Reduced vascular responsiveness to adiponectin in hyperlipidemic rats--mechanisms and significance.

Deficiency of adiponectin (APN), an adipocyte-derived vascular protective molecule, contributes to diabetic vascular injury. The current study determined whether obesity/hyperlipidemia may alter the vascular response to APN, and investigated the involved mechanisms and pathologic significance. Adult male Sprague-Dawley rats were fed a regular or high-fat diet (HF) for 4-16 weeks.

Cardiomyocyte-derived adiponectin is biologically active in protecting against myocardial ischemia-reperfusion injury.

Adiponectin (APN) has traditionally been viewed as an adipocyte-specific endocrine molecule with cardioprotective effects. Recent studies suggest that APN is also expressed in cardiomyocytes. However, biological significances of this locally produced APN remain completely unknown.

Adiponectin: an indispensable molecule in rosiglitazone cardioprotection following myocardial infarction.

Rationale: Patients treated with peroxisome proliferator-activated receptor (PPAR)-gamma agonist manifest favorable metabolic profiles associated with increased plasma adiponectin (APN). However, whether increased APN production as a result of PPAR-gamma agonist treatment is an epiphenomenon or is causatively related to the cardioprotective actions of PPAR-gamma remains unknown.

Objective: To determine the role of APN in rosiglitazone (RSG) cardioprotection against ischemic heart injury.

Roles of Wnt/beta-catenin signaling in epithelial differentiation of mesenchymal stem cells.

Bone marrow-derived mesenchymal stem cells (MSCs) have been demonstrated to be able to differentiate into epithelial lineage, but the precise mechanisms controlling this process are unclear. Our aim is to explore the roles of Wnt/beta-catenin in the epithelial differentiation of MSCs. Using indirect co-culture of rat MSCs with rat airway epithelial cells (RTE), MSCs expressed several airway epithelial markers (cytokeratin 18, tight junction protein occudin, cystic fibrosis transmembrance regulator).

Cardioprotective effect of adiponectin is partially mediated by its AMPK-independent antinitrative action.

Adiponectin (APN) exerts its metabolic regulation largely through AMP-dependent protein kinase (AMPK). However, the role of AMPK in APN's antiapoptotic effect in ischemic-reperfused (I/R) adult cardiomyocytes remains incompletely understood. The present study was designed to determine the involvement of AMPK in the antiapoptotic signaling of APN.

AMP-activated protein kinase deficiency enhances myocardial ischemia/reperfusion injury but has minimal effect on the antioxidant/antinitrative protection of adiponectin.

Background: Diabetes increases the morbidity/mortality of ischemic heart disease, but the underlying mechanisms are incompletely understood. Deficiency of both AMP-activated protein kinase (AMPK) and adiponectin occurs in diabetes, but whether AMPK is cardioprotective or a central mediator of adiponectin cardioprotection in vivo remains unknown.

Methods And Results: Male adult mice with cardiomyocyte-specific overexpression of a mutant AMPKalpha2 subunit (AMPK-DN) or wild-type (WT) littermates were subjected to in vivo myocardial ischemia/reperfusion (MI/R) and treated with vehicle or adiponectin.

INO-4885 [5,10,15,20-tetra[N-(benzyl-4'-carboxylate)-2-pyridinium]-21H,23H-porphine iron(III) chloride], a peroxynitrite decomposition catalyst, protects the heart against reperfusion injury in mice.

Oxidative/nitrative stress caused by peroxynitrite, the reaction product of superoxide (O2(.-)) and nitric oxide (NO), is the primary cause of myocardial ischemia/reperfusion injury. The present study determined whether INO-4885 [5,10,15,20-tetra[N-(benzyl-4'-carboxylate)-2-pyridinium]-21H,23H-porphine iron(III) chloride], a new peroxynitrite decomposition catalyst, may provide cellular protection and protect heart from myocardial ischemia/reperfusion injury.

Endothelial dysfunction in adiponectin deficiency and its mechanisms involved.

Endothelial dysfunction is the earliest pathologic alteration in diabetic vascular injury and plays a critical role in the development of atherosclerosis. Plasma levels of adiponectin (APN), a novel vasculoprotective adipocytokine, are significantly reduced in diabetic patients, but its relationship with endothelial dysfunction remains unclear. The present study aims to determine whether APN deficiency may cause endothelial dysfunction and to investigate the involved mechanisms.

Methyl tert-butyl ether (MTBE) induced Ca(2+)-dependent cytotoxicity in isolated rabbit tracheal epithelial cells.

As a volatile synthetic organic chemical, methyl tert-butyl ether (MTBE) was the most common gasoline additive. The increasing use of MTBE raised concern over its health safety. Inhalation was the principle route of exposure for the general population.

[Molecular and chemical mechanism of Trichomonas vaginalis-induced contact-dependent cytotoxicity].

Trichomonas vaginalis parasitizes in human genitourinary tract. The protozoon adhering to target cell plays a critical role in its contact-dependent cytotoxicity. The enzymes synthesized by T.

[Construction of eukaryotic expression recombinant plasmid of trichomonas vaginalis ferredoxin gene].

Total DNA was extracted from T. vaginalis with Chelex-100 method and used as templates for PCR. The ferredoxin gene was directionally cloned into plasmid pMD-18T vector and subcloned into eukaryotic expression vector pcDNA3.

Estrogen down-regulates nicotine-induced adhesion molecule expression via nongenomic signal pathway in endothelial cells.

Although gonadal hormone mostly causes genotropic actions through the members of nuclear receptor family, it also can regulate these actions via membrane receptor. To explore the possibility of plasma membrane estrogen receptors (mER) mediating genotropic events, we have investigated estrogen's effect on nicotine-stimulated adhesion molecule expression and evaluated whether this effect depends on calcium, MAPK signal pathway. Fluorescence Spectroscopy analysis of Ca2+ from human umbilical vein endothelial cells (HUVECs) showed through mER, estrogen induced a rapid rise of intracellular free Ca2+ concentration and this rise could not be inhibited by tamoxifen (classic ER inhibitor).

Testosterone attenuates p38 MAPK pathway during Leishmania donovani infection of macrophages.

Leishmania donovani (L. donovani) is an obligatory intracellular pathogen that resides and multiplies in the macrophages and has been found to alter the signaling parameters of the host. Testosterone plays a key role as signaling molecules in the regulation of parasite infections and could increase L.

Characterization and quantification of mRNA transcripts in ejaculated spermatozoa of fertile men by serial analysis of gene expression.

Background: Accumulated evidence proves that mature spermatozoa contain a complex yet specific array of mRNA, which could provide information on the past events of spermatogenesis.

Objective: To quantitatively microdissect these mRNA transcripts by a digital approach.

Methods: Serial analysis of gene expression (SAGE) was used to study the mRNA transcripts from ejaculate of a fertile individual and of a pool of 10 fertile men.

Nicotine stimulates adhesion molecular expression via calcium influx and mitogen-activated protein kinases in human endothelial cells.

To evaluate the effect of nicotine on endothelium dysfunction and development of vascular diseases, we investigated the influence on adhesion molecular expression mediated by nicotine and the mechanism of this effect in human umbilical vein endothelial cells (HUVECs). The result showed that nicotine could induce surface/soluble vascular cell adhesion molecule (VCAM-1) and endothelial selectin (E-selectin) expression in a time-response decline manner and the peak appeared at 15 min. This action could be mediated by mitogen-activated protein kinase/extracellular signal regulated kinase 1/2 (MAPK/ERK1/2) and MAPK/p38 because their activation could be distinctly blocked by MAPK inhibitors, PD098059 or SB203580.

[Expression and activity of tissue-type plasminogen activator mutant reteplase with deletion of PAI-1 binding sites].

Aim: To construct a mutant of human tissue plasminogen activator (t-PA) with activity not inhibited by plasminogen activator inhibitor-1 (PAI-1).

Methods: The finger, epidermal growth factor and kringle-1 domains were removed from native t-PA to obtain a t-PA mutant with the PAI-1 binding sites. A pUC18 plasmid containing the human t-PA full-length cDNA sequence was used as template, and the DNA sequences encoding 1-3 and 176-527 amino acids were amplified by PCR.

[Cloning and sequence analysis of Trichomonas vaginalis ferredoxin gene].

Objective: To construct a recombinant plasmid containing ferredoxin gene of Trichomonas vaginalis.

Methods: Total DNA was extracted from Trichomonas vaginalis with Chelex-100 method and used as templates for PCR. Primers were designed based on the published sequence of the ferredoxin gene and used to amplify the Trichomonas vaginalis gene using PCR method.

Modulation of Leishmania donovani infection and cell viability by testosterone in bone marrow-derived macrophages: signaling via surface binding sites.

Androgens can increase susceptibility toward numerous parasitic infections as well as modulate apoptosis of immune cells. According to the current view, androgens mediate immune cell activities not only through classical intracellular androgen receptors (AR), but also through membrane receptors on the cell surface. Here, using murine bone marrow-derived macrophages (BMMs), we examined the influence of testosterone on Leishmania donovani infection and cell viability in vitro as well as the possible mechanisms.

[Analysis of CpG motifs in endoflagellar gene (flaB2) and expression vector (VR1012) of leptospiral DNA vaccine].

Objective: To provide basis for the exploring of the mechanism and improvement of the efficacy of DNA vaccines, through the analysis of CpG motifs in endoflagellar gene (flaB2) and expression vector (VR1012) of the Leptospiral DNA vaccine.

Methods: Directed by Kreig's immunostimulatory nucleic acid molecules, we undertook the computer-assisted analysis of the total number and locations of CpG motifs in flaB2 and VR1012 sequences.

Results: The CpG motifs was flanked by two 5'purines and 3'pyrimidines.

Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-alpha, IL-1beta.

Nicotine, the major immunomodulatory components of cigarette smoking, is among the leading risk factors in atherosclerosis and various other diseases. The subject of this study is to observe how nicotine affects the function of macrophages and vascular endothelial cells. The changes of nicotine on releasing of cytokines from Ana-1 were detected by radio-immunoassay (RIA) or enzyme-link immunosorbent assay (ELISA).

[Construction of LACK gene recombinant plasmid and detection of its expression in eukaryotic cell].

The LACK gene from Leishmania, an analogue of the receptor of activated protein kinase C, was discovered recently. In this study, the LACK gene of Leishmania donovani was obtained from the recombinant plasmid T-LACK by PCR. The gene was cloned into eukaryotic expressed plasmid pcDNA3.