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PubMed2006

Branching morphogenesis in the prostate gland and seminal vesicles.

The prostate gland and seminal vesicles are the major exocrine glands in the male reproductive tracts of mammals. Although the morphology of these organs varies widely among species, epithelial branching morphogenesis is a key feature of organ development in most mammals including rodents and humans. Insight into the mechanisms that control prostatic and seminal vesicle branching morphogenesis has come from experimental embryological work as well as from the study of mice and humans harboring mutations that alter branching morphogenesis. These studies have demonstrated a requirement for androgens to initiate branching morphogenesis as well as a role for androgens in sustaining the normal rate and extent of branching. In addition, these studies have revealed a series of reciprocal paracrine signals between the developing prostatic epithelium and prostatic mesenchyme that are essential for regulating branching morphogenesis. Key growth factors that participate in these signaling events include members of the fibroblast growth factor, Hedgehog, and transforming growth factor-beta families. Additional genes including several homeobox-containing transcription factors have also been implicated as key regulators of prostatic and seminal vesicle branching morphogenesis. While research in recent years has greatly enhanced our understanding of the molecular control of prostatic and seminal vesicle development, known genes cannot yet explain in molecular terms the complex biological interactions that descriptive and experimental embryological studies have elucidated in the control of branching morphogenesis in these organs.

Animals↗

PubMed2005

An immunohistochemical study of the development of sensorimotor components of the early fetal human spinal cord.

Sections from all spinal cord levels from 20 human fetuses, age range 7.5-17 gestational weeks (GW) were immunostained for non-phosphorylated neurofilaments (to reveal motoneurones, spinocerebellar neurones and other large neurones), the calcium-binding protein parvalbumin (large proprioreceptive afferents), growth-associated protein 43 kDa (growing axons), glial fibrillary acidic protein (radial glia), synaptophysin (synaptic terminals) the cell-cell recognition molecule ephrin A4 (EphA4) and the ETS transcription factor Er81 (subclasses of motoneurone and proprioreceptive neurone). Muscle afferents crossed the dorsal horn by 7.5 GW and innervated motoneurones by 9 GW. An alignment of glial fibres guided them from dorsal columns to ventral horn, at right angles to the radial glia. They continued to provide a dense innervation of motoneurone pools up to 17 GW. By 13 GW motoneurones were segregated into distinct columns, all of which expressed EphA4 although only certain lateral groups expressed Er81. However, Er81 expression was more widespread amongst dorsal root ganglion neurones. From 9 GW Clarke's column neurones were identified and by 14 GW were heavily innervated by parvalbumin-positive afferents whilst their efferent axons could be traced to the lateral funiculus. This investigation contributes towards a timetable for the functional development of human motor control and makes comparisons with well-studied rodent models.

Biomarkers↗

PubMed1987

Activation of adenovirus promoters by the adenovirus E1A protein in cell-free extracts.

The primary product of the adenovirus E1A gene is a protein that is sufficient for controlling host-cell proliferation and immortalizing primary rodent cells. The mechanism by which the protein induces these cellular effects is poorly understood, but might be linked to its ability to regulate RNA transcription from a number of viral and cellular genes. The mechanism of E1A's transcriptional-activation (trans-activation) was studied here by monitoring the protein's effect on specific adenovirus promoters in two types of transcriptional systems in vitro. One of these systems consisted of extracts from transformed cells constitutively expressing E1A, and the other consisted of extracts of HeLa cells supplemented with a plasmid-encoded E1A protein purified from Escherichia coli. The results show that the E1A protein specifically stimulates transcription from adenovirus promoters; thus, the induction of cellular transcription factors is not necessary to explain the stimulation of transcription by E1A.

Adenoviridae↗

PubMed2000

Gene gun-mediated DNA immunization primes development of mucosal immunity against bovine herpesvirus 1 in cattle.

Vaccination by a mucosal route is an excellent approach to the control of mucosally acquired infections. Several reports on rodents suggest that DNA vaccines can be used to achieve mucosal immunity when applied to mucosal tissues. However, with the exception of one study with pigs and another with horses, there is no information on mucosal DNA immunization of the natural host. In this study, the potential of inducing mucosal immunity in cattle by immunization with a DNA vaccine was demonstrated. Cattle were immunized with a plasmid encoding bovine herpesvirus 1 (BHV-1) glycoprotein B, which was delivered with a gene gun either intradermally or intravulvomucosally. Intravulvomucosal DNA immunization induced strong cellular immune responses and primed humoral immune responses. This was evident after BHV-1 challenge when high levels of both immunoglobulin G (IgG) and IgA were detected. Intradermal delivery resulted in lower levels of immunity than mucosal immunization. To determine whether the differences between the immune responses induced by intravulvomucosal and intradermal immunizations might be due to the efficacy of antigen presentation, the distributions of antigen and Langerhans cells in the skin and mucosa were compared. After intravulvomucosal delivery, antigen was expressed early and throughout the mucosa, but after intradermal administration, antigen expression occurred later and superficially in the skin. Furthermore, Langerhans cells were widely distributed in the mucosal epithelium but found primarily in the basal layers of the epidermis of the skin. Collectively, these observations may account for the stronger immune response induced by mucosal administration.

Animals↗

PubMed2003

Food-entrained circadian rhythms are sustained in arrhythmic Clk/Clk mutant mice.

Daily scheduled feeding is a potent time cue that elicits anticipatory activity in rodents. This food-anticipatory activity (FAA) is controlled by a food-entrainable oscillator (FEO) that is distinct from light-entrained oscillators of the suprachiasmatic nucleus (SCN). Circadian rhythms within the SCN depend on transcription-translation feedback loops in which CLOCK protein is a key positive regulator. The Clock gene is expressed in rhythmic tissues throughout the brain and periphery, implicating its widespread involvement in the functioning of circadian oscillators. To examine whether CLOCK protein is also necessary for the FEO, the effect of daily food restriction was studied in homozygous Clock mutant (Clk/Clk) mice. The results show that Clk/Clk mutant mice exhibit FAA, even when their circadian wheel-running behavior is arrhythmic. As in wild-type controls, FAA in Clk/Clk mutants persists after temporal feeding cues are removed for several cycles, indicating that the FEO is a circadian timer. This is the first demonstration that the Clock gene is not necessary for the expression of a circadian, food-entrained behavior and suggests that the FEO is mediated by a molecular mechanism distinct from that of the SCN.

Animals↗

PubMed1992

Tissue-specific nutritional regulation of angiotensinogen in adipose tissue.

Recent studies have found that angiotensinogen is expressed in white and brown fat pads, and adipocytes have been implicated as a primary source of angiotensinogen in several other tissues. The functional significance of this unexpected expression is unknown. To address this, we studied angiotensinogen messenger RNA (mRNA) expression and angiotensinogen secretion in adipose tissue and isolated adipocytes comparing fasted and refed rodents and those with genetic obesity with normal controls. Control 2-month-old Sprague-Dawley rats, those fasted for 3 days, or those fasted for 2 days and refed for 6 days were killed, and adipocytes were isolated from epididymal fat pads using collagenase digestion. Angiotensinogen mRNA was reduced to 14.6 +/- 2.3% of control levels under fasted conditions and increased to 228 +/- 53% of control levels after refeeding. Angiotensinogen release from adipocytes was reduced to 33% of control levels by fasting and increased to 183% by refeeding. These effects of fasting and refeeding on angiotensinogen regulation were tissue specific since liver angiotensinogen mRNA and serum angiotensinogen concentrations were unaffected. Systolic blood pressure, however, was modulated by fasting and refeeding in a manner parallel to adipocyte angiotensinogen expression. In related experiments, angiotensinogen secretion per epididymal fat pad of the ob/ob mouse model of obesity was increased an average of 3.4-fold compared with control. We conclude angiotensinogen expression in white adipocytes is regulated nutritionally in a tissue-specific manner. We propose that adipocyte angiotensinogen could play a previously unrecognized role in regulating adipose tissue blood supply and thereby fatty acid efflux from fat.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1994

Abnormal lipid composition of bronchoalveolar lavage fluid obtained from individuals with AIDS-related lung disease.

Surfactant lipids are not only important to the physiologic function of the lungs, but may also influence disease processes like Pneumocystis pneumonia, in which the interaction of host-defense cells with pathogen occurs within the confines of the surfactant-rich alveolar hypophase. In the present studies the lipid profile of bronchoalveolar lavage fluid (BALF) was characterized in subjects with AIDS-related lung diseases including Pneumocystis pneumonia. BALF lipid and total protein measurements were made in 43 subjects with acquired immune deficiency syndrome (AIDS)-related lung disease and compared with those made in 50 normal human immunodeficiency virus (HIV)-seronegative controls. The AIDS patient samples contained significantly greater amounts of total cholesterol, phosphatidylglycerol (PG), and protein than the control samples; in contrast to previous observations in rodent P. carinii infection, no differences were seen in total phospholipid (PL) or phosphatidylcholine (PC) in the two groups. The proportions of several of these lipids were deranged in BALF obtained from the patient group: PG/PL and PC/cholesterol differed significantly from normal samples. In the subset of patients with AIDS-related Pneumocystis pneumonia, no correlation was apparent between discrete BALF lipids and clinical indices reflective of disease severity. Using these measurements to approximate the lipid composition of the alveolar microenvironment in AIDS-related lung disease, we performed experiments in which normal human alveolar macrophages were exposed to exogenous liposomal lipids and then challenged with P. carinii. The ingestion but not binding of P. carinii by macrophages was diminished as a result of lipid exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Opportunistic Infections↗

PubMed2003

Glucocorticoid-like effects of antihepatocarcinogen Rotenone are mediated via enhanced serum corticosterone levels: Molecular Fitting and Receptor Activation Studies.

BACKGROUND: Recent studies suggest that rotenone alters cell signal transduction pathways in a manner similar to glucocorticoids. Histological and biochemical markers of glucocorticoid effects in vivo, evaluated in our laboratories, provide further evidence for similarities in the activity of glucocorticoids and rotenone. The purpose of this study was to investigate the mechanism by which rotenone produces glucocorticoid-like effects. METHODS: Male B6C3F1 mice were treated for 7 days with rotenone (600 ppm in diet), the glucocorticoid antagonist RU486 (2 mg/kg/day, ip), corticosterone (2 mg/kg/day, ip), or both rotenone and RU 486. Control mice received drug-free diet and the vehicle (corn oil, ip). Following preservation in 10% neutral buffered formalin, tissues were embedded in paraffin. Sections were stained with hematoxylin, eosin, and were examined by light microscopy. Tissue sections were processed for in situ enzymatic end labeling of 3'-hydroxy-DNA strand breaks, a measure of apoptosis. Corticosterone was quantified in sera, using a solid phase radioimmunoassay kit. Cells (cell line 1470.2 derived from C127 mouse mammary adenocarcinoma cells) were transiently transfected with 5 &mgr;g of pLTRLuc and 1 &mgr;g of beta-Galactosidase expression vectors using a BTX square-wave pulser at 155 V, 4 pulses (40 ms each). Cells were then treated with dexamethasone, rotenone, or a mixture of both for 6 hr, harvested and assayed for luciferase and beta-Galactosidase activity. Using Root Mean Square (RMS) fit analysis (Alchemy trade mark, Tripose, Inc., St Louis, MO), we assessed possible structural similarities between rotenone and corticosterone, dehydrocorticosterone, glucocorticoid antagonists ZK 98.299, and RU 486. RMS fit was calculated by selecting three atoms in each of the molecules, followed by calculating the distance between these atoms. An RMS value of zero between two molecules indicates identical molecular characteristics. A positive value suggests diminished similarity with a value of 1 or higher excluding any such similarities. RESULTS: Although the stimulatory effect exerted by rotenone on hepatocellular apoptosis was in the opposite direction of that produced by the glucocorticoid antagonist RU 486, data suggested that rotenone does not directly activate the glucocorticoid receptor. Molecular fitting of rotenone to glucocorticoid receptor agonists and antagonists as well as examination of the transcriptional activation of a glucocorticoid-responsive reporter gene (Mouse MammaryTumorVirus) in response to rotenone indicated that it is highly unlikely that rotenone interacts directly with the glucocorticoid receptor. However, feeding male B6C3F1 mice a diet containing rotenone (600 ppm for 7 days) resulted in a 3-fold increase in serum levels of corticosterone relative to control animals. Corticosterone is the major glucocorticoid in rodents. CONCLUSION: Rotenone does not interact directly with the glucocorticoid receptor. Elevation of serum corticosterone levels in response to rotenone may explain the glucocorticoid-like effects of this compound, and may play a role in its anti-hepatocarcinogenic effect.

Journal Article↗

PubMed2004

Lack of correlation between mitochondrial reactive oxygen species production and life span in Drosophila.

The free radical theory of aging proposes that mitochondrial production of reactive oxygen species (ROS) determines the rate of aging. Supporting this hypothesis, longer-lived species produce fewer ROS than shorter-lived ones, and calorically restricted rodents live longer and produce fewer ROS than controls. We studied such correlation in Drosophila melanogaster in caloric restriction and in mutant flies overexpressing the mitochondrial adenine nucleotide translocase (ANT). Caloric restriction extended life span, but there was no significant difference in mitochondrial ROS production compared with controls. ANT overexpressers had significantly lower ROS production (because they had lower membrane potential), but their life span was not extended compared to wild type. Our results show two examples in which mitochondrial ROS production and life span are not correlated.

Aging↗

PubMed1992

Estrogen inhibits calbindin-D28k expression in mouse uterus.

The cellular localization and hormonal controls of calbindin-D9k expression in the rodent reproductive tract have suggested new functions for this protein. The present studies were undertaken to extend the earlier studies of calbindin-D9k to the related protein, calbindin-D28k. Immunohistochemical studies revealed that calbindin-D28k was absent from female rat reproductive tissues, but was abundantly expressed in immature mouse uterus and oviduct. Immunoreactivity was restricted to the endometrial and glandular epithelium of the uterus and the oviductal epithelium. Neither 1,25-dihydroxyvitamin D- nor strontium-containing diets (to blunt 1,25-dihydroxyvitamin D production) affected expression of calbindin-D28k. Uterine, but not oviductal, calbindin-D28k decreased markedly at sexual maturity; this pattern persisted in pregnant mice and was reproduced in immature mice by the administration of estradiol (3 micrograms/day for 3 days). RNA extraction and Northern analyses demonstrated that estrogen markedly decreased calbindin-D28k mRNA abundance in the uterus, but not in the oviduct. These findings suggest that estrogen affects mammalian calbindin-D28k expression and represent a rare example of estrogen-induced down-regulation of gene expression.

Animals↗

PubMed2006

Reversal of brain injury-induced prefrontal glutamic acid decarboxylase expression and working memory deficits by D1 receptor antagonism.

Working memory (WM), the ability to transiently hold information in mind, is essential for high-level cognitive functions that are often impaired in brain-injured patients. The cellular and molecular mechanisms contributing to WM deficits, which can manifest in the absence of overt damage, in these patients are unknown. The function of the dorsolateral prefrontal cortex in humans and monkeys, and the medial prefrontal cortex (mPFC), in rodents is critical for WM. We demonstrate that controlled cortical impact injury of rats causes a long-lasting WM impairment that is associated with increased levels of the GABA-synthesizing enzyme glutamic acid decarboxylase 67 (GAD67) in the mPFC for up to 1 month after injury. A single administration of dopamine D1 antagonists at 14 d after injury is sufficient to decrease GAD67 levels and restore WM for at least 1 week. These findings indicate that inhibition of prefrontal neuronal activity contributes to WM deficits and that strategies to reduce GAD67 expression can offer prolonged WM improvement in brain-injured patients.

Animals↗

PubMed2006

Microbiological contamination of laboratory mice and rats in Korea from 1999 to 2003.

To survey the microbiological contamination of laboratory mice and rats in Korea during a 5-year period, we monitored animals housed in mouse and rat facilities with either barrier or conventional systems. At barrier and conventional mouse facilities, the most important pathogen identified was mouse hepatitis virus (MHV), while Mycoplasma pulmonis was the most important pathogen at conventional rat facilities. Interestingly, hantavirus was recovered from both barrier and conventional mouse facilities. The most common protozoon identified was Tritrichomonas muris in mouse facilities and Entamoeba muris in rat facilities. In addition, we found that the microbiological contamination of mice and rats in conventional facilities was severe. These results suggest that conventional facilities should be renovated and monitored regularly to decrease microbiological contamination. We also propose that hantavirus should be monitored in Korea as an important mouse pathogen.

Animal Husbandry↗

PubMed1995

Dietary vitamin E supplementation ameliorates renal injury in chronic puromycin aminonucleoside nephropathy.

Chronic puromycin aminonucleoside nephropathy (PAN) is an experimental analog of focal segmental glomerulosclerosis. Progressive renal damage in this model is partly mediated by excessive production of oxidant species. Whether dietary supplementation with vitamin E, an endogenous lipophilic antioxidant, ameliorates the severity of chronic PAN was tested. PAN was induced by seven serial injections of the glomerular epithelial cell toxin puromycin aminonucleoside, 2 mg/100 g body wt per dose, over a 12-wk period. Experimental animals (N = 8) received vitamin E-enriched chow (100 IU/kg), whereas control PAN rats (N = 10) were fed standard rodent diet containing vitamin E (30 IU/kg of chow). The administration of vitamin E had no effect on somatic growth or blood pressure; however, rats with PAN fed the vitamin E-enriched diet had an increased hematocrit. In addition, the experimental diet resulted in a 50% reduction in urinary total protein and albumin excretion and stabilization of the serum albumin, cholesterol, and triglyceride concentrations (P < 0.01). The inulin clearance was 69% higher in the vitamin E-supplemented animals (P < 0.001). Tubular function, namely, phosphate reabsorption and beta 2-microglobulin excretion, was improved in rats with chronic PAN treated with the vitamin E-enriched diet. There was a significant decrease in glomerulosclerosis and glomerular planar area, and tubulointerstitial scarring was diminished in vitamin E-treated animals with chronic PAN (P < 0.01). These beneficial effects on renal structure and function were associated with reduced malondialdehyde content in the kidney and liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Galanin receptor antagonists : a potential novel pharmacological treatment for mood disorders.

The pathophysiology of mood disorders involves several genetic and social predisposing factors, as well as a dysregulated response to chronic stress. Accumulated evidence during the last two decades has implicated disturbances in brain serotonin and/or noradrenaline (norepinephrine) neurotransmission in the aetiology of depression. In fact, current pharmacological treatment for mood disorders is based on the use of drugs that act mainly by enhancing brain serotonin and noradrenaline neurotransmission by blockade of the active reuptake mechanism for these neurotransmitters. However, current antidepressant drugs have a delayed onset of therapeutic action, and a substantial number of patients do not respond adequately to them. In addition, these drugs have a number of adverse effects that limit patient compliance. In view of this, there is an intense search to identify novel (receptor) targets for antidepressant therapy. Recent studies have indicated that several neuropeptides and their receptors are potential candidates for the development of novel antidepressant treatment. In this context, galanin is of particular interest, since it is co-localised with serotonin in the dorsal raphe nucleus and with noradrenaline in the locus coeruleus, nuclei known to play a major role in affective disorders and in the action of antidepressant drugs. The actions of galanin are mediated by three receptor subtypes (GAL1, GAL2 and GAL3), which are coupled to different intracellular effector systems. Studies in rats have shown that galanin administered intracerebroventricularly is a potent inhibitor of mesencephalic serotonergic neurotransmission, as indicated by a long-lasting reduction in the release of serotonin in the hippocampus. This inhibitory effect is related to activation of the galanin receptors located on the dorsal raphe neurons. Moreover, intracerebroventricular galanin alters the gene expression of serotonin 5-HT1A autoreceptors in the dorsal raphe and also changes their functional activity. In addition, galanin produces a functional blockade of postsynaptic 5-HT1A receptor-mediated responses. Both pharmacological and genetic studies suggest a role for galanin in depression-like behaviour in rodent models. Transgenic mice overexpressing galanin under the control of the platelet-derived growth factor-beta promoter display increased immobility in the forced swim test. Intracerebroventricular administration of galanin in the rat increases depression-like behaviour, and this is fully blocked by the nonselective peptide galanin receptor antagonist M35. Importantly, M35 alone administered intracerebroventricularly produces an antidepressant-like effect. Recently, newly developed receptor-specific nonpeptidergic galanin GAL3 receptor antagonists (SNAP-37889 and SNAP-398299), which cross the blood-brain barrier after systemic administration, have shown antidepressant-like activity in several animal models. On the other hand, stimulation of the GAL2 receptor at the raphe level by local application of the GAL2 receptor agonist galanin (2-11) has been shown to increase serotonin levels in the hippocampus and dorsal raphe. These results indicate an important (mainly inhibitory) role of galanin as a regulator of brain serotonin and 5-HT1A receptor-mediated transmission, which may be of potential importance for understanding mood disorders and for the development of antidepressant drugs. Taken together, the present evidence suggests that antidepressant efficacy may be associated with compounds acting as antagonists at the GAL3 and/or possibly GAL1 receptors, and/or agonists at the GAL2 receptor.

Animals↗

PubMed1995

Effects of D1 dopamine agonists on schedule-controlled behavior in the squirrel monkey.

Behavioral effects of several dopamine D1 receptor agonists were compared with those of cocaine and (+)-amphetamine in squirrel monkeys trained to press a response key under a fixed-interval schedule of electric shock presentation. Cocaine (0.03 to 0.3mg/kg) and (+)-amphetamine (0.01 to 0.1mg/kg) at low to intermediate doses increased rates of responding under the fixed-interval schedule; at higher doses each of these drugs decreased response rates. In contrast, neither full nor partial D1 receptor agonists produced reliable increases in response rates. Rather, these drugs decreased rates of responding in a dose-related manner. These results with schedule-controlled behavior in primates support earlier findings in rodents that indicate that D1 agonist actions result in effects quite different from the characteristic psychomotor stimulant effects produced by cocaine or (+)-amphetamine; and they further suggest that those characteristic stimulant effects are more probably due to stimulation of other dopamine receptors.

Journal Article↗

PubMed2002

Morphological effects on the hard palatine mucosa of Calomys callosus submitted to experimental chronic alcoholism.

The morphological effects of ethanol ingestion on the hard palatine mucosa of adult male Calomys callosus were observed. Twenty rodents were divided into two experimental groups: the control group received solid diet, Purina rat chow, and tap water ad libitum; the alcoholic group received the same solid diet and ethanol P.A. diluted 20% in water (v/v). After 270 days of treatment, all animals were sacrificed and the hard palatine mucosa were prepared for TEM and SEM methods. The epithelial cells of the alcoholic group showed some alterations like cytoplasmatic lipid droplets, pycnotic nucleus and increased mitochondrial size. The lamina propria also presented intense lipid droplets accumulation. The morphological changes suggested that chronic ethanol consumption was able to modify the integrity of the mucosa.

Alcoholism↗

PubMed2002

Colonization of Anopheles maculatus from Central Java, Indonesia.

The routine colonization of Anopheles maculatus, a reputed malaria vector from Central Java, is described. The strain is free mating and long lived in the laboratory. This species will readily bloodfeed on small rodents and artificial membrane systems. Either natural or controlled temperatures, humidity, and lighting provide acceptable conditions for continuous rearing. A simple larval diet incorporating a 10:4 powdered mixture of dried beef and rice hulls proved acceptable. Using a variety of simple tools and procedures, this colony strain appears readily adaptable to rearing under most laboratory conditions. This appears to be the first report of continuous colonization using a free-mating strain of An. maculatus. Using this simple, relatively inexpensive method of mass colonization adds to the short list of acceptable laboratory populations used in the routine production of human-infecting plasmodia.

Animals↗

PubMedDate not supplied

[Activity of the natural foci of plague in the Northern Caucasus in recent years].

During the last two years the natural foci of plague in the North Caucasus were controlled with relatively low intensity. Nevertheless, every year rodents of different species and their fleas, both infected with Yersinia pestis, were detected in all 5 foci. According to the available data, no intensive, expanding epizootics were registered at the period under consideration. In the areas where stable manifestations of plague, irrespective of the density of the population of vector rodents, were observed for decades only a few infected rodents or local epizootics of plague were mainly registered.

Animals↗