Estrogen receptor α (ESR1) over-expression mediated apoptosis in Hep3B cells by binding with SP1 proteins.

Previous studies have reported that estrogen receptors (ERs) are expressed in normal human liver, chronic hepatitis, and benign hepatic tumor tissues. However, decreased expression of ERs can be observed in hepatocellular carcinoma (HCC) and the role of ERs in HCC is not fully understood. Thus, the present study aimed to investigate the molecular mechanism induced by the overexpression of ERα (ERα (ESR1)) in Hep3B cells.

Association of hypoxia inducible factor-1α polymorphisms with susceptibility to non-small-cell lung cancer.

Hypoxia-inducible factor-1α (HIF-1α) is a key regulator of cellular response to hypoxia and has been suggested to play an important role in tumorigenesis and metastasis. The aim of this study was to investigate the role of HIF-1α-1772 C/T (P582S) and -1790 G/A (A588T) polymorphisms in the susceptibility to and severity of non-small-cell lung cancer (NSCLC). Using a case-control study design and polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) analysis, the allele frequencies and genotype distributions of each single nucleotide polymorphism in 285 NSCLC cases and 300 gender-matched controls were compared.

IGF-II/mannose 6-phosphate receptor activation induces metalloproteinase-9 matrix activity and increases plasminogen activator expression in H9c2 cardiomyoblast cells.

The IGF-II/mannose 6-phosphate receptor (IGF2R) function in extracellular matrix (ECM) remodeling is known to occur as a result of transforming growth factor-beta (TGF-beta) activation and plasmin in the proteolytic cleavage level caused by the interaction between latent TGF-beta and urokinase plasminogen activator receptor (uPAR) respectively. In one of our previous studies, we found IGF-II and IGF2R dose-dependently correlated with the progression of pathological hypertrophy remodeling following complete abdominal aorta ligation. However, how this IGF2R signaling pathway responds specifically to IGF-II and regulates the myocardial ECM remodeling process is unclear.

Immunoglobulin E and matrix metalloproteinase-9 in patients with different stages of coronary artery diseases.

The aims of this study were to identify levels of total immunoglobulin E (IgE) and matrix metalloproteinase (MMP)-9 in patients with different stages of coronary artery diseases. IgE, MMP-9, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), total cholesterol, low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL) and triglyceride (TG) were measured by fluorescence enzyme immunoassay, gelatin zymography, and autoanalyzer in normal subjects (n = 40), patients with stable angina pectoris (SAP, n = 40), patients with unstable angina pectoris (UAP, n = 40), patients with acute myocardial infarction (AMI, n = 40), or post-CABG-surgery of those acute myocardial infarction (P-CABG, n = 40). Compared with normal subjects, increased IgE but unchanged MMP-9, CPK, LDH were found in SAP group and UAP group, whereas IgE, MMP-9, CPK and LDH levels were all significantly increased in AMI group.

Down regulation of IGF-I and IGF-IR gene expression in right atria tissue of ventricular septal defect infants with right atria hypoxemia.

Background: Our previous studies showed serum insulin-like growth factor-I (IGF-I) concentrations significantly decreased in infants with congenital ventricular septal defect (VSD) and that they were associated with increased concentrations of growth hormone. In order to confirm the relationship between IGF-I axis and VSD, we further compared the IGF-I and insulin-like growth factor-I receptor(IGF-IR) gene expressions in the cardiac tissue of VSD infants.

Methods: Right atrium biopsies of 27 infants were studied.

Serum MMP-9 activity as a diagnosing marker for the developing heart failure of post MI patients.

Myocardial infarction (MI) is the result, in mostly cases, of the destabilization and rupture of atherosclerotic lesions. The destruction of cardiac tissue resulting from myocardial ischemia could further result in heart failure. It has been suggested that plaque instability may be mediated by matrix metalloproteinase (MMP) family.

Serum insulin-like growth factor-axis and matrix metalloproteinases in patients with rheumatic arthritis or rheumatic heart disease.

Background: Insulin-like growth factor (IGF)-I plays an important role for maintaining cardiac functions. We clarified the unknown role of IGF-axis in rheumatic heart disease (RHD).

Method: Interleukin (IL)-10, growth hormone (GH), IGF, IGF binding protein (IGFBP)-3 and matrix metalloproteinase (MMP) were measured by ELISA and zymography in 30 age range-matched normal subjects (control), 36 patients with acute phase of rheumatoid arthritis (RA) with positive rheumatoid factor (RF) and C-reactive protein (CRP), and in 43 patients with RHD with negative RF and CRP.

Differential expression of carbonic anhydrase isoenzymes in various types of anemia.

Background: The aim of the present study was to determine the concentrations of cytosolic carbonic anhydrase (CA) isoenzymes in erythrocytes of patients with aplastic, autoimmune hemolytic, iron deficiency or beta-thalassemia anemia.

Methods: Western blotting and CA esterase activity analysis were used to analyze cytosolic erythrocyte CA isoenzymes in 118 subjects with various types of anemia and 35 healthy controls.

Results: Total CA activity and CAII concentration of anemia patients were significantly higher than that of the control subjects while CAI concentration was significantly lower in patients of autoimmune hemolytic anemia (P<0.

The differential expression of cytosolic carbonic anhydrase in human hepatocellular carcinoma.

Cytosolic carbonic anhydrases (CAs), including CAI, CAII and CAIII are present in normal hepatocytes. This study was aimed to investigate the expression status of CAs in hepatocellular carcinomas (HCC) and cholangiocellular carcinoma (CCC) and the role of tumor progression. The activity, protein expression pattern and messenger RNA of cytosolic CA were analyzed by CA activity analysis, immunoblot and RT-PCR in 60 human hepatocellular carcinomas and 10 human cholangiocellular carcinoma surgical specimens.

Differential inductions of matrix metalloproteinase-2 and -9 in host tissues during the growth of ascitic sarcoma 180 cells in mice.

This study was designed to investigate the changes of matrix metalloproteinase (MMP)-2 and MMP-9 in host tissues in response to the growth of tumor cells. Zymogram showed that the responses of both MMPs in the host tissues were differential but concurrent. The liver, a prime target of metastases, had profound increases in MMP-2 and -9.

Significant differences in serum activities of matrix metalloproteinase-2 and -9 between HCV- and HBV-infected patients and carriers.

To examine the possible involvement of MMP-9 and -2 in the development of liver diseases caused by HCV or HBV infection, serum activities of both enzymes were studied by zymograph. Eight groups of subjects (60 for each) were examined in the study: healthy control, patients with hepatoma, liver cirrhosis, chronic hepatitis B or chronic hepatitis C, and carriers positive for HBsAg, both HBsAg and HBeAg, or anti-HCV. The results showed significant changes in the MMP-9 and -2 activities in the carriers.