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Van Gieson Staining (van + gieson_staining)
Selected Abstractsl -Arginine Inhibits Isoproterenol-Induced Cardiac Hypertrophy through Nitric Oxide and Polyamine PathwaysBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2008Yan Lin Nitric oxide exhibits antihypertrophic functions and inhibits cardiac remodelling. However, the metabolism of polyamines and the potential interactions with nitric oxide in cardiac hypertrophy remain unclear. We randomly divided Wistar rats into four treatment groups: controls, isoproterenol (ISO), ISO and l -arginine, and l -arginine. Isoproterenol (5 mg/kg/day, subcutaneously) and/or l -arginine (800 mg/kg/day, intraperitoneally) was administered once daily for 7 days. The expression of atrial natriuretic peptide mRNA was determined by reverse transcription,polymerase chain reaction, and fibrogenesis of heart was assessed by Van Gieson staining. Polyamines were measured with high-performance liquid chromatography, and plasma nitric oxide content and lactate dehydrogenase (LDH) activity were determined with a spectrophotometer. The expression levels of ornithine decarboxylase, spermidine/spermine N1-acetyltransferase (SSAT), endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were analysed by Western blot. Heart-to-body weight ratio, left ventricle-to-body weight ratio, atrial natriuretic peptide mRNA expression, collagen fibres and LDH activity were elevated, both ornithine decarboxylase and SSAT proteins were up-regulated, and total polyamines were increased in the group treated with ISO. Additionally, the expression of iNOS was up-regulated, eNOS was down-regulated, and nitric oxide levels were low. Notably, cotreatment with l -arginine reversed most of these changes except for SSAT expression, which was further up-regulated. We propose that increased polyamines and decreased nitric oxide are involved in cardiac hypertrophy induced by ISO and suggest that l -arginine pre-treatment can attenuate cardiac hypertrophy through the regulation of key enzymes of the polyamine and nitric oxide pathways. [source] Immunohistochemical investigation of mid-dermal elastolysisCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 2 2004T. Gambichler Summary We report a 31-year-old Caucasian woman presenting with remarkable wrinkling on her trunk and proximal extremities. Diagnosis of mid-dermal elastolysis (MDE) was confirmed by Van Gieson's staining. Immunohistochemical investigations revealed enhanced expression of CD34+ and CD68+ cells accompanied by slightly increased expression of CD3+ and CD4+ lymphocytes in lesional skin. Furthermore an elevated cellular expression of matrix metalloproteinase (MMP)-1 and slightly increased presence of MMP-12 positive cells combined with a decrease of tissue inhibitor of metalloproteinases 1 (TIMP-1) positive cells was observed in lesional skin as compared with a control specimen obtained from nonlesional skin. Our data may indicate inflammatory processes and an altered balance between MMPs and TIMPs in MDE. Furthermore CD34+ dendritic fibroblasts and/or histiocytes are possibly involved in the pathogenesis of MDE. [source] Irradiated cultured apoptotic peripheral blood mononuclear cells regenerate infarcted myocardiumEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2009H. J. Ankersmit Abstract Background, Acute myocardial infarction (AMI) is followed by post AMI cardiac remodelling, often leading to congestive heart failure. Homing of c-kit+ endothelial progenitor cells (EPC) has been thought to be the optimal source for regenerating infarcted myocardium. Methods, Immune function of viable peripheral blood mononuclear cells (PBMC) was evaluated after co-culture with irradiated apoptotic PBMC (IA-PBMC) in vitro. Viable PBMC, IA-PBMC and culture supernatants (SN) thereof were obtained after 24 h. Reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay were utilized to quantify interleukin-8 (IL-8), vascular endothelial growth factor, matrix metalloproteinase-9 (MMP9) in PBMC, SN and SN exposed fibroblasts. Cell suspensions of viable- and IA-PBMC were infused in an experimental rat AMI model. Immunohistological analysis was performed to detect inflammatory and pro-angiogenic cells within 72 h post-infarction. Functional data and determination of infarction size were quantified by echocardiography and Elastica van Gieson staining. Results, The IA-PBMC attenuated immune reactivity and resulted in secretion of pro-angiogenic IL-8 and MMP9 in vitro. Fibroblasts exposed to viable and IA-PBMC derived SN caused RNA increment of IL-8 and MMP9. AMI rats that were infused with IA-PBMC cell suspension evidenced enhanced homing of endothelial progenitor cells within 72 h as compared to control (medium alone, viable-PBMC). Echocardiography showed a significant reduction in infarction size and improvement in post AMI remodelling as evidenced by an attenuated loss of ejection fraction. Conclusion, These data indicate that infusion of IA-PBMC cell suspension in experimental AMI circumvented inflammation, caused preferential homing of regenerative EPC and replaced infarcted myocardium. [source] Role of Chlamydia pneumoniae -infected macrophages in atherosclerosis developments of the carotid arteryNEUROPATHOLOGY, Issue 1 2003Satoshi Kuroda Chlamydia pneumoniae (C. pneumoniae) infection has been recently accepted as an important cause of atherosclerosis. However, the precise mechanisms remain unclear. The present study was aimed to clarify the distribution link among C. pneumoniae, chlamydial HSP 60, and activated macrophages. Atheromatous carotid plaques were obtained from 40 consecutive carotid endarterectomies (CEA). The specimens were prepared for HE and elastica,van Gieson staining. Parallel sections were stained immunocytochemically with monoclonal antibodies for a C. pneumoniae -specific antigen, chlamydial HSP 60, activated macrophages, and smooth muscle cells. Immunoreactivity for the C. pneumoniae -specific antigen was observed within the endothelial cells, activated macrophages, and smooth muscle cells in 36 of 40 specimens (90%). Chlamydial HSP 60 was found in all specimens positive for the C. pneumoniae -specific antigen, and mainly co-localized with the C. pneumoniae -specific antigen within the activated macrophages. The present results suggest that C. pneumoniae is a key microbial organ that causes atheroma developments in the carotid artery. Chlamydia pneumoniae -infected macrophages may come into the arterial intima and mediate inflammatory and autoimmune processes through the production of chlamydial HSP 60, leading to atherosclerosis. [source] | ||||||||||