14K prolactin derived 14-mer antiangiogenic peptide targets bradykinin-/nitric oxide-cGMP-dependent angiogenesis.

Over the past few decades, VEGF-targeted antiangiogenic therapy for cancers has gained increasing attention. Nevertheless, there are still several limitations such as the potential resistance mechanisms arising in cancer cells against these therapies and their potential adverse effects. These limitations highlight the need for novel anti-angiogenesis molecules and better understanding of the mechanisms of tumor angiogenesis.

Decreased ascorbic acid biosynthesis in response to PMSG in the pre-pubertal female rat ovary.

Ascorbic acid (AA) is known to be an important antioxidant serving as a cofactor in collagen synthesis, and thus facilitates follicular growth in the ovary. Many studies have shown that AA is synthesized in the liver and transported to other organs including ovary, however, there is no direct evidence of ascorbic acid synthesis in the ovary. Hence, we examined the expression pattern of different proteins (SMP30/GNL and GULO) involved in the AA synthesis in pre-pubertal rat, which showed significant expression of these proteins, suggesting the synthesis of AA in the ovary.

Unraveling the mechanism of l-gulonate-3-dehydrogenase inhibition by ascorbic acid: Insights from molecular modeling.

l-Gulonate dehydrogenase (GuDH) is a crucial enzyme in the non-phosphorylated sugar metabolism or glucuronate-xylulose (GX) pathway. Some naturally occurring compounds inhibit GuDH. Ascorbic acid is one of such inhibitors for GuDH.

Deterioration of epithelium mediated mechanisms in diabetic-antigen sensitized airways of guinea pigs.

Background: The onset of diabetes causes disruption of respiratory epithelial mediators. The present study investigates whether diabetes modifies the epithelium mediated bronchial responses in hyper-reactive airway smooth muscle (ASM) primarily through nitric oxide (NO), cyclooxygenase (COX), and epithelium derived hyperpolarizing factor (EpDHF) pathways.

Methods: Experimental model of guinea pigs having hyper-reactive airways with or without diabetes were developed.

Onset of diabetes modulates the airway smooth muscle reactivity of guinea pigs: role of epithelial mediators.

Background: Diabetes induces lung dysfunction, leading to alteration in the pulmonary functions. Our aim was to investigate whether the early stage of diabetes alters the epithelium-dependent bronchial responses and whether nitric oxide (NO), KATP channels and cyclooxygenase (COX) pathways contribute in this effect.

Methods: Guinea pigs were treated with a single injection of streptozotocin (180 mg/kg, i.

Inhibitory activity of the peptides derived from buffalo prolactin on angiogenesis.

The peptide fragments obtained by cathepsin digestion of purified buffalo prolactin (buPRL) monomer have been characterized using SDS-PAGE and FPLC with regard to size and pI. Their antiangiogenic activity was tested in chick embryo chorioallantoic membrane (CAM) assay and the human endothelial cells wound healing assay. Antiangiogenic activity was observed in cathepsin-cleaved fragments from buPRL.

Purification and biological characterization of bacterially expressed recombinant buffalo prolactin.

Recombinant prolactin (PRL) from water buffalo (Bubalus bubalis) has been cloned and expressed in a prokaryotic expression system. The hormone was also successfully refolded into a biologically active form. Total RNA was purified from buffalo pituitaries and the buPRL cDNA was synthesized using primers designed on bovine PRL sequence.

Pseudo-affinity chromatographic approach to probe heterogeneity in buffalo pituitary luteinizing hormone: probable pseudolectin-like behavior of immobilized Cibacron Blue 3GA.

The alpha (α) and beta (β) subunits of buffalo pituitary luteinizing hormone (LH) were chromatographed on Cibacron Blue 3GA agarose and their immunoreactivity was quantitated using anti-α and anti-β anti sera. Subsequent analyses showed α subunits were relatively more hydrophilic than β subunits. Further, the naturally occurring free α and β subunits were more hydrophobic than their native counterparts which were dissociated and isolated from heterodimeric LH.

Thioredoxin reductase-1 negatively regulates HIV-1 transactivating protein Tat-dependent transcription in human macrophages.

Epidemiological studies suggest a correlation between severity of acquired immunodeficiency syndrome (AIDS) and selenium deficiency, indicating a protective role for this anti-oxidant during HIV infection. Here we demonstrate that thioredoxin reductase-1 (TR1), a selenium-containing pyridine nucleotide-disulfide oxidoreductase that reduces protein disulfides to free thiols, negatively regulates the activity of the HIV-1 encoded transcriptional activator, Tat, in human macrophages. We used a small interfering RNA approach as well as a high affinity substrate of TR1, ebselen, to demonstrate that Tat-dependent transcription and HIV-1 replication were significantly increased in human macrophages when TR1 activity was reduced.

Association of polymorphisms in pulmonary surfactant protein A1 and A2 genes with high-altitude pulmonary edema.

Study Objectives: A potential pathogenetic cofactor for the development of high-altitude pulmonary edema (HAPE) is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free-radical-mediated injury to the lung. Pulmonary surfactant protein A (SP-A), the most abundant surfactant protein, has potent antioxidant properties and protects unsaturated phospholipids and growing cells from oxidative injury. Single-nucleotide polymorphisms (SNPs) in SP-A1 and SP-A2, genes encoding SP-A, have been associated with susceptibility to respiratory distress syndrome, COPD, and pulmonary infections.

Association of polymorphisms in the collagen region of SP-A2 with increased levels of total IgE antibodies and eosinophilia in patients with allergic bronchopulmonary aspergillosis.

Background: Studies from our group have shown a protective role of pulmonary surfactant protein A (SP-A) against lung allergy and infections caused by Aspergillus fumigatus.

Objective: Present study investigated the association of polymorphisms in the collagen region of SP-A1 and SP-A2 (genes encoding SP-A) with allergic bronchopulmonary aspergillosis (ABPA) and its clinical markers.

Methods: Genomic DNA was extracted from blood samples of patients with ABPA and age-matched, unrelated control subjects.

Association of polymorphisms in the collagen region of human SP-A1 and SP-A2 genes with pulmonary tuberculosis in Indian population.

Surfactant protein A (SP-A) binds to and modulates phagocytosis of Mycobacterium tuberculosis by macrophages. We investigated the relationship between polymorphisms in the collagen regions of SP-A1 and SP-A2 genes and pulmonary tuberculosis. In the present study, seven single nucleotide polymorphisms (SNPs) (4 exonic and 3 intronic) have been identified in the collagen regions of SP-A1 and SP-A2 genes in Indian population.