ABSTRACT
BACKGOUND: Platelet-derived growth factor (PDGF) is a widely expressed growth factor with both mitogenic and chemotactic activities in many connective tissue cell types. There are four members of PDGF family; PDGF-A, PDGF-B, PDGF-C, PDGF-D. Their biological effects are mediated via two tyrosine kinase receptors, PDGF receptor-alpha and PDGF receptor-beta, and PDGF-mediated signaling is critical for development of many organ systems and acquired disease. The aims of this study were to determine the changes of PDGF-A, PDGF-C and PDGF receptor (PDGFR)-alpha expression in ischemia reperfusion acute renal failure model. METHODS: We examined the expression and localization of PDGF-A, PDGF-C and PDGF receptor-alpha protein using Western blot analysis and immunohistochemistry and PDGF-C mRNA using RNase protection assay after ischemia reperfusion renal failure model. RESULTS: PDGF-A expression showed no change after ischemia reperfusion injury. Proliferating cell nuclear antigen expression increased at day 2 after ischemia reperfusion injury. PDGF-C expression increased at day 2 after ischemia reperfusion injury, and was localized in tubular epithelial cells of outer medulla. PDGFR-alpha increased at day 2 after ischemia reperfusion injury, and was localized in tubular interstitium of outer medulla. CONCLUSION: These results indicated that PDGF-C and PDGF receptor-alpha may have an important role in the renal regeneration after ischemia reperfusion renal injury.
Subject(s)
Humans , Acute Kidney Injury , Blood Platelets , Blotting, Western , Connective Tissue Cells , Epithelial Cells , Immunohistochemistry , Ischemia , Platelet-Derived Growth Factor , Proliferating Cell Nuclear Antigen , Receptor Protein-Tyrosine Kinases , Receptors, Platelet-Derived Growth Factor , Regeneration , Renal Insufficiency , Reperfusion Injury , Reperfusion , Ribonucleases , RNA, MessengerABSTRACT
BACKGROUND: Agonists of the peroxisome proliferator-activated receptor gamma may help to regulate inflammation by modulating the production of inflammatory mediators and adhesion molecules. The purpose of this study was to determine the anti- inflammatory effects of rosiglitazone on renal injury in sepsis model. METHODS: In lipopolysaccharide (LPS)-induced mouse sepsis, we examined the effect of rosiglitazone on LPS-induced overproduction of inflammatory mediators, on the expression of adhesion molecules, on the infiltration of inflammatory cells and on renal function. RESULTS: Rosiglitazone significantly decreased serum tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta levels during sepsis. The levels of blood urea nitrogen and creatinine were significantly lower in mice pretreated with rosiglitazone than that in LPS-treated mice. Rosiglitazone reduced the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in renal tissue of LPS-treated mice. Pretreatment with rosiglitazone reduced the infiltration of macrophages/ monocytes in renal tissue. CONCLUSION: These results indicate that pretreatment with rosiglitazone attenuated the production of TNF-alpha and IL-1beta and reduced adhesion molecule expression and infiltration of inflammatory cells in renal tissue of LPS-treated mice. Therefore, rosiglitazone may have a protective effect in maintaining renal function and reducing mortality and morbidity in sepsis.
Subject(s)
Animals , Mice , Blood Urea Nitrogen , Creatinine , Inflammation , Intercellular Adhesion Molecule-1 , Interleukins , Monocytes , Mortality , PPAR gamma , Sepsis , Tumor Necrosis Factor-alpha , Vascular Cell Adhesion Molecule-1ABSTRACT
C1 esterase inhibitor deficiency with consequent angioedma is an uncommon condition. Nonhereditary C1 inhibitor deficiency includes underlying disorders; lymphoproliferative disorder, autoimmune disease, hypereosinophilia, drug-induced, allergic, and idiopathic forms. The as sociation of hereditary C1 esterase inhibitor deficiency with systemic lupus erythematosus has been previously described. We experienced a case with transiently decreased C1 inactivator activity and angioedema in lupus nephritis. This present case is a previously healthy 22-year-old woman, who developed intermittent facial angioedema and decreased urine amount. After steroid treatment, the C1 inactivator activity was recovered and angioedema was disappeared.
Subject(s)
Female , Humans , Young Adult , Angioedema , Angioedemas, Hereditary , Autoimmune Diseases , Lupus Erythematosus, Systemic , Lupus Nephritis , Lymphoproliferative DisordersABSTRACT
Left ventricular mural thrombi can occur in setting of acute myocarditis. Major thromboembolism may occur according to the echocardiographic characteristics of the thrombi. Mobile, irregular and protruding thrombi are known to raise systemic embolism more easily than immobile laminar clot. We experienced a case of a hypermobile pedunculated left ventricular thrombus complicated to acute myocarditis in a 49-year-old woman. Mobility of it increased day by day in spite of the proper anticoagulation. Surgical removal of the thrombus was performed to prevent major thromboembolism.
Subject(s)
Female , Humans , Middle Aged , Echocardiography , Embolism , Heart Ventricles , Myocarditis , Thromboembolism , ThrombosisABSTRACT
BACKGROUND: The Angiopoietin-1 (Ang1), Angiopoietin-2 (Ang2) and Tie2 have essential role in angiogenesis in development. Ang1 and Ang2 are ligands which binds to their receptor, Tie2. METHODS: Expression of these proteins was sought during mouse kidney maturation from embryonic day 16 (E16) to 28 days postnatal (P28). RESULTS: Using RNase protection assay and Western blot, these three molecules were expressed throughout the experimental period with peak levels at P28 (Ang1), P14 (Ang2) and P7 (Tie2). By immunohistochemical analysis, Ang1 protein was found to localize to condensing renal mesenchymal cells, and tubules. Ang2 proteins were detected in differentiating outer medullary tubules and the vasa recta bundle area. Tie2 protein was detected in a portion of glomerular tufts and cortical interstitium, and medulla including vessels in the vasa recta. CONCLUSIONS: These data suggest that Ang1, Ang2 and Tie2 proteins are expressed in renal development.