Miklós Mózes
YOU?
Author Swipe
View article: Effects of in vivo chlorobenzene exposure on bone tissue in a rat model
Effects of in vivo chlorobenzene exposure on bone tissue in a rat model Open
Calcipaenic bone disorders (e.g., osteoporosis) are becoming an epidemic as a significant public health concern. The underlying genetic, epigenetic, and homeostatic factors and the determinants of bone tissue expression are triggered by en…
View article: Renal Epithelial Complement C3 Expression Affects Kidney Fibrosis Progression
Renal Epithelial Complement C3 Expression Affects Kidney Fibrosis Progression Open
Kidney fibrosis is a hallmark of chronic kidney diseases. Evidence shows that genetic variability and complement component 3 (C3) might influence tubulointerstitial fibrosis. Still, the role of renal C3 production in the epithelial-to-mese…
View article: Study of endocrine disruptor effects in AVP and OT mediated behavioral and reproductive processes in female rat models
Study of endocrine disruptor effects in AVP and OT mediated behavioral and reproductive processes in female rat models Open
Environmental exposures may have endocrine disruptor (ED) effects, e.g., a role for halogenated hydrocarbon chlorobenzenes in increasing vasopressin (AVP), oxytocin (OT) secretion and, in association, anxiety and aggression in male rats ha…
View article: Pioglitazone Protects Tubular Epithelial Cells during Kidney Fibrosis by Attenuating miRNA Dysregulation and Autophagy Dysfunction Induced by TGF-β
Pioglitazone Protects Tubular Epithelial Cells during Kidney Fibrosis by Attenuating miRNA Dysregulation and Autophagy Dysfunction Induced by TGF-β Open
Excessive renal TGF-β production and pro-fibrotic miRNAs are important drivers of kidney fibrosis that lack any efficient treatment. Dysfunctional autophagy might play an important role in the pathogenesis. We aimed to study the yet unknow…
View article: #5503 PIOGLITAZONE REVERSES MIR-130A AND MIR-199 DYSREGULATION INDUCED BY TGF-BETA DURING KIDNEY FIBROSIS
#5503 PIOGLITAZONE REVERSES MIR-130A AND MIR-199 DYSREGULATION INDUCED BY TGF-BETA DURING KIDNEY FIBROSIS Open
Background and Aims The peroxisome proliferator-activated receptor-γ (PPARγ) agonists have been shown to dampen TGF-β signaling and suppress miR-130a in VSMCs and also profibrotic miR-21-5p in the kidney. We have recently demonstrated that…
View article: Susceptibility to kidney fibrosis in mice is associated with early growth response-2 protein and tissue inhibitor of metalloproteinase-1 expression
Susceptibility to kidney fibrosis in mice is associated with early growth response-2 protein and tissue inhibitor of metalloproteinase-1 expression Open
Patients with chronic kidney disease and experimental animal models of kidney fibrosis manifest diverse progression rates. Genetic susceptibility may contribute to this diversity, but the causes remain largely unknown. We have previously d…
View article: MO612: Relationship of Renal Timp-1, Stat3 and Inflammatory Factors in Diabetes
MO612: Relationship of Renal Timp-1, Stat3 and Inflammatory Factors in Diabetes Open
BACKGROUND AND AIMS The balance of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMP) is disrupted in diabetic nephropathy and renal TIMP-1 overexpression is observed in both animal experimental models and human biopsies. …
View article: MO404: Autophagy and Fibrotic Response is Genetically Determined in Mouse Mesangial Cells
MO404: Autophagy and Fibrotic Response is Genetically Determined in Mouse Mesangial Cells Open
BACKGROUND AND AIMS C57Bl6/J (B6) mouse strain is resistant to several experimental models of renal fibrosis. Mesangial cells play an important role in the pathogenesis of glomerulosclerosis. Also, autophagy dysregulation was recently rela…
View article: P0721PPAR-GAMMA ACTIVATION INHIBITS TGF-BETA INDUCED RENAL COMPLEMENT AND GALECTIN-3 EXPRESSION IN VIVO AND IN VITRO
P0721PPAR-GAMMA ACTIVATION INHIBITS TGF-BETA INDUCED RENAL COMPLEMENT AND GALECTIN-3 EXPRESSION IN VIVO AND IN VITRO Open
Background and Aims Reduced peroxisome proliferator-activated receptor-γ (PPARγ) activity has been observed in chronic kidney disease and fibrosis. We have recently shown that the PPARγ agonist pioglitazone dampens TGF-β induced renal pro-…
View article: P0681TIMP-1 DEFICIENCY DAMPENS RENAL GALECTIN-3 RESPONSE IN DIABETES
P0681TIMP-1 DEFICIENCY DAMPENS RENAL GALECTIN-3 RESPONSE IN DIABETES Open
Background and Aims Overexpression of tissue inhibitors of metalloproteases (TIMPs) are a hallmark of renal fibrosis, and elevated TIMP-1 has been reported in experimental and human diabetes. Also, renal galectin-3 (Lgals3) overproduction …
View article: The PPARγ agonist pioglitazone prevents TGF-β induced renal fibrosis by repressing EGR-1 and STAT3
The PPARγ agonist pioglitazone prevents TGF-β induced renal fibrosis by repressing EGR-1 and STAT3 Open
View article: FP345TIMP-1 DEFICIENCY REDUCES TGF-BETA EXPRESSION AND DAMPENS RENAL FIBROSIS AFTER RENAL ABLATION
FP345TIMP-1 DEFICIENCY REDUCES TGF-BETA EXPRESSION AND DAMPENS RENAL FIBROSIS AFTER RENAL ABLATION Open
View article: SP257EARLY RENAL INFLAMMATORY MOLECULE EXPRESSION DIFFERENCES AFTER UNILATERAL URETER OBSTRUCTION IN MICE
SP257EARLY RENAL INFLAMMATORY MOLECULE EXPRESSION DIFFERENCES AFTER UNILATERAL URETER OBSTRUCTION IN MICE Open
View article: SP270GENETIC SUSCEPTIBILITY TO TGF-BETA INDUCED RENAL FIBROSIS IS ASSOCIATED WITH ALTERED MIR-199 EXPRESSION
SP270GENETIC SUSCEPTIBILITY TO TGF-BETA INDUCED RENAL FIBROSIS IS ASSOCIATED WITH ALTERED MIR-199 EXPRESSION Open
View article: Sustained hyperosmolarity increses TGF-ß1 and Egr-1 expression in the rat renal medulla
Sustained hyperosmolarity increses TGF-ß1 and Egr-1 expression in the rat renal medulla Open
We conclude that both TGF-ß and Egr-1 are upregulated by sustained hyperosmolarity in the rat renal medulla, and it favors the expression of extracellular matrix components.
View article: SP271PIOGLITAZONE EFFECTIVELY REDUCES RENAL INTERSTITIAL FIBROSIS IN TGF-ß TRANSGENIC MICE
SP271PIOGLITAZONE EFFECTIVELY REDUCES RENAL INTERSTITIAL FIBROSIS IN TGF-ß TRANSGENIC MICE Open
View article: MP051GENETIC BACKGROUND DETERMINES MURINE PRIMARY MESANGIAL CELL RESPONSE TO TGF-ß
MP051GENETIC BACKGROUND DETERMINES MURINE PRIMARY MESANGIAL CELL RESPONSE TO TGF-ß Open
View article: PPARγ Links BMP2 and TGFβ1 Pathways in Vascular Smooth Muscle Cells, Regulating Cell Proliferation and Glucose Metabolism
PPARγ Links BMP2 and TGFβ1 Pathways in Vascular Smooth Muscle Cells, Regulating Cell Proliferation and Glucose Metabolism Open
View article: MP360DELAYED PROGRESSION OF RENAL FIBROSIS IN C57BL6/J MICE IS ASSOCIATED WITH ROBUST MMP ACTIVITY
MP360DELAYED PROGRESSION OF RENAL FIBROSIS IN C57BL6/J MICE IS ASSOCIATED WITH ROBUST MMP ACTIVITY Open
View article: MP097SUSTAINED HYPEROSMOLARITY LEADS TO THE EXPRESSION OF PROFIBROTIC FACTORS IN VIVO
MP097SUSTAINED HYPEROSMOLARITY LEADS TO THE EXPRESSION OF PROFIBROTIC FACTORS IN VIVO Open
View article: Ductular reaction correlates with fibrogenesis but does not contribute to liver regeneration in experimental fibrosis models
Ductular reaction correlates with fibrogenesis but does not contribute to liver regeneration in experimental fibrosis models Open
The stringent connection between ductular reaction and fibrosis, which cannot be influenced by any of our treatment regimens, suggests that there is a close mutual interaction between them instead of a unidirectional causal relationship. O…
View article: The Effect of Combined Treatment with the (Pro)Renin Receptor Blocker HRP and Quinapril in Type 1 Diabetic Rats
The Effect of Combined Treatment with the (Pro)Renin Receptor Blocker HRP and Quinapril in Type 1 Diabetic Rats Open
Background/Aims: Diabetic nephropathy remains a major clinical problem. The effects of prorenin might be adverse, but the literature data are controversial. We compared the renal effects of the (pro)renin receptor ((P)RR) blo…
View article: MP299EARLY AND SUSTAINED RUNX1 ACTIVATION AFTER UNILATERAL URETER OBSTRUCTION IN MICE: A POSSIBLE NEW PLAYER IN RENAL FIBROSIS
MP299EARLY AND SUSTAINED RUNX1 ACTIVATION AFTER UNILATERAL URETER OBSTRUCTION IN MICE: A POSSIBLE NEW PLAYER IN RENAL FIBROSIS Open
View article: MP245MICRORNA NETWORKS IN THE PROGRESSION OF TGF-BETA INDUCED RENAL FIBROSIS
MP245MICRORNA NETWORKS IN THE PROGRESSION OF TGF-BETA INDUCED RENAL FIBROSIS Open
View article: Treatment protocols for LPS preconditioning.
Treatment protocols for LPS preconditioning. Open
Saline: physiological saline, LPS: bacterial lipopolysaccharide endotoxin, p: preconditioning dose, L: lethal dose, NB: novobiocin.
View article: Western blot analysis of Hsp70 (A), and Hsp90 (B) protein expression.
Western blot analysis of Hsp70 (A), and Hsp90 (B) protein expression. Open
Results are normalized to actin protein expression, and presented as fold increase relative to the saline-treated group with its mean set to 1. **, ***: p<0.01, 0.001 vs. the saline-treated controls, respectively, or between the groups ind…
View article: Plasma urea levels at the time of organ harvest i.e. at 24 hours after the second treatment.
Plasma urea levels at the time of organ harvest i.e. at 24 hours after the second treatment. Open
LPS: bacterial lipopolysaccharide endotoxin, p: preconditioning, L: lethal, NB: novobiocin. *, **, ***: p<0.05, 0.01, 0.001 vs. the saline-treated controls, respectively, or between the groups indicated.
View article: Northern blot analysis of Hsp70 (A), Hsp90α (B) and Hsp90β (C) mRNA expression.
Northern blot analysis of Hsp70 (A), Hsp90α (B) and Hsp90β (C) mRNA expression. Open
Results are normalized to S14 expression and presented as fold increase relative to the saline-treated group with its mean set to 1. *, **, ***: p<0.05, 0.01, 0.001 vs. the saline-treated controls, respectively, or between the groups indic…
View article: FP301STRAIN-DEPENDENT RENAL COMPLEMENT EXPRESSION IN KIDNEY FIBROSIS OF TGF-ß TRASGENIC MICE
FP301STRAIN-DEPENDENT RENAL COMPLEMENT EXPRESSION IN KIDNEY FIBROSIS OF TGF-ß TRASGENIC MICE Open
View article: FP307SUBTOTAL RENAL ABLATION INDUCES TUBULOINTERSTITIAL EGR-2 OVEREXPRESSION IN MICE
FP307SUBTOTAL RENAL ABLATION INDUCES TUBULOINTERSTITIAL EGR-2 OVEREXPRESSION IN MICE Open