1
40
4
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/jnr.20690" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jnr.20690</a>
Pages
875–889
Issue
6
Volume
82
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Activation and circuitry of uterine-cervix-related neurons in the lumbosacral dorsal root ganglia and spinal cord at parturition.
Publisher
An entity responsible for making the resource available
Journal of neuroscience research
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-12
Subject
The topic of the resource
Analysis of Variance; Animals; Blotting; Cell Count/methods; Cervix Uteri/*cytology; Cyclic AMP Response Element-Binding Protein/metabolism; Estrogen Receptor alpha/metabolism; Female; Ganglia; Gene Expression Regulation/physiology; Immunohistochemistry/methods; Lumbosacral Region; Models; Nerve Net/cytology/*physiology; Neurological; Neurons/classification/*physiology; Oncogene Proteins v-fos/metabolism; Parturition/*physiology; Pregnancy; Rats; Spinal Cord/*cytology; Spinal/*cytology; Sprague-Dawley; Stilbamidines/metabolism; Time Factors; Western/methods
Creator
An entity primarily responsible for making the resource
Puder B A; Papka R E
Description
An account of the resource
Stimulation of the uterine cervix at parturition activates neural circuits involving primary sensory nerves and supraspinally projecting neurons of the lumbosacral spinal cord, resulting in output of hypothalamic neurohormones. Dorsal root ganglia (DRG) and spinal neurons of these circuits are not well-characterized. The objectives of this study were to detail the activation of DRG and spinal neurons of the L6/S1 levels that are stimulated at late pregnancy, verify hypothalamic projections of activated spinal neurons, and determine whether activated neurons express estrogen receptor-alpha (ERalpha). Expression of phosphorylated cyclic-AMP response element-binding protein (PCREB) and Fos immunohistochemistry were used to "mark" activated DRG and spinal neurons, respectively. Retrograde tracing identified uterine-cervix-related and spinohypothalamic neurons. Baseline PCREB expression in the DRG increased during pregnancy and peaked during the last trimester. Some PCREB-expressing neurons contained retrograde tracer identifying them as cervix-related neurons. Fos-expressing neurons were few in spinal cords of nonpregnant and day 22 pregnant rats but were numerous in parturient animals. Some Fos-expressing neurons located in the dorsal half of the spinal cord contained retrograde tracer identifying them as spinohypothalamic neurons. Some DRG neurons expressing PCREB also expressed ERalpha, and some spinal neurons activated at parturition projected axons to the hypothalamus and expressed ERalpha. These results indicate that DRG and spinal cord neurons are activated at parturition; that those in the spinal cord are present in areas involved in autonomic and sensory processing; that some spinal neurons project axons to the hypothalamus, ostensibly part of a neuroendocrine reflex; and that sensory and spinal neurons can respond to estrogens. Moreover, some activated sensory neurons may be involved in the animal's perception of labor pain.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jnr.20690" target="_blank" rel="noreferrer noopener">10.1002/jnr.20690</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2005
Analysis of Variance
Animals
Blotting
Cell Count/methods
Cervix Uteri/*cytology
Cyclic AMP Response Element-Binding Protein/metabolism
Estrogen Receptor alpha/metabolism
Female
Ganglia
Gene Expression Regulation/physiology
Immunohistochemistry/methods
Journal of neuroscience research
Lumbosacral Region
Models
Nerve Net/cytology/*physiology
Neurological
Neurons/classification/*physiology
Oncogene Proteins v-fos/metabolism
Papka R E
Parturition/*physiology
Pregnancy
Puder B A
Rats
Spinal Cord/*cytology
Spinal/*cytology
Sprague-Dawley
Stilbamidines/metabolism
Time Factors
Western/methods
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/s0006-8993(01)02803-7" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/s0006-8993(01)02803-7</a>
Pages
1–10
Issue
1
Volume
915
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Aberrant induction of Par-4 is involved in apoptosis of hippocampal neurons in presenilin-1 M146V mutant knock-in mice.
Publisher
An entity responsible for making the resource available
Brain research
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-10
Subject
The topic of the resource
*Intracellular Signaling Peptides and Proteins; Alzheimer Disease/*genetics/metabolism/physiopathology; Animals; Apoptosis Regulatory Proteins; Apoptosis/*genetics; Carrier Proteins/*genetics/metabolism; Caspases/metabolism; Gene Expression Regulation/physiology; Glucose/deficiency; Hippocampus/*metabolism/physiopathology; Membrane Proteins/*genetics; Mice; Mitochondria/metabolism/pathology; Mutation/*genetics; Neurons/*metabolism/pathology; Presenilin-1; Signal Transduction/genetics; Transgenic/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Xie J; Chang X; Zhang X; Guo Q
Description
An account of the resource
Mutations in presenilin-1 (PS-1) have been shown to increase neuronal vulnerability to apoptosis in Alzheimer's disease (AD). Par-4 is a novel cell-death-promoting protein associated with neuronal degeneration in AD. We previously reported that, in transfected PC12 cells, Par-4 seems to be involved in the neurodegenerative mechanisms of PS-1 mutations. However, direct evidence for a necessary role of Par-4 in the pathogenic mechanisms of PS-1 mutations in neurons is lacking. We recently generated and characterized presenilin-1 mutant M146V knock-in (PS-1 M146V KI) mice. We now report that expression of the mutant presenilin-1 in these mice induces early and exaggerated increase in Par-4 expression in hippocampal neurons following glucose deprivation (an insult relevant to the pathogenesis of AD). Importantly, inhibition of Par-4 expression by antisense par-4 oligonucleotide treatment counteracts neuronal apoptosis promoted by M146V mutation of PS-1. Mitochondrial dysfunction and caspase-3 activity induced by glucose deprivation was significantly exacerbated in hippocampal neurons expressing the mutant PS-1. Antisense par-4 treatment largely suppressed the adverse effect of the mutant PS-1 on mitochondrial dysfunction and caspase activation. These results provide evidence in hippocampal neurons that Par-4 is involved in the neurodegenerative cascades associated with PS-1 M146V mutation by acting relatively early in the apoptotic process before mitochondrial dysfunction and caspase-3 activation. Since levels of Par-4 are significantly increased in the hippocampus in human AD brain, the results of this study may provide a significant link between aberrant induction of Par-4 and the neurodegenerative cascades promoted by PS-1 mutations in AD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0006-8993(01)02803-7" target="_blank" rel="noreferrer noopener">10.1016/s0006-8993(01)02803-7</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Intracellular Signaling Peptides and Proteins
2001
Alzheimer Disease/*genetics/metabolism/physiopathology
Animals
Apoptosis Regulatory Proteins
Apoptosis/*genetics
Brain research
Carrier Proteins/*genetics/metabolism
Caspases/metabolism
Chang X
Gene Expression Regulation/physiology
Glucose/deficiency
Guo Q
Hippocampus/*metabolism/physiopathology
Membrane Proteins/*genetics
Mice
Mitochondria/metabolism/pathology
Mutation/*genetics
Neurons/*metabolism/pathology
Presenilin-1
Signal Transduction/genetics
Transgenic/genetics/metabolism
Xie J
Zhang X
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpcell.00008.2012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpcell.00008.2012</a>
Pages
C179–191
Issue
2
Volume
303
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Upregulation of thrombospondin-1 expression by leptin in vascular smooth muscle cells via JAK2- and MAPK-dependent pathways.
Publisher
An entity responsible for making the resource available
American journal of physiology. Cell physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-07
Subject
The topic of the resource
Animals; Cell Movement/physiology; Cells; Cultured; Gene Expression Regulation/physiology; Humans; Inbred C57BL; Janus Kinase 2/*biosynthesis; Knockout; Leptin/*physiology; Male; MAP Kinase Signaling System/*physiology; Mice; Muscle; Myocytes; Smooth; Smooth Muscle/enzymology/metabolism; Thrombospondin 1/*biosynthesis; Up-Regulation/*physiology; Vascular/enzymology/*metabolism
Creator
An entity primarily responsible for making the resource
Chavez Ronaldo J; Haney Rebecca M; Cuadra Rene H; Ganguly Rituparna; Adapala Ravi K; Thodeti Charles K; Raman Priya
Description
An account of the resource
Hyperleptinemia, characteristic of diabetes and a hallmark feature of human obesity, contributes to the increased risk of atherosclerotic complications. However, molecular mechanisms mediating leptin-induced atherogenesis and gene expression in vascular cells remain incompletely understood. Accumulating evidence documents a critical role of a potent antiangiogenic and proatherogenic matricellular protein, thrombospondin-1 (TSP-1), in atherosclerosis. Although previous studies reported elevated TSP-1 levels in both diabetic and obese patients and rodent models, there is no direct information on TSP-1 expression in vascular cells in response to leptin. In the present study, we show that leptin upregulates TSP-1 expression in cultured human aortic smooth muscle cells (HASMC) in vitro, and this increase occurs at the level of transcription, revealed by mRNA stability and TSP-1 promoter-reporter assays. Utilizing specific pharmacological inhibitors and siRNA approaches, we demonstrate that upregulation of TSP-1 expression by leptin is mediated by JAK2/ERK/JNK-dependent mechanisms. Furthermore, we report that while ERK and JNK are required for both the constitutive and leptin-induced expression of TSP-1, JAK-2 appears to be specifically involved in leptin-mediated TSP-1 upregulation. Finally, we found that increased HASMC migration and proliferation in response to leptin is significantly inhibited by a TSP-1 blocking antibody, thereby revealing the physiological significance of leptin-TSP-1 crosstalk. Taken together, these findings demonstrate, for the first time, that leptin has a direct regulatory effect on TSP-1 expression in HASMCs, underscoring a novel role of TSP-1 in hyperleptinemia-induced atherosclerotic complications.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpcell.00008.2012" target="_blank" rel="noreferrer noopener">10.1152/ajpcell.00008.2012</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Adapala Ravi K
American journal of physiology. Cell physiology
Animals
Cell Movement/physiology
Cells
Chavez Ronaldo J
Cuadra Rene H
Cultured
Department of Integrative Medical Sciences
Ganguly Rituparna
Gene Expression Regulation/physiology
Haney Rebecca M
Humans
Inbred C57BL
Janus Kinase 2/*biosynthesis
Knockout
Leptin/*physiology
Male
MAP Kinase Signaling System/*physiology
Mice
Muscle
Myocytes
NEOMED College of Medicine
Raman Priya
Smooth
Smooth Muscle/enzymology/metabolism
Thodeti Charles K
Thrombospondin 1/*biosynthesis
Up-Regulation/*physiology
Vascular/enzymology/*metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpgi.00417.2002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00417.2002</a>
Pages
G349–356
Issue
3
Volume
284
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Bile acid regulation of hepatic physiology: III. Bile acids and nuclear receptors.
Publisher
An entity responsible for making the resource available
American journal of physiology. Gastrointestinal and liver physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
2003-03
Subject
The topic of the resource
Animals; Bile Acids and Salts/biosynthesis/genetics/*physiology; Bile/*physiology; Cardiovascular Diseases/genetics/physiopathology; Cholesterol/physiology; Cytoplasmic and Nuclear/*physiology; Feedback/physiology; Gene Expression Regulation/physiology; Humans; Liver Diseases/genetics/physiopathology; Liver/*physiology; Receptors
Creator
An entity primarily responsible for making the resource
Chiang John Y L
Description
An account of the resource
Bile acids are physiological detergents that facilitate excretion, absorption, and transport of fats and sterols in the intestine and liver. Recent studies reveal that bile acids also are signaling molecules that activate several nuclear receptors and regulate many physiological pathways and processes to maintain bile acid and cholesterol homeostasis. Mutations of the principal regulatory genes in bile acid biosynthetic pathways have recently been identified in human patients with hepatobiliary and cardiovascular diseases. Genetic manipulation of key regulatory genes and bile acid receptor genes in mice have been obtained. These advances have greatly improved our understanding of the molecular mechanisms underlying complex liver physiology but also raise many questions and controversies to be resolved. These developments will lead to early diagnosis and discovery of drugs for treatment of liver and cardiovascular diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpgi.00417.2002" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00417.2002</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2003
American journal of physiology. Gastrointestinal and liver physiology
Animals
Bile Acids and Salts/biosynthesis/genetics/*physiology
Bile/*physiology
Cardiovascular Diseases/genetics/physiopathology
Chiang John Y L
Cholesterol/physiology
Cytoplasmic and Nuclear/*physiology
Department of Integrative Medical Sciences
Feedback/physiology
Gene Expression Regulation/physiology
Humans
Liver Diseases/genetics/physiopathology
Liver/*physiology
NEOMED College of Medicine
Receptors