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Tissue Specific (tissue + specific)
Terms modified by Tissue Specific Selected AbstractsThe VpreB1 enhancer drives developmental stage-specific gene expression in vivoEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2003Steve Licence Abstract In adult mice, the VpreB genes are expressed in bone marrow progenitor (pro-) and precursor (pre-) B,cells. As part of the pre-B,cell receptor, the proteins are crucial for the proliferation of these cells and consequently normal B,lymphocyte development. Using cell lines, we identified a lineage- and developmental-stage-specific VpreB1 enhancer. Here, we analyze its specificity in vivo by generating transgenic mice in which expression of a reporter gene (human CD122) is regulated by the VpreB1 enhancer in the context of its own promoter. All transgenic lines expressed thereporter gene in the bone marrow in a copy number-independent manner, whereas expression levels were integration site-dependent. While the enhancer is not tissue specific, within the B,cell lineage the expression pattern of human CD122 mimicked that of endogenous VpreB1. Thus, low levels were detected in pro-B,cells, high levels in pre-BI and slightly lower levels in pre-BII cells; no expression was detected in immature/mature B,cells. Furthermore, when in vitro cultured transgenic pre-B,cells differentiated into immature B,cells there was concomitant down-regulation of human CD122 andendogenous VpreB1. Thus the VpreB1 enhancer is sufficient to ensure developmental stage-specific expression of a reporter gene in B,lymphocytes in vivo. [source] Developmental impact on trans -acting dosage effects in maize aneuploidsGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 2 2001Jennifer L. Cooper Abstract Summary: The reduction in vigor or viability caused by aneuploidy may be the result of trans -acting dosage effects that reduce gene expression. To investigate the molecular and developmental parameters of aneuploid syndromes, the expression of sucrose synthase1 (sus1) and shrunken1 (sh1) was studied in 2-week-old plants. Expression of sus1 and sh1 was first investigated in euploids, where it was found that both transcripts varied in a diurnal fashion. Chromosome arm number can be varied in a series from one to three doses in maize. In the 14 aneuploid dosage series examined, most caused changes in sus1 and sh1 RNA levels that were both gene and tissue specific. Results were compared to previous data from embryo and endosperm tissue. More dosage effects were detected and the magnitude of RNA level modulation was greater in 2-week-old plant tissue. These findings suggest that the molecular consequences of aneuploidy might become more severe as development progresses. genesis 31:64,71, 2001. © 2001 Wiley-Liss, Inc. [source] Molecular characterization of two novel milk proteins in the tsetse fly (Glossina morsitans morsitans)INSECT MOLECULAR BIOLOGY, Issue 2 2010G. Yang Abstract Purpose: Milk proteins are an essential component of viviparous reproduction in the tsetse fly. Milk proteins are synthesized in and secreted from the milk gland tissue and constitute 50% of the secretions from which the intrauterine larva derives its nourishment. To understand milk protein function and regulation during viviparous reproduction, milk proteins need to be identified and characterized. Methods: Two putative unknown secretory proteins (GmmMGP2 and GmmMGP3) were selected by bioinformatic analysis of tissue specific tsetse cDNA libraries. RT-PCR analysis was performed to verify their milk gland/fat body specific expression profile. Detailed characterization of developmental and tissue specific expression of these proteins was performed by northern blot analysis and fluorescent in situ hybridization. Functional analysis of the milk gland proteins during the tsetse gonotrophic cycle was performed using RNA interference (RNAi). Results: The predicted proteins from gmmmgp2 and gmmmgp3 are small ,22 kD and contain a high proportion of hydrophobic amino acids and potential phosphorylation sites. Expression of both genes is tissue specific to the secretory cells of the milk gland. Transcript abundance for both genes increases over the course of intrauterine larval development and parallels that of gmmmgp, a well characterized milk protein gene considered to be the major milk protein. Phenotypic analysis of flies after RNA interference treatment revealed a significant effect upon fecundity in the gmmmgp2 knockdown flies, but not the gmmmgp3 flies. Knockdown of gmmmgp2 resulted in disruption of ovulation and consequent oocyte accumulation and degradation. Gmmmgp2 knockdown also had a significant impact on fly mortality. Conclusions: This work identifies two novel genes, the proteins of which appear to function in response to intrauterine larvigenesis in tsetse. These proteins may be nutritional components of the milk secretions provided to the larva from the mother. Phenotypic data from knockdown of gmmmgp2 suggests that this protein may also have a regulatory function given the defect in ovulation observed in knockdown flies. Further analysis of these genes will be important (in conjunction with other milk proteins) for identification of transcriptional regulation mechanisms that direct milk gland/pregnancy specific gene expression. [source] Effects of nickel poisoning on expression pattern of the 72/73 and 94 kDa stress proteins in rat organs and in the COS-7, HepG2, and A549 cell linesJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 1 2005N. Hfaiedh Abstract The present study deals with the effects of Ni on the expression level of three stress proteins, namely, the cytosolic HSP72 and HSP73, and the reticulum-associated GRP94. Experiments were carried out on "Wistar" female rats daily injected with 4 mg NiCl2 per kg body weight for 1, 3, 5, and 10 days. Another set of experiments were carried out using cell lines, derived from the monkey kidney (COS-7), and from human tumors of the lung (A549) and liver (HepG2). Cells were cultured for 4 days in the permanent presence of 100, 200, or 400 µM NiCl2. In control rats, stress proteins pattern was found to be tissue specific: two protein bands of 96 and 94 kDa were immunodetected with the anti-GRP94 antibody in kidney and liver extracts, whereas only the 96 kDa band was present in ovary extracts. HSP73 was present in kidney, liver, and ovary whereas HSP72 was only found in kidney. In kidney of nickel-treated animals, HSP73 and the 96 kDa proteins were overexpressed whereas HSP72 was strongly down regulated. No such effect was observed in liver or ovary. Similarly, in nickel-treated cell lines, HSP72 was downregulated and GRP94 (96 kDa protein) was overexpressed. HSP73 expression appeared moderately increased in A549 cells but decreased in COS-7 cells. Because long-term caloric restriction was reported to reduce free radical generation in cells, the effect of 1 month food restriction (50%) was tested in rats as a possible way to lower oxidative damages induced by Ni. No significant effect on HSP expression was observed. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:12,18, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20056 [source] Nuclear matrix proteins as biomarkers in prostate cancerJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2002Eddy S. Leman Abstract The nuclear matrix (NM) is the structural framework of the nucleus that consists of the peripheral lamins and pore complexes, an internal ribonucleic protein network, and residual nucleoli. The NM contains proteins that contribute to the preservation of nuclear shape and its organization. These protein components better known as the NM proteins have been demonstrated to be tissue specific, and are altered in many cancers, including prostate cancer. Alterations in nuclear morphology are hallmarks of cancer and are believed to be associated with changes in NM protein composition. Prostate cancer is the most frequently diagnosed cancer in American men and many investigators have identified unique NM proteins that appear to be specific for this disease. These NM protein changes are associated with the development of prostate cancer, as well as in some cases being indicative of cancer stage. Identification of these NM proteins specific for prostate cancer provides an insight to understanding the molecular changes associated with this disease. This article reviews the role of NM proteins as tumor biomarkers in prostate cancer and the potential application of these proteins as therapeutic targets in the treatment of this disease. J. Cell. Biochem. 86: 213,223, 2002. © 2002 Wiley-Liss, Inc. [source] Neurophysiological monitoring of alveolar nerve function during sensor-controlled Er:YAG laser corticotomy in rabbitsLASERS IN SURGERY AND MEDICINE, Issue 3 2005Stephan Rupprecht DDS Abstract Background and Objectives The sensor-controlled Er:YAG laser system may be a potent tool for tissue specific cutting in surgery. In order to investigate the impact of the laser on neural tissues, inferior alveolar nerve (IAN) function was monitored by the jaw-opening reflex (JOR) during specific corticotomy in rabbits. Study Design/Materials and Methods Laser jaw corticotomy was performed in 13 anesthetized rabbits. During and after specific corticotomy the JOR was evoked by electric intraoral stimulation to monitor effects on IAN function. Results The JOR permanently abolished in one case and transiently failed immediately after surgery but largely recovered within days in another rabbit. In one experiment JOR threshold increased 7 days after corticotomy. Histology did not prove any objective nerve pathology. Conclusions Monitoring IAN function by the JOR demonstrated the relatively low risk of nerve damaging during sensor-controlled laser corticotomy. © 2005 Wiley-Liss, Inc. [source] Regulation of Endothelial Cell Adhesion Molecule Expression in an Experimental Model of Cerebral MalariaMICROCIRCULATION, Issue 6 2002PHILLIPE R. BAUER ABSTRACT Objective: Plasmodium falciparum malaria in humans and animal models of this disease have revealed changes in the infected host that are consistent with a systemic inflammatory response. Although it has been proposed that endothelial cell adhesion molecules (CAM) contribute to the adhesive interactions of Plasmodium -infected erythrocytes and immune cells with vascular endothelial cells, ECAM expression has not been systematically studied in Plasmodium -infected animals. Methods: In this study, the dual radiolabeled monoclonal antibody method was used to quantify the expression of different ECAMs (ICAM-1, VCAM-1, P-selectin, E-selectin) in different regional vascular beds of Plasmodium berghei ANKA-inffected mice (PbA), a well-recognized model of human cerebral malaria. The roles of T lymphocytes and certain cytokines (TNF-,, IL-12, IFN-,) in mediating the infection-induced expression of ICAM-1 and P-selectin were assessed by using relevant mutant mice. Results: Wild-type (WT) mice exhibited highly significant increases in the expression of ICAM-1, VCAM-1, and P-selectin (but not E-selectin) in all vascular beds on the 6th day of PbA infection. The PbA -induced upregulation of ICAM-1 was significantly blunted in mice that were either deficient in IFN-,, IL-12 (but not TNF1b) or T lymphocytes (Rag-1 deficiency); however, these responses were tissue specific. Conclusions: These findings indicate that vascular endothelial cells in most regional circulations assume an inflammatory phenotype and that cytokines and immune cells mediate this response in a tissue-specific manner. [source] Histopathological and immunohistochemical characterization of canine prostate cancerTHE PROSTATE, Issue 5 2008Chen-Li Lai Abstract Background In this study we try to identify the origin of canine prostate cancer (cPC) by classifying the tumors histological subtypes and relate these subtypes to their combined expressional characteristics of several tissue specific and differentiation markers. Methods cPCs were examined histomorphologically and by immunohistochemical detection of the cytokeratin markers CK14, HMWCK, CK5, CK18, and CK7, and of the markers UPIII, PSA and PSMA. Results Histopathologically, six growth patterns could be differentiated. The most frequent patterns were solid, cribriform and micropapillary growth patterns, while sarcomatoid, small acinar/ductal, and tubulo-papillary growth patterns were less frequent present. Solid growth patterns were significantly (P,=,0.027) more often seen in castrated dogs. Immunohistochemically, about half of the cPC cases showed expression of PSA (8/20) and PSMA (10/20); 85% and 60% of the cPC expressed UPIII (17/20) and CK7 (12/20), while 13 and 12 cPC expressed CK5 and CK14, respectively; all cPC expressed CK18. CK14 was significantly more often and UPIII less frequent expressed in the solid growth patterns than in the micropapillary and cribriform patterns, respectively. Conclusions Canine prostate cancer appear to be more aggressive and of a less differentiated type than most common human prostate cancers. Comparing the expression patterns of the markers in cPC to those in normal canine prostate tissue, cPC most likely originates from the collecting ducts rather than from the peripheral acini. Given also the fact that canine prostate cancer is unresponsive to androgen withdrawal therapy, canine prostate cancer mostly resembles human, androgen refractory, poorly differentiated prostate cancer. Prostate 68: 477,488, 2008. © 2008 Wiley-Liss, Inc. [source] Influence of Hyperglycaemia on Chemical-Induced Toxicity: Study with Cyclophosphamide in RatBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2009Kalavatala Saandeep Hyperglycaemia perturbs the critical balance between oxidative stress and anti-oxidant defence mechanisms in the body and thereby alters the response of biological system towards various toxic chemicals. Cyclophosphamide (CP) is a widely prescribed anticancer drug, well-known genotoxic agent as well as used in the development of immunocompromised animal models. The present study investigated the modulating effect of diabetes on the cyclophosphamide-induced cytotoxicity and genotoxicity. The study was performed on male Sprague-Dawley rats (200 ± 10 g). Cyclophosphamide (10 mg/kg) was administered five consecutive days in a week for 3 weeks to both control and diabetic rats. Thiobarbituric acid reactive substances (TBARS) levels were measured in the plasma, liver, kidney and lung tissues. DNA damaging potential of cyclophosphamide under diabetic condition was evaluated using comet and halo assay as an endpoint. To further ascertain the mode of cell death, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assay and immunohistochemical evaluation of p53 was performed. Significant increase in DNA damage was revealed by the comet assay parameters, halo assay indicated the level of cytotoxicity and the oxidative stress was measured using the TBARS assay in the diabetic rats receiving cyclophosphamide treatment. The toxic effects were more prominent in diabetic animals as compared to non-diabetic rats. Cyclophosphamide treatment and diabetic condition per se led to increase in the p53 + and TUNEL + cells in the liver and kidney of rats. Under diabetic condition, further increase in the p53 + and TUNEL + cells was observed in response to cyclophosphamide. In the present study, we report that hyperglycaemic condition exaggerates the cyclophosphamide-induced toxicity and the response was found to be tissue specific. [source] Renal carcinogenesis: Genotype, phenotype and dramatypeCANCER SCIENCE, Issue 2 2003Okio Hino Cancer is a heritable disorder of somatic cells. Environment and heredity are both important in the carcinogenic process. The Eker rat model of hereditary renal carcinoma (RC) is an example of a Mendelian dominantly inherited predisposition to a specific cancer in an experimental animal. Forty years after the discovery of the Eker rat in Oslo, we and Knudson's group independently identified a germline retrotransposon insertion in the rat homologue of the human tuberous sclerosis (TSC2) gene. To our knowledge, this was the first isolation of a Mendelian dominantly predisposing cancer gene in a naturally occurring animal model. Recently, we discovered a new hereditary renal carcinoma in the rat. This rat was named the "Ninon''rat and its predisposing (Nihon) gene could be a novel renal tumor suppressor gene. This article will review the utility of these unique models for the study of problems in carcinogenesis; e.g., species-specific differences in tumorigenesis, cell stage and tissue/cell-type specific tumorigene-sis, multistep carcinogenesis, modifier gene(s) in renal carcinogenesis, cancer prevention and the development of therapeutic treatments which can be translated to human patients, as well as how environmental factors interact with cancer susceptibility gene(s). (Cancer Sci 2003; 94: 142,147) [source] | |||||||||||||