage ◽  
Urinary Enzymes

scholarly journals AT1 and AT2 receptors modulate renal tubular cell necroptosis in angiotensin II-infused renal injury mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yongjun Zhu ◽  
Hongwang Cui ◽  
Jie Lv ◽  
Haiqin Liang ◽  
Yanping Zheng ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Injury ◽  
Critical Role ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Tubular Cell ◽  
Tubular Damage ◽  
Renal Tubular Cell ◽  
Ang Ii ◽  
Renal Tubular

AbstractAbnormal renin-angiotensin system (RAS) activation plays a critical role in the initiation and progression of chronic kidney disease (CKD) by directly mediating renal tubular cell apoptosis. Our previous study showed that necroptosis may play a more important role than apoptosis in mediating renal tubular cell loss in chronic renal injury rats, but the mechanism involved remains unknown. Here, we investigate whether blocking the angiotensin II type 1 receptor (AT1R) and/or angiotensin II type 2 receptor (AT2R) beneficially alleviates renal tubular cell necroptosis and chronic kidney injury. In an angiotensin II (Ang II)-induced renal injury mouse model, we found that blocking AT1R and AT2R effectively mitigates Ang II-induced increases in necroptotic tubular epithelial cell percentages, necroptosis-related RIP3 and MLKL protein expression, serum creatinine and blood urea nitrogen levels, and tubular damage scores. Furthermore, inhibition of AT1R and AT2R diminishes Ang II-induced necroptosis in HK-2 cells and the AT2 agonist CGP42112A increases the percentage of necroptotic HK-2 cells. In addition, the current study also demonstrates that Losartan and PD123319 effectively mitigated the Ang II-induced increases in Fas and FasL signaling molecule expression. Importantly, disruption of FasL significantly suppressed Ang II-induced increases in necroptotic HK-2 cell percentages, and necroptosis-related proteins. These results suggest that Fas and FasL, as subsequent signaling molecules of AT1R and AT2R, might involve in Ang II-induced necroptosis. Taken together, our results suggest that Ang II-induced necroptosis of renal tubular cell might be involved both AT1R and AT2R and the subsequent expression of Fas, FasL signaling. Thus, AT1R and AT2R might function as critical mediators.

scholarly journals Changes in Cerebrospinal Fluid Balance of TNF and TNF Receptors in Naïve Multiple Sclerosis Patients: Early Involvement in Compartmentalised Intrathecal Inflammation

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1712
Author(s):  
Roberta Magliozzi ◽  
Francesco Pezzini ◽  
Mairi Pucci ◽  
Stefania Rossi ◽  
Francesco Facchiano ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Immune Cell ◽  
Protein Pattern ◽  
Fold Change ◽  
Cortical Lesion ◽  
Control Group ◽  
Lesion Volume ◽  
Mri Features ◽  
Csf Levels ◽  
Multiple Sclerosis Patients

An imbalance of TNF signalling in the inflammatory milieu generated by meningeal immune cell infiltrates in the subarachnoid space in multiple sclerosis (MS), and its animal model may lead to increased cortical pathology. In order to explore whether this feature may be present from the early stages of MS and may be associated with the clinical outcome, the protein levels of TNF, sTNF-R1 and sTNF-R2 were assayed in CSF collected from 122 treatment-naïve MS patients and 36 subjects with other neurological conditions at diagnosis. Potential correlations with other CSF cytokines/chemokines and with clinical and imaging parameters at diagnosis (T0) and after 2 years of follow-up (T24) were evaluated. Significantly increased levels of TNF (fold change: 7.739; p < 0.001), sTNF-R1 (fold change: 1.693; p < 0.001) and sTNF-R2 (fold change: 2.189; p < 0.001) were detected in CSF of MS patients compared to the control group at T0. Increased TNF levels in CSF were significantly (p < 0.01) associated with increased EDSS change (r = 0.43), relapses (r = 0.48) and the appearance of white matter lesions (r = 0.49). CSF levels of TNFR1 were associated with cortical lesion volume (r = 0.41) at T0, as well as with new cortical lesions (r = 0.56), whilst no correlation could be found between TNFR2 levels in CSF and clinical or MRI features. Combined correlation and pathway analysis (ingenuity) of the CSF protein pattern associated with TNF expression (encompassing elevated levels of BAFF, IFN-γ, IL-1β, IL-10, IL-8, IL-16, CCL21, haptoglobin and fibrinogen) showed a particular relationship to the interaction between innate and adaptive immune response. The CSF sTNF-R1-associated pattern (encompassing high levels of CXCL13, TWEAK, LIGHT, IL-35, osteopontin, pentraxin-3, sCD163 and chitinase-3-L1) was mainly related to altered T cell and B cell signalling. Finally, the CSF TNFR2-associated pattern (encompassing high CSF levels of IFN-β, IFN-λ2, sIL-6Rα) was linked to Th cell differentiation and regulatory cytokine signalling. In conclusion, dysregulation of TNF and TNF-R1/2 pathways associates with specific clinical/MRI profiles and can be identified at a very early stage in MS patients, at the time of diagnosis, contributing to the prediction of the disease outcome.

scholarly journals Bisphenol A Modulates Autophagy and Exacerbates Chronic Kidney Damage in Mice

2021 ◽  
Vol 22 (13) ◽  
pp. 7189
Author(s):  
Alberto Ruiz Priego ◽  
Emilio González Parra ◽  
Sebastián Mas ◽  
José Luis Morgado-Pascual ◽  
Marta Ruiz-Ortega ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Hepatitis A Virus ◽  
Antioxidant Response ◽  
Heme Oxygenase 1 ◽  
Tubular Damage ◽  
Related Factor ◽  
Related Gene ◽  
Inflammatory Infiltration ◽  
Proximal Tubular Epithelial Cells

BACKGROUND: Bisphenol A (BPA) is a ubiquitous environmental toxin that accumulates in chronic kidney disease (CKD). Our aim was to explore the effect of chronic exposition of BPA in healthy and injured kidney investigating potential mechanisms involved. METHODS: In C57Bl/6 mice, administration of BPA (120 mg/kg/day, i.p for 5 days/week) was done for 2 and 5 weeks. To study BPA effect on CKD, a model of subtotal nephrectomy (SNX) combined with BPA administration for 5 weeks was employed. In vitro studies were done in human proximal tubular epithelial cells (HK-2 line). RESULTS: Chronic BPA administration to healthy mice induces inflammatory infiltration in the kidney, tubular injury and renal fibrosis (assessed by increased collagen deposition). Moreover, in SNX mice BPA exposure exacerbates renal lesions, including overexpression of the tubular damage biomarker Hepatitis A virus cellular receptor 1 (Havcr-1/KIM-1). BPA upregulated several proinflammatory genes and increased the antioxidant response [Nuclear factor erythroid 2-related factor 2 (Nrf2), Heme Oxygenase-1 (Ho-1) and NAD(P)H dehydrogenase quinone 1 (Nqo-1)] both in healthy and SNX mice. The autophagy process was modulated by BPA, through elevated autophagy-related gene 5 (Atg5), autophagy-related gene 7 (Atg7), Microtubule-associated proteins 1A/1B light chain 3B (Map1lc3b/Lc3b) and Beclin-1 gene levels and blockaded the autophagosome maturation and flux (p62 levels). This autophagy deregulation was confirmed in vitro. CONCLUSIONS: BPA deregulates autophagy flux and redox protective mechanisms, suggesting a potential mechanism of BPA deleterious effects in the kidney.

scholarly journals Changes in membrane protein pattern in relation to lens cell differentiation

FEBS Letters ◽  
1977 ◽  
Vol 83 (2) ◽  
pp. 301-306 ◽  
Author(s):  
A.J.M. Vermorken ◽  
J.M.H.C. Hilderink ◽  
I. Dunia ◽  
E.L. Benedetti ◽  
H. Bloemendal
Keyword(s):  
Cell Differentiation ◽  
Membrane Protein ◽  
Protein Pattern ◽  
Lens Cell

scholarly journals Snail mucus from the mantle and foot of two land snails, Lissachatina fulica and Hemiplecta distincta, exhibits different protein profile and biological activity

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Nattaphop Noothuan ◽  
Kantamas Apitanyasai ◽  
Somsak Panha ◽  
Anchalee Tassanakajon
Keyword(s):  
Biological Activities ◽  
Protein Pattern ◽  
Protein Profile ◽  
Antibacterial Properties ◽  
Biological Properties ◽  
Specific Protein ◽  
Land Snails ◽  
Snail Species ◽  
Significant Difference ◽  
Different Types

Abstract Objective Snails secrete different types of mucus that serve several functions, and are increasingly being exploited for medical and cosmetic applications. In this study, we explored the protein pattern and compared the biological properties of the mucus secreted from the mantle collar and foot of two snail species, Lissachatina fulica and Hemiplecta distincta. Result Protein profile showed a different pattern between the two species and between the two secretory parts. The mantle-specific protein bands were further characterized and among them was an antibacterial protein, achacin. Accordingly, the mucus from the mantle exhibited the higher antibacterial activity than that from the foot in both snail species. The mucus from H. distincta, first reported here, also showed antibacterial properties, but with a lower activity compared to that for L. fulica. Snail mucus also exhibited anti-tyrosinase activity and antioxidant activity but with no significant difference between the foot and mantle mucus. These results indicate some different protein compositions and biological activities of snail slime from the mantle and foot, which might be associated with their specific functions in the animal and are useful for medical applications.

scholarly journals Renal Involvement in Children with Type 2 Diabetes Mellitus Onset: A Pilot Study

Children ◽  
2021 ◽  
Vol 8 (8) ◽  
pp. 627
Author(s):  
Pierluigi Marzuillo ◽  
Anna Di Sessa ◽  
Pier Luigi Palma ◽  
Giuseppina Rosaria Umano ◽  
Cesare Polito ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Renal Involvement ◽  
Kidney Injury ◽  
Fractional Excretion ◽  
Tubular Damage ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Type 2 Diabetes Mellitus (T2DM) is a main cause of chronic kidney disease (CKD) in adulthood. No studies have examined the occurrence of acute kidney injury (AKI)—that enhances the risk of later CKD—and renal tubular damage (RTD)—that can evolve to AKI—in children with onset of T2DM. We aimed to evaluate the prevalence and possible features of AKI and RTD in a prospectively enrolled population of children with onset of T2DM. We consecutively enrolled 10 children aged 12.9 ± 2.3 years with newly diagnosed T2DM. AKI was defined according to the KDIGO criteria. RTD was defined by abnormal urinary beta-2-microglobulin and/or tubular reabsorption of phosphate (TRP) < 85% and/or fractional excretion of Na > 2%. None of the patients developed AKI, whereas 3/10 developed RTD with high beta-2-microglobulin levels (range: 0.6–1.06 mg/L). One of these three patients also presented with reduced TRP levels (TRP = 70%). Proteinuria was observed in two out of three patients with RTD, while none of patients without RTD had proteinuria. Patients with RTD presented higher beta-2-microglobulin, acute creatinine/estimated basal creatinine ratio, and serum ketones levels compared with patients without RTD. In conclusion, in our pilot observation, we found that none of the 10 children with T2DM onset developed AKI, whereas three of them developed RTD.

scholarly journals Differential organ-specific inflammatory response to progranulin in high-fat diet-fed mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maki Murakoshi ◽  
Tomohito Gohda ◽  
Eri Adachi ◽  
Saki Ichikawa ◽  
Shinji Hagiwara ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Kidney Injury ◽  
Proximal Tubules ◽  
Tubular Damage ◽  
Standard Diet ◽  
Mrna Levels ◽  
High Fat ◽  
Organ Specific

AbstractProgranulin (PGRN) has been reported to bind tumor necrosis factor (TNF) receptor and to inhibit TNFα signaling. We evaluated the effect of augmentation of TNFα signaling by PGRN deficiency on the progression of kidney injury. Eight-week-old PGRN knockout (KO) and wild-type (WT) mice were fed a standard diet or high-fat diet (HFD) for 12 weeks. Albuminuria, markers of tubular damage, and renal mRNA levels of inflammatory cytokines were higher in HFD-fed KO (KO-HFD) mice than in HFD-fed WT (WT-HFD) mice. Body weight, vacuolization in proximal tubules, and systemic and adipose tissue inflammatory markers were lower in the KO-HFD mice than in the WT-HFD mice. The renal megalin expression was lower in the KO mice than in the WT mice regardless of the diet type. The megalin expression was also reduced in mouse proximal tubule epithelial cells stimulated with TNFα and in those with PGRN knockdown by small interfering RNA in vitro. PGRN deficiency was associated with both exacerbated renal inflammation and decreased systemic inflammation, including that in the adipose tissue of mice with HFD-induced obesity. Improved tubular vacuolization in the KO-HFD mice might partially be explained by the decreased expression of megalin in proximal tubules.

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