Immunoexpression of vascular endothelial growth factor and vWF-regulating angiogenesis in cyclic corpus luteum of Indian buffalo.

The present study was conducted to localize the immunoexpression of VEGF-A (Vascular Endothelial Growth Factor) and von Willebrand factor (vWF) in corpora lutea of healthy buffaloes (24) collected from local slaughterhouses. CL collected were categorized into early (stage I, 1-5 days, n = 6), mid (stage II, 6-11 days, n = 6), late luteal phase (stage III, 12 to 16 days, n = 6) and regressing phase (stage IV, 17 to 20 days, n = 6). The percent positive immunostaining for VEGF-A was significantly (p < 0.05) higher in mid-luteal phase than the other three stages of CL. However, it was higher in early luteal phase as well indicated intense angiogenesis in both early and mid-luteal phases. The number of capillary endothelium expressing vWF was significantly (p < 0.05) highest in mid-luteal phase among all the phases. However, in late luteal phase, the percent area positive for VEGF-A immunostaining was reduced but it was significantly (p < 0.05) higher than corpus albicans phase. Thus, in regressing phase or corpus albicans, it was lowest and reduced considerably. However, in late luteal phase, the number of capillaries with vWF immunoexpression reduced significantly (p < 0.05) but it was lowest in corpus albicans phase. Therefore, the immunotaining pattern for VEGF-A and vWF concluded that there was a spositive linear correlation between the two, that is, as the VEGF-A expression was increased, the number of vWF positive capillaries also increased and vice versa. The VEGF-A expressed by the luteal parenchyma in different stages of development and regression of corpus luteum was thus observed to be involved in promoting the angiogenesis and luteal cell proliferation as supported by vWF expressed by endothelium of proliferating capillaries in buffalo corpus luteum throughout the estrous cycle.

Biomarker-assisted assessment of aquatic health using the cosmopolitan common carp, Cyprinus carpio (L): a case study of bisphenol-A exposures.

Monitoring aquatic health from environmental pollutants is critical, none more so than bisphenol-A (BPA), a ubiquitous endocrine-disrupting chemical (EDC). The present study brings out the responses of selected transcripts, hormone levels, and tissue histomorphology in a widely distributed fish species Cyprinus carpio (Linn.), following exposure to environmentally relevant (10, 100 ng/L) and higher (1000 ng/L) concentration of BPA. The response of cyp19a1a, cyp19a1b, and c3 significantly decreased, while that of vtg increased in their respective tissue domains. The hematological parameters TEC, Hb, and Hct decreased significantly in contrast to TLC (p < 0.05) at all exposure concentrations, whereas none of the erythrocytic indices (MCV, MCH, and MCHC) was perturbed. The steroidogenic hormone levels, such as estradiol and progesterone, increased significantly with increasing BPA concentrations. In contrast, the testosterone and all the thyroid hormones (T3, T4, and TSH) were suppressed significantly (p < 0.05). At the histological level, the BPA induced chondrocyte proliferation, which was accompanied by hemorrhage of the gill lamellae, increased melanomacrophagic centers (MMCs), and degeneration of tubules and fluid accumulation in the kidney. In parallel, binucleated hepatocytes and inflammations were prominent in the liver. Collectively, the histomorphology confirmed induction of degenerative effects in all the tissues investigated, while the cyclic responses of biochemical markers suggest an ability to regulate the impacts. However, a chronic exposure could result in overriding the endemic reproductive pathways with potential population-level effects. In conclusion, the study identified multiple molecular, cellular, and physiological markers that could be employed to detect early signs of BPA and more broadly EDC exposures. These markers in combination with a wide distribution of C. carpio should allow comparative studies of pollutants at environmental concentrations.

P-coumaric acid ameliorates fipronil induced liver injury in mice through attenuation of structural changes, oxidative stress and inflammation.

Fipronil is a broad-spectrum phenylpyrazole insecticide and has been used effectively in the agriculture. Due to its widespread use and bioaccumulation in the environment, it possesses significant threat to human and animals. P-coumaric acid is a natural dietary polyphenolic compound that has anti-oxidant and anti-inflammatory property. The present study was aim to investigate the ameliorative effect of p-coumaric acid on fipronil induced liver injury. The mice were divided into five groups (SHAM, FPN, FPN/PCA/50, FPN/PCA/100 and PCA/100) and challenged with fipronil @ 25 mg/kg bw (half of LD50). Haematological, liver function biomarkers (ALT, AST, ALP, GGT), biochemical parameters (MPO, oxidative, nitrosative stress and anti-oxidant enzyme activity), levels of serum and liver inflammatory cytokines (TNF-α, IL-1ß and IL-10), histopathology were monitored. Fipronil administration caused a significant increase in liver enzymes with concomitant significant increase in inflammatory cytokines (TNF-α, IL-1ß, IL-10) and myeloperoxidase activity. A significant increase in oxidative stress (lipid peroxidation, nitric oxide) as well as down regulation of anti-oxidant enzymes like superoxide dismutase (SOD) and catalase (CAT) along with histopathological changes such as microsteatosis, hypertrophy of the hepatocytes and necrosis were observed on fipronil administration. Administration of p-coumaric acid against fipronil caused decreased serum liver enzymes, inflammatory cytokines, myeloperoxidase activity and oxidative stress along with improvement in anti-oxidant enzyme levels and structural changes induced by fipronil. Thus p-coumaric acid ameliorates the FPN induced liver injury in mice through attenuation of structural changes, oxidative stress, and inflammation.

Expression of Certain Pulmonary Proteins in the Tracheal Mucosa and Lungs of Pashmina, Bakerwali and Non-Descript Goats of U.T.s of Ladakh and Jammu & Kashmir

Abstract The aim of this present study was to localize alveolar macrophages, Proliferating cell nuclear antigen (PCNA), Smooth muscle actin (SMA), Vimentin and Vasculo-endothelial growth factor (VEGF) in the tracheal epithelium and lung alveoli in three important breeds of goats namely, Pashmina, Bakerwali and non-descript goats by standard immunohistochemical methods. Large pulmonary macrophages were observed in the lung sections of all the three breeds of goat. Macrophages were observed in the alveolar septa and airway epithelium. The mean macrophage count for Pashmina, Bakerwali and non-descript goat were recorded as 23.4±1.47, 27.8±0.68 and 21.4±0.70, respectively. The PCNA activity was intense in the alveolar epithelial cells of lungs in Pashmina and Bakerwali goats and very high in the lung tissue of non-descript goat. The PCNA activity was intense in the bronchial epithelial cells of lungs in Bakerwali goat. Strong reaction of SMA was observed in the submucosa of bronchioles of Pashmina and Bakerwali goats. The submucosa of the tracheal tissue showed a strong reaction of SMA in the non-descript goat and moderate in the submucosa of trachea in the Bakerwali goat. A number of vimentin-positive cells were found in the lung parenchyma in both Pashmina and Bakerwali goats. Also, there was a strong reaction of vimentin mainly in submucosal area in non-descript goat. The VEGF activity was found to be intense in the lung alveoli of Bakerwali goat and strong in Pashmina and non-descript goats. The tracheal epithelium was moderately reactive to VGEF in all the three goats.

Long non-coding RNA: its evolutionary relics and biological implications in mammals: a review.

The central dogma of gene expression propounds that DNA is transcribed to mRNA and finally gets translated into protein. Only 2-3% of the genomic DNA is transcribed to protein-coding mRNA. Interestingly, only a further minuscule part of genomic DNA encodes for long non-coding RNAs (lncRNAs) which are characteristically more than 200 nucleotides long and can be transcribed from both protein-coding (e.g. H19 and TUG1) as well as non-coding DNA by RNA polymerase II. The lncRNAs do not have open reading frames (with some exceptions), 3`-untranslated regions (3'-UTRs) and necessarily these RNAs lack any translation-termination regions, however, these can be spliced, capped and polyadenylated as mRNA molecules. The flexibility of lncRNAs confers them specific 3D-conformations that eventually enable the lncRNAs to interact with proteins, DNA or other RNA molecules via base pairing or by forming networks. The lncRNAs play a major role in gene regulation, cell differentiation, cancer cell invasion and metastasis and chromatin remodeling. Deregulation of lncRNA is also responsible for numerous diseases in mammals. Various studies have revealed their significance as biomarkers for prognosis and diagnosis of cancer. The aim of this review is to overview the salient features, evolution, biogenesis and biological importance of these molecules in the mammalian system.

Over-expression of mammaglobin-B in canine mammary tumors.

BACKGROUND: Mammaglobin, a member of secretoglobin family has been recognized as a breast cancer associated protein. Though the exact function of the protein is not fully known, its expression has been reported to be upregulated in human breast cancer.We focused on studying the expression of mammaglobin-B gene and protein in canine mammary tumor (CMT) tissue. Expression of mammaglobin-B mRNA and protein were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC), respectively. RESULTS: High levels of mammaglobin-B mRNA expression (6.663 ± 0.841times) was observed in CMT as compared to age and breed matched healthy controls. Further, expression of mammaglobin-B protein was detected in paraffin-embedded mammary tumor tissues from the same subjects by IHC. Mammaglobin-B protein was overexpressed only in 6.67% of healthy mammary glands while, a high level of its expression was scored in 76.7% of the CMT subjects. Moreover, no significant differences in terms of IHC score and qRT-PCR score with respect to CMT histotypes or tumor grades were observed, indicating that mammaglobin-B over-expression occurred irrespective of CMT types or grades. CONCLUSION: Overall, significantly increased expression of mammaglobin-B protein was found in CMTs with respect to healthy mammary glands, which positively correlates to its transcript. These findings suggest that overexpression of mammaglobin-B is associated with tumors of canine mammary glands.

Characterization of the lung epithelium of wild-type and TLR9(-/-) mice after single and repeated exposures to chicken barn air.

Exposure to chicken barn air causes lung injury resulting in lower and upper respiratory symptoms in the poultry workers, and mechanisms of which are not fully understood. The lung injury can initiate modifications such as proliferation of the airway epithelial cells such as Clara cells, type II alveolar (T2) cells and mucus producing goblet cells as part of the innate immune response. Toll-like receptors (TLR) have been suggested to play a role in cell division and proliferation. To understand the effect of TLR9 on Clara cells, T2 and mucus-producing goblet cells, we quantified the numbers of these cells in the lungs of wild-type (WT) and TLR9(-/-) mice exposed to chicken barn air. The mice were exposed for either one day or five or 20 days for 8 h/day. Clara cells and T2 cells were labelled with antibodies, and the mucus cells were identified with Periodic-acid Schiff stain, and quantified in per unit tissue section area. The data show decrease in the number of Clara cells and increase in mucus-producing goblet cells after exposure to chicken barn air in both WT and TLR9(-/-) mice. Numbers of T2 cells increased and decreased in WT and TLR9(-/-) mice, respectively, after exposure to poultry barn air. These data show that exposure to chicken barn air can affect major lung epithelial cells, and allude to the role of TLR9 in regulation of some of these responses.