Transforming growth factor-beta increases breast cancer stem cell population partially through upregulating PMEPA1 expression.

The prostate transmembrane protein, androgen-induced 1 (PMEPA1) has been previously shown to promote solid malignancies in a variety of cancers, but the role and mechanisms of PMEPA1 in breast cancer has not been fully addressed. Here, we found that PMEPA1 was upregulated in breast cancer cell lines as well as in a set of clinical invasive breast ductal carcinomas. Interestingly, depletion of PMEPA1 decreased breast cancer stem cell (CSC)-enriched populations, while ectopic overexpression of PMEPA1 increased breast CSC-enriched populations.

A short report: PAMM, a novel antioxidant protein, induced by oxidative stress.

Reactive oxygen species (ROS) play a central role in estrogen deficiency-induced bone loss. We previously identified and characterized a novel member of the Peroxiredoxin (PRX) like 2 family that we called PAMM: Peroxiredoxin Activated in M-CSF stimulated Monocytes, a redox regulatory protein that modulates osteoclast differentiation in vitro. In this study, we report increased PAMM expression in H2O2-treated cells and in bones from ovariectomized (OVX) mice 4 weeks after surgery, models for oxidative stress in vitro and in vivo, respectively.

[Differential expression of miRNAs in myocardial tissues of rats with lipopolysaccharide- induced endotoxemia].

Objective: To analyze the differential miRNA expression profile in the myocardium of rats with lipopolysaccharide (LPS)-induced endotoxemia and explore the role of miRNA in endotoxin-induced myocardial injury.

Methods: Twenty male SD rats received intraperitoneal injection of 10 mg/kg LPS (n=10) or an equivalent amount of saline solution (n=10). At 24 h after LPS injection, the rats were sacrificed to detect myocardial expressions of TLR4, TNF-α and IL-1β using real-time PCR and for observing myocardial ultrastructures under transmission electron microscopy.

The comparison of methods to identify the presence of fibrocytes in formalin-fixed, paraffin-embedded archival cardiac tissue with coronary heart disease.

The purpose of this study was to find the optimal technical approach to identify the presence of fibrocytes in formalin-fixed, paraffin-embedded archival cardiac tissue with CHD (coronary heart disease). Using the coexpression markers CD45 and αSMA, the presence of fibrocytes was examined by three different methods, including double immunohistochemistry staining, combination labeling of immunohistochemistry and immunofluorescence and double immunofluorescence labeling. Double immunohistochemistry staining was very difficult to identify the CD45(+)/αSMA(+) fibrocytes.

[Expression of PEPT2 mRNA in lung tissue of rats with pulmonary fibrosis].

Background And Objective: Pulmonary fibrosis is a common pathological phenomenon in lung cancer patients after chemotherapy or radiotherapy. It is also a key hindrance to the transport of drugs to lung tissue. Peptide transporters have become a target of the rational design of peptides and peptide drugs.

Extracorporeal cardiac shock wave therapy ameliorates myocardial fibrosis by decreasing the amount of fibrocytes after acute myocardial infarction in pigs.

Objectives: Extracorporeal shock wave (SW) therapy ameliorates cardiac remodeling after acute myocardial infarction (AMI). However, it remains to be examined whether and how SW therapy ameliorates myocardial fibrosis after AMI. Fibrocytes are associated with myocardial fibrosis.

siRNA-Act1 inhibits the function of IL-17 on lung fibroblasts via the NF-κB pathway.

Background: Interleukin (IL)-17-producing T lymphocytes play a role in pulmonary fibrosis, but the possible mechanism of IL-17 on lung fibroblasts remains uncertain.

Objectives: To explore the role and possible mechanism of IL-17 on lung fibroblasts.

Methods: A mouse model of pulmonary fibrosis was established by intratracheal administration of 5 mg/kg bleomycin.

Protective mechanisms of sevoflurane against one-lung ventilation-induced acute lung injury: role of cyclooxygenase-2 and 5-lipoxygenase pathways.

Objective: To explore the protective mechanisms of sevoflurane against acute lung injury (ALI) induced by one-lung ventilation (OLV) in view of cyclooxygenase-2 (COX2) and 5-lipoxygenase (5-LOX) pathways.

Method: Eighteen healthy Japanese white rabbits were randomized into sham-operated group (S group), OLV group (O group) and OLV + sevoflurane group (OS group). COX2 and 5-LOX protein and mRNA expressions in the lungs were detected by Western blotting and real-time PCR, respectively.

[Relationship between adipose expression of 3-phosphoinositide-dependent protein kinase 1 and glycometabolism in a mouse model of hyperhomocysteinemia].

Objective: To study the effect of homcysteine on the expression of 3-phosphoinositide-dependent protein kinase 1 (PDK1) in the adipose tissue and explore whether PDK1 inhibits p-Akt(Thr-308) expression and affect PI3K/Akt signal pathway to decrease glucose uptake and utilization.

Methods: Forty mice were randomly divided into 4 groups (n=10), namely the fasting control group, feeding control group, fasting hyperhomocysteinemia group, and feeding hyperhomocysteinemia group. In the two hyperhomocysteinemia groups, the mice were given water containing 1.

Effects of sevoflurane on pulmonary cytosolic phospholipase A₂ and clara cell secretory protein expressions in rabbits with one-lung ventilation-induced lung injury.

Objective: To investigate the effects of sevoflurane on cytosolic phospholipase A₂ (C-PLA₂) and clara cell secretory protein (CCSP) in lung tissues of rabbits with one-lung ventilation (OLV)-induced lung injuries.

Methods: Thirty-six healthy Japanese white rabbits were randomized into sham-operated group, OLV group, and OLV plus sevoflurane group subdivided into 4 subgroups with sevoflurane concentrations of 1%, 2%, 3% and 4%. CCSP and C-PLA₂ mRNA and protein expressions in rabbit lung tissues were detected by Western blotting and real-time PCR, and the content of arachidonic acid (AA) was measured using ELISA.

Fibrocytes are associated with the fibrosis of coronary heart disease.

Fibrocytes contribute significantly to fibrosis in many cardiac diseases. However, it is not clear whether fibrocytes are associated with the fibrosis in coronary heart disease (CHD). The aim of this study was to determine whether fibrocytes are involved in cardiac fibrosis in CHD.

Therapeutic effect of intravenous bone marrow-derived mesenchymal stem cell transplantation on early-stage LPS-induced acute lung injury in mice.

Objective: To investigate the effect of intravenous bone marrow-derived mesenchymal stem cell (MSC) transplantation for early intervention of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.

Methods: Thirty-six mice were randomized into control group, PBS-treated ALI group, and MSC-treated ALI group. In the latter two groups, mouse models of ALI were established by intranasal instillation of LPS, and 1 h later, the 4th passage of MSCs isolated from the bone marrow of mice or PBS were administered via the tail vein.

[Effects of interleukin-17 on murine pulmonary fibroblast proliferation, transformation and collagen synthesis].

Objective: To investigate the effects of interleukin-17 (IL-17) on the proliferation, transformation and collagen synthesis of the lung fibroblasts in mice with bleomycin-induced pulmonary fibrosis.

Methods: In a mouse model of pulmonary fibrosis established by intratracheal administration of 5 mg/kg bleomycin, the dynamic expressions of IL-17/IL-17 receptor (IL-17R) mRNAs were detected by RT-PCR. At 14 days following bleomycin administration, the pulmonary fibroblasts were isolated, cultured and identified.

The role of all-trans retinoic acid in bleomycin-induced pulmonary fibrosis in mice.

Much evidence suggests that immune imbalance in the lung plays a crucial role in the development of pulmonary fibrosis. Recently, all-trans retinoic acid (ATRA) shifting the regulatory T/T-helper 17 (Treg/Th17) profile had been proven in some diseases. However, to date, the effect of ARTA of pulmonary fibrosis has not been examined from this aspect.

Role of asymmetric dimethylarginine in acute lung injury induced by cerebral ischemia/reperfusion injury in rats.

Objective: To determine the role of asymmetric dimethylarginine (ADMA) in acute lung injury induced by cerebral ischemia/reperfusion (I/R) injury in rats.

Methods: Adult male SD rats were randomly divided into 4 groups, namely the sham-operated group (S), cerebral I/R model group, ADMA+I/R group, and dimethylarginine dimethylaminohydrolase (DDAH)+I/R group. In the latter 3 groups, acute lung injury was induced by left middle cerebral artery occlusion for 120 min.

Paragonimus worm from a New Guinea native in 1926.

Objective: To reobserve and research the specimen of Paragonimus worm found in the left lung of a New Guinea native in 1926, which was previously identified as Paragonimus westermani Kerbert or Paragonimus ringeri Cobbold.

Methods: Using reconstructive software and microscopy to observe some organs of the worm, and compared with other species of paragonimus.

Results: The three dimensional (3D) views of ovary and two testes of New Guinea specimen showed that the ovary was clearly divided into six lobes.

Effect of asymmetric dimethylarginine on MIF expression and TNF-α and IL-8 secretion in THP-1 monocytes-derived macrophages.

Objective: To investigate the effect of ADMA on macrophage migration inhibitory factor (MIF) expression and tumor necrosis factor-α (TNF-α) and IL-8 secretion in THP-1 monocyte-derived macrophages. METHIDS: THP-1 monocytes were induced to differentiate into macrophages by a 24-h incubation with 160 nmol/L PMA. The THP-1 monocyte-derived macrophages were exposed to different concentrations of ADMA for 24 h, and the changes in MIF mRNA and protein expressions were analyzed with RT-PCR and Western blotting, respectively.

Asymmetric dimethylarginine upregulates the expression of ACAT-1 in THP-1 macrophage-derived foam cells.

Objective: To investigate the effects of asymmetric dimethylarginine (ADMA) on ACAT-1 expression and cholesterol content in THP-1-derived macrophages and foam cells.

Methods: THP-1 cells were induced to differentiate into macrophages and further into foam cells. The macrophages and foam cells were exposed to different concentrations (0, 3.

[Change of cytochrome c in postconditioning attenuating ischemia-reperfusion-induced mucosal apoptosis in rat intestine].

The present study aimed to investigate the change of cytochrome c in postconditioning-attenuated ischemia-reperfusion (I/R)-induced mucosal apoptosis in rat intestine compared with ischemic preconditioning (IPC). Using rat model of intestine I/R injury, male Sprague-Dawley rats weighing 220-250 g were divided into 4 groups which were Sham operation group, I/R group, IPC group and ischemic postconditioning (IPOST) group. In these groups, I/R procedure was performed by the occlusion of the superior mesenteric artery (SMA) for 45 min followed by reperfusion for 1 h.

[Role of nuclear factor-kappaB in apoptosis pathway of HUVEC].

Aim: To investigate the role of nuclear factor-kappaB in apoptosis pathway of HUVEC.

Methods: The cell lines of HUVEC cultured in vitro were divided into three groups: normal control group, Ang II group, and Gliotoxin group. We investigated the effects of Ang II (0.

Protection of preconditioning, postconditioning and combined therapy against hepatic ischemia/reperfusion injury.

Objective: To study the protective effect of ischemic preconditioning (I-pre) and ischemic postconditioning (I-post) against ischemia/reperfusion (I/R) injury in rat's liver.

Methods: Using rat model of hepatic segmental I/R injury, rats were divided into 5 groups: Group A (sham group), Group B (I/R injury), Group C (I-pre group), Group D (I-post group) and Group E (combined treatment of I-pre and I-post). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) in hepatic tissues were determined, respectively.