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Mouse advanced glycation end products,AGEs ELISA Kit SpeciesMouse

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[#CSB-E09414m] Mouse advanced glycation end products,AGEs ELISA Kit SpeciesMouse

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CSB-E09414m | Mouse advanced glycation end products,AGEs ELISA Kit SpeciesMouse, 96T
More informations about Mouse advanced glycation end products,AGEs ELISA Kit SpeciesMouse in Antibody-antibodies.com

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(1) Diabetes with heart failure increases methylglyoxal modifications in the sarcomere, which inhibit function.[TOP]

Pubmed ID :30333300
Publication Date : //
Patients with diabetes are at significantly higher risk of developing heart failure. Increases in advanced glycation end products are a proposed pathophysiological link, but their impact and mechanism remain incompletely understood. Methylglyoxal (MG) is a glycolysis byproduct, elevated in diabetes, and modifies arginine and lysine residues. We show that left ventricular myofilament from patients with diabetes and heart failure (dbHF) exhibited increased MG modifications compared with nonfailing controls (NF) or heart failure patients without diabetes. In skinned NF human and mouse cardiomyocytes, acute MG treatment depressed both calcium sensitivity and maximal calcium-activated force in a dose-dependent manner. Importantly, dbHF myocytes were resistant to myofilament functional changes from MG treatment, indicating that myofilaments from dbHF patients already had depressed function arising from MG modifications. In human dbHF and MG-treated mice, mass spectrometry identified increased MG modifications on actin and myosin. Cosedimentation and in vitro motility assays indicate that MG modifications on actin and myosin independently depress calcium sensitivity, and mechanistically, the functional consequence requires actin/myosin interaction with thin-filament regulatory proteins. MG modification of the myofilament may represent a critical mechanism by which diabetes induces heart failure, as well as a therapeutic target to avoid the development of or ameliorate heart failure in these patients.

Authors : Papadaki Maria, Holewinski Ronald J, Previs Samantha Beck, Martin Thomas G, Stachowski Marisa J, Li Amy, Blair Cheavar A, Moravec Christine S, Van Eyk Jennifer E, Campbell Kenneth S, Warshaw David M, Kirk Jonathan A,



(2) Reduced Susceptibility to Sugar-Induced Metabolic Derangements and Impairments of Myocardial Redox Signaling in Mice Chronically Fed with D-Tagatose when Compared to Fructose.[TOP]

Pubmed ID :30327714
Publication Date : //
D-tagatose is an isomer of fructose and is ~90% as sweet as sucrose with less caloric value. Nowadays, D-tagatose is used as a nutritive or low-calorie sweetener. Despite clinical findings suggesting that D-tagatose could be beneficial in subjects with type 2 diabetes, there are no experimental data comparing D-tagatose with fructose, in terms of metabolic derangements and related molecular mechanisms evoked by chronic exposure to these two monosaccharides.

Authors : Collotta Debora, Lucarini Laura, Chiazza Fausto, Cento Alessia Sofia, Durante Mariaconcetta, Sgambellone Silvia, Chini Jacopo, Baratta Francesca, Aragno Manuela, Mastrocola Raffaella, Masini Emanuela, Collino Massimo,



(3) Inhibiting Receptor of Advanced Glycation End Products Attenuates Pressure Overload-Induced Cardiac Dysfunction by Preventing Excessive Autophagy.[TOP]

Pubmed ID :30319444
Publication Date : //
The receptor for advanced glycation end products (RAGE) is involved in heart failure (HF) by mediating diverse pathologic processes, including the promotion of inflammation and autophagy. However, the role of RAGE in pressure overload-induced HF is not well understood. We found that stimulation of RAGE triggered the death of neonatal rat ventricular myocytes (NRVMs), while cell death was alleviated by ATG5 knockdown. Using transverse aortic constriction (TAC) in mice as a model of pressure overload-induced HF, we demonstrated that RAGE knockout or RAGE blockade attenuated cardiac hypertrophy and fibrosis as well as cardiac dysfunction at 8 weeks after TAC. Importantly, RAGE knockout reversed upregulation of autophagy related proteins (LC3BII/I and Beclin 1) and reduced cardiomyocyte death, indicating that excessive autophagy after TAC was inhibited. Moreover, RAGE knockout or blockade reduced the upregulation of pp65-NFκB and BNIP3, which mediate autophagy. Taken together, these results suggest that RAGE plays an important role in the progression of HF by regulating autophagy. Therefore, inhibition of the RAGE-autophagy axis could be a promising new strategy for treatment of heart failure.

Authors : Gao Wenbin, Zhou Zheng, Liang Birong, Huang Yusheng, Yang Zhongqi, Chen Yang, Zhang Lu, Yan Cui, Wang Jiajia, Lu Lu, Wen Zhaorui, Xian Shaoxiang, Wang Lingjun,



(4) Synthetic Fragments of Receptor for Advanced Glycation End Products Bind Beta-Amyloid 1-40 and Protect Primary Brain Cells From Beta-Amyloid Toxicity.[TOP]

Pubmed ID :30319347
Publication Date : //
Receptor for advanced glycation end products (RAGE) is involved in the pathogenesis of Alzheimer's disease. We have previously revealed that RAGE fragment sequence (60-76) and its shortened analogs sequence (60-70) and (60-65) under intranasal insertion were able to restore memory and improve morphological and biochemical state of neurons in the brain of bulbectomized mice developing major AD features. In the current study, we have investigated the ability of RAGE peptide (60-76) and five shortened analogs to bind beta-amyloid (Aβ) 1-40 in an fluorescent titration test and show that all the RAGE fragments apart from one [sequence (65-76)] were able to bind Aβ . Moreover, we show that all RAGE fragments apart from the shortest one (60-62), were able to protect neuronal primary cultures from amyloid toxicity, by preventing the caspase 3 activation induced by Aβ 1-42. We have compared the data obtained in the present research with the previously published data in the animal model of AD, and offer a probable mechanism of neuroprotection of the RAGE peptide.

Authors : Kamynina Anna V, Esteras Noemi, Koroev Dmitriy O, Bobkova Natalia V, Balasanyants Samson M, Simonyan Ruben A, Avetisyan Armine V, Abramov Andrey Y, Volpina Olga M,



(5) Visualization of methylglyoxal in living cells and diabetic mice model with a 1,8-naphthalimide-based two-photon fluorescent probe.[TOP]

Pubmed ID :30310608
Publication Date : //
Methylglyoxal (MGO), a dicarbonyl metabolite, is the most studied precursor of advanced glycation end-products (AGEs) and its elevated levels have also been associated with various pathologies. Hence, the development of effective methods for monitoring MGO in live cells and is of great importance for ascertaining the onset and progress of related diseases. Herein, we designed and synthesized an endoplasmic reticulum-targeting two-photon fluorescent probe called for the detection of MGO with high selectivity, sensitivity, and hypotoxicity. The probe was successfully applied for monitoring MGO in living cells and a diabetic mice model. The two-photon fluorescence images confirmed that the endogenous MGO in the liver and kidney tissues of diabetic mice is higher than that of normal mice. Furthermore, it revealed that after treatment with metformin, a widely used hypoglycemia drug, the diabetic mice showed a decreased concentration of MGO in liver and kidney tissues. Thus, may serve as a useful tool for the detection of MGO and for studying the relationships between MGO and pathological and biological processes in biosystems.

Authors : Yang Mingwang, Fan Jiangli, Zhang Junwei, Du Jianjun, Peng Xiaojun,



(6) Compensatory mechanisms for methylglyoxal detoxification in experimental & clinical diabetes.[TOP]

Pubmed ID :30287091
Publication Date : //
The deficit of Glyoxalase I (Glo1) and the subsequent increase in methylglyoxal (MG) has been reported to be one the five mechanisms by which hyperglycemia causes diabetic late complications. Aldo-keto reductases (AKR) have been shown to metabolize MG; however, the relative contribution of this superfamily to the detoxification of MG in vivo, particularly within the diabetic state, remains unknown.

Authors : Schumacher Dagmar, Morgenstern Jakob, Oguchi Yoko, Volk Nadine, Kopf Stefan, Groener Jan Benedikt, Nawroth Peter Paul, Fleming Thomas, Freichel Marc,



(7) Correlation between Diabetes Mellitus and Knee Osteoarthritis: A Dry-To-Wet Lab Approach.[TOP]

Pubmed ID :30282957
Publication Date : //
Recent years have witnessed an increased prevalence of knee osteoarthritis (KOA) among diabetes mellitus (DM) patients-conditions which might share common risk factors such as obesity and advanced aging. Therefore, we conducted dry-to-wet lab research approaches to assess the correlation of type 1 DM (T1DM) and type 2 DM (T2DM) with KOA among all age and genders of Taiwanese population. The strength of association (odds ratio: OR) was analyzed using a phenome-wide association study portal. Populations of 37,353 T1DM and 1,218,254 T2DM were included. We observed a significant association of KOA with T1DM (OR: 1.40 (1.33⁻1.47), < 0.0001) and T2DM (OR: 2.75 (2.72⁻2.78), < 0.0001). The association between T1DM and KOA among the obese (OR: 0.99 (0.54⁻1.67), = 0.0477) was insignificant compared to the non-obese (OR: 1.40 (1.33⁻1.48), < 0.0001). Interestingly, a higher association between T2DM and KOA among non-obese persons (OR: 2.75, (2.72⁻2.79), < 0.0001) compared to the obese (OR: 1.71 (1.55⁻1.89), < 0.0001) was noted. Further, histopathologic and Western blot studies of diabetic mice knee joints revealed enhanced carboxymethyl lysine (advanced glycation end product), matrix metalloproteinase-1, and reduced cartilage-specific proteins, including type II collagen (Col II), SOX9, and aggrecan (AGN), indicating deteriorated articular cartilage and proteoglycans. Results indicate that DM is strongly associated with KOA, and obesity may not be a confounding factor.

Authors : Dubey Navneet Kumar, Ningrum Dina Nur Anggraini, Dubey Rajni, Deng Yue-Hua, Li Yu-Chuan, Wang Peter D, Wang Joseph R, Syed-Abdul Shabbir, Deng Win-Ping,



(8) Limited field radiation therapy results in decreased bone fracture toughness in a murine model.[TOP]

Pubmed ID :30281657
Publication Date : //
Fragility fractures are a well-known complication following oncologic radiotherapy, and it is suspected that radiation-induced embrittlement of bone within the treatment field may contribute to fracture risk. To explore this phenomenon, a mouse model (BALB/cJ) of fractionated, limited field, bilateral hindlimb irradiation (4x5 Gy) was used. The effects of radiation on femoral (cortical) bone fracture toughness, morphology, and biochemistry-including advanced glycation end products (AGEs)-were quantified and compared to Sham group samples prior to irradiation and at 0, 4, 8, and 12 weeks post-irradiation. Additionally, alterations to bone fracture toughness mediated directly by radiation (independent of cellular mechanisms) were determined using devitalized mouse cadaver femurs. Finally, the contribution of AGEs to reduced fracture toughness was examined by artificially ribosylating mouse femurs ex vivo. These data demonstrate that in vivo irradiation results in an immediate (-42% at 0 weeks, p < 0.001) and sustained (-28% at 12 weeks, p < 0.001) decrease in fracture toughness with small changes in morphology (-5% in cortical area at 12 weeks), and minimal changes in bone composition (tissue mineral density, mineral:matrix ratio, and AGE content). Irradiation of devitalized femurs also reduced fracture toughness (-29%, p < 0.001), but to a lesser extent than was seen in vivo. While artificial ribosylation decreased fracture toughness with time, the extent of glycation needed to induce this effect exceeded the AGE accumulation that occurred in vivo. Overall, hindlimb irradiation induced a substantial and sustained decrease in bone fracture toughness. Approximately half of this decrease in fracture toughness is due to direct radiation damage, independent of cellular remodeling. Collagen glycation in vivo was not substantially altered, suggesting other matrix changes may contribute to post-radiotherapy bone embrittlement.

Authors : Bartlow Christopher M, Mann Kenneth A, Damron Timothy A, Oest Megan E,



(9) FOXO1 Deletion Reverses the Effect of Diabetic-Induced Impaired Fracture Healing.[TOP]

Pubmed ID :30279162
Publication Date : //
Type 1 diabetes mellitus impairs fracture healing. We tested the hypothesis that diabetes affects chondrocytes to impair fracture healing through a mechanism that involves the transcription factor FOXO1. Type-1 diabetes was induced by streptozotocin in mice with FOXO1 deletion in chondrocytes (Col2α1CreFOXO1) or littermate controls, (Col2α1CreFOXO1) and closed femoral fractures induced. Diabetic mice had 77% less cartilage and 30% less bone than normoglycemics evaluated histologically and by micro-CT. Both were reversed with lineage-specific FOXO1 ablation. Diabetic mice had a 3-fold increase in osteoclasts and a 2 to 3-fold increase in RANKL mRNA or RANKL expressing chondrocytes compared to normoglycemics. Both parameters were rescued by FOXO1 ablation in chondrocytes. Conditions present in diabetes, high glucose (HG) and increased advanced glycation end products (AGE) stimulated FOXO1 association with the RANKL promoter and overexpression of FOXO1 increased RANKL promoter activity in luciferase reporter assays. HG and AGE stimulated FOXO1 nuclear localization, which was reversed by insulin and inhibitors of TLR4, HDAC, NO, and ROS. The results indicate that chondrocytes play a prominent role in diabetes-impaired fracture healing and that high levels of glucose, AGEs, and TNF-α, which are elevated by diabetes, alter RANKL expression in chondrocytes via FOXO1.

Authors : Alharbi Mohammed A, Zhang Citong, Lu Chanyi, Milovanova Tatyana N, Yi Leah, Ryu Je Dong, Jiao Hongli, Dong Guangyu, O'Connor J Patrick, Graves Dana T,



(10) Advanced Glycation End Products Increase MDM2 Expression via Transcription Factor KLF5.[TOP]

Pubmed ID :30271790
Publication Date : //
Type 2 diabetes increases the risk for all-site cancers including colon cancer. Diabetic patients present typical pathophysiological features including an increased level of advanced glycation end products (AGEs), which comes from a series of nonenzymatic reactions between sugars and biological macromolecules, positively associated with the occurrence of diabetic complications. MDM2 is an oncogene implicated in cancer development. The present study investigated whether diabetes promoted MDM2 expression in colon cells and the underlying mechanisms. Our results showed that AGE increased the protein level of MDM2 in a cell model and promoted binding between MDM2 and Rb as well as p53, which led to degradation of Rb and p53. KLF5 was able to bind to the regulatory sequence of the MDM2 gene, and knockdown of the KLF5 protein level inhibited the AGE-triggered MDM2 overexpression, which indicated that KLF5 was the transcription factor for MDM2. In a mouse model of diabetes, we found that AGE level was increased in serum. The protein levels of both KLF5 and MDM2 were increased. KLF5 was able to bind to the regulatory sequence of the MDM2 gene. In conclusion, our results suggest that diabetes increases the level of AGE which enhances the expression of MDM2 via transcription factor KLF5 in colon cells. MDM2 overexpression is a candidate biological link between type 2 diabetes and colon cancer development.

Authors : Wang Pu, Lu Yu Cheng, Li Yuan Fei, Wang Lan, Lee Shao Chin,