Hormonal Regulation of Calcification, with Particular Reference to the Hormonal Control of Eggshell Formation in Birds and Shell Growth in Molluscs

Abstract Thirst has evolved for vertebrate terrestrial adaptation. We previously showed that buccal drying induced a series of drinking behaviours (migration to water–taking water into the mouth–swallowing) in the amphibious mudskipper goby, thereby discovering thirst in ray-finned fish. However, roles of dipsogenic/antidipsogenic hormones, which act on the thirst center in terrestrial tetrapods, have remained unclear in the mudskipper thirst. Here we examined the hormonal effects on the mudskipper drinking behaviours, particularly the antagonistic interaction between angiotensin II (AngII) and atrial natriuretic peptide (ANP) which is important for thirst regulation in mammalian ‘forebrain’. Expectedly, intracerebroventricular injection of ANP in mudskippers reduced AngII-increased drinking rate. ANP also suppressed the neural activity at the ‘hindbrain’ region for the swallowing reflex, and the maintenance of buccopharyngeal water due to the swallowing inhibition may attenuate the motivation to move to water. Thus, the hormonal molecules involved in drinking regulation, as well as the influence of buccopharyngeal water, appear to be conserved in distantly related species to solve osmoregulatory problems, whereas hormonal control of thirst at the forebrain might have been acquired only in tetrapod lineage during evolution.

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Regulation of the immunoexpression of aquaporin 9 by ovarian hormones in the rat oviductal epithelium

AJP Cell Physiology ◽

10.1152/ajpcell.00420.2003 ◽

2005 ◽

Vol 288 (5) ◽

pp. C1048-C1057 ◽

Cited By ~ 44

Author(s):

María C. Brañes ◽

Bernardo Morales ◽

Mariana Ríos ◽

Manuel J. Villalón

Keyword(s):

Steroid Hormones ◽

Estrous Cycle ◽

Hormonal Regulation ◽

Water Movement ◽

Water Channels ◽

Hormonal Control ◽

Apical Plasma Membrane ◽

Functional Assay ◽

Mrna Levels ◽

Oviductal Epithelium

The volume of oviductal fluid fluctuates during the estrous cycle, suggesting that water availability is under hormonal control. It has been postulated that sex-steroid hormones may regulate aquaporin (AQP) channels involved in water movement across cell membranes. Using a functional assay (oocytes of Xenopus laevis), we demonstrated that the rat oviductal epithelium contains mRNAs coding for water channels, and we identified by RT-PCR the mRNAs for AQP5, -8, and -9, but not for AQP2 and -3. The immunoreactivity for AQP5, -8, and -9 was localized only in epithelial cells of the oviduct. The distribution of AQP5 and -8 was mainly cytoplasmic, whereas we confirmed, by confocal microscopy, that AQP9 localized to the apical plasma membrane. Staining of AQP5, -8, and -9 was lost after ovariectomy, and only AQP9 immunoreactivity was restored after estradiol and/or progesterone treatments. The recovery of AQP9 reactivity after ovariectomy correlated with increased mRNA and protein levels after treatment with estradiol alone or progesterone administration after estradiol priming. Interestingly, progesterone administration after progesterone priming also induced AQP9 expression but without a change in mRNA levels. Levels of AQP9 varied along the estrous cycle with their highest levels during proestrus and estrus. These results indicate that steroid hormones regulate AQP9 expression at the mRNA and protein level and that other ovarian signals are involved in the expression of AQP5 and -8. Thus hormonal regulation of the type and quantity of water channels in this epithelium might control water transport in the oviductal lumen.

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Hormonal control of the renal immune response and antibacterial host defense by arginine vasopressin

Journal of Experimental Medicine ◽

10.1084/jem.20071032 ◽

2007 ◽

Vol 204 (12) ◽

pp. 2837-2852 ◽

Cited By ~ 46

Author(s):

Cécilia Chassin ◽

Mathias W. Hornef ◽

Marcelle Bens ◽

Michael Lotz ◽

Jean-Michel Goujon ◽

...

Keyword(s):

Immune Response ◽

Host Defense ◽

Arginine Vasopressin ◽

Hormonal Regulation ◽

Collecting Duct ◽

Hormonal Control ◽

Innate Immune ◽

Duct Cells ◽

Collecting Duct Cells ◽

Antibacterial Host Defense

Ascending urinary tract infection (UTI) and pyelonephritis caused by uropathogenic Escherichia coli (UPEC) are very common infections that can cause severe kidney damage. Collecting duct cells, the site of hormonally regulated ion transport and water absorption controlled by vasopressin, are the preferential intrarenal site of bacterial adhesion and initiation of inflammatory response. We investigated the effect of the potent V2 receptor (V2R) agonist deamino-8-D-arginine vasopressin (dDAVP) on the activation of the innate immune response using established and primary cultured collecting duct cells and an experimental model of ascending UTI. dDAVP inhibited Toll-like receptor 4–mediated nuclear factor κB activation and chemokine secretion in a V2R-specific manner. The dDAVP-mediated suppression involved activation of protein phosphatase 2A and required an intact cystic fibrosis transmembrane conductance regulator Cl− channel. In vivo infusion of dDAVP induced a marked fall in proinflammatory mediators and neutrophil recruitment, and a dramatic rise in the renal bacterial burden in mice inoculated with UPECs. Conversely, administration of the V2R antagonist SR121463B to UPEC-infected mice stimulated both the local innate response and the antibacterial host defense. These findings evidenced a novel hormonal regulation of innate immune cellular activation and demonstrate that dDAVP is a potent modulator of microbial-induced inflammation in the kidney.

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A re-evaluation of the role of mitochondrial pyruvate transport in the hormonal control of rat liver mitochondrial pyruvate metabolism

Biochemical Journal ◽

10.1042/bj2230677 ◽

1984 ◽

Vol 223 (3) ◽

pp. 677-685 ◽

Cited By ~ 34

Author(s):

A P Halestrap ◽

A E Armston

Keyword(s):

Respiratory Chain ◽

Hormonal Regulation ◽

Hormone Treatment ◽

Liver Mitochondria ◽

Hormonal Control ◽

Protonmotive Force ◽

Pyruvate Metabolism ◽

Carboxylase Activity ◽

Computer Simulation Studies

The inhibitor of mitochondrial pyruvate transport alpha-cyano-beta-(1-phenylindol-3-yl)-acrylate was used to inhibit progressively pyruvate carboxylation by liver mitochondria from control and glucagon-treated rats. The data showed that, contrary to our previous conclusions [Halestrap (1978) Biochem. J. 172, 389-398], pyruvate transport could not regulate metabolism under these conditions. This was confirmed by measuring the intramitochondrial pyruvate concentration, which almost equilibrated with the extramitochondrial pyruvate concentration in control mitochondria, but was significantly decreased in mitochondria from glucagon-treated rats, where rates of pyruvate metabolism were elevated. Computer-simulation studies explain how this is compatible with linear Dixon plots of the inhibition of pyruvate metabolism by alpha-cyano-4-hydroxycinnamate. Parallel measurements of the mitochondrial membrane potential by using [3H]triphenylmethylphosphonium ions showed that it was elevated by about 3 mV after pretreatment of rats with both glucagon and phenylephrine. There was no significant change in the transmembrane pH gradient. It is shown that the increase in pyruvate metabolism can be explained by a stimulation of the respiratory chain, producing an elevation in the protonmotive force and a consequent rise in the intramitochondrial ATP/ADP ratio, which in turn increases pyruvate carboxylase activity. Mild inhibition of the respiratory chain with Amytal reversed the effects of hormone treatment on mitochondrial pyruvate metabolism and ATP concentrations, but not on citrulline synthesis. The significance of these observations for the hormonal regulation of gluconeogenesis from L-lactate in vivo is discussed.

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Hormones as adaptive control systems in juvenile fish

10.1101/768689 ◽

2019 ◽

Author(s):

Jacqueline Weidner ◽

Camilla Håkonsrud Jensen ◽

Jarl Giske ◽

Sigrunn Eliassen ◽

Christian Jørgensen

Keyword(s):

Food Availability ◽

Hormonal Regulation ◽

Juvenile Fish ◽

Optimal Strategies ◽

Evolutionary Optimization ◽

Hormonal Control ◽

Fish Growth ◽

Growth And Survival ◽

Hormone Levels ◽

Regulation Of Growth

AbstractGrowth is an important theme in many biological disciplines. Physiologists often relate growth rates to hormonal control of essential processes. Ecologists often study growth as function of gradients or combinations of environmental factors. Fewer studies have investigated the combined effects of environmental and hormonal control on growth. Here, we present an evolutionary optimization model of fish growth that combines internal regulation of growth by hormone levels with the external influence of food availability and predation risk. Hormones are represented by growth hormone, thyroid hormone and orexin functions. By studying a range from poor to rich environments, we find that the level of food availability in the environment results in different evolutionarily optimal strategies of hormone levels. With more food available, higher levels of hormones are optimal, resulting in higher food uptake and growth. By using this fitness-based approach we also find a consequence of evolutionary optimization of survival on optimal hormone use. Where foraging is risky, aerobic scope can be used strategically to increase the chance of escaping from predators. By comparing model results to empirical observations, many mechanisms can be recognized, for instance a change in pace-of-life due to resource availability, and reduced emphasis on reserves in more stable environments.Summary statementWe combine physiological, environmental and evolutionary aspects of fish growth in a state-dependent model where the optimal regulation of growth and survival is achieved through hormonal regulation of behaviour.

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256. Ovarian lymphatic vascular development is hormonally regulated and Adamts1-dependent

Reproduction Fertility and Development ◽

10.1071/srb08abs256 ◽

2008 ◽

Vol 20 (9) ◽

pp. 56

Author(s):

H. M. Brown ◽

R. L. Robker ◽

D. L. Russell

Keyword(s):

Granulosa Cells ◽

Hormonal Regulation ◽

Lymphatic System ◽

Immune Cell ◽

Vascular Development ◽

Lymphatic Vessels ◽

Hormonal Control ◽

Cell Trafficking ◽

Reproductive Tissues ◽

Reproductive Cycles

The lymphatic system is important for return of extra-vascular fluid to the blood circulation, conductance of hormones and immune cell trafficking. Delicate hormonal control of fluid conductance during reproductive cycles is exemplified by the ovarian hyperstimulation syndrome, a dangerous condition of hypovolemia caused by fluid accumulation in the abdomen and reproductive tissues, in response to hormonal hyperstimulation. This study is the first to investigate the relationship between ovarian lymphatic development and follicle growth. Quantitative morphometric analysis of vessel size and number in mouse ovary revealed, for the first time, that the ovarian lymphatic vasculature develops postnatally and in synchrony with the induction of ovarian CYP19a1 (Aromatase); the time when secondary follicles become FSH-responsive and estrogenic. Mechanistically, we found that the FSH-analogue eCG mediates induction of lymphatic vascular endothelial growth factor Vegfd and the receptor Vegfr3 (Flt4) in granulosa cells. Importantly, stimulation with eCG also enhanced ovarian lymphatic vessel number and size. However, formation of ovarian lymphatics also required the matrix-remodelling protease Adamts1, since ovaries from Adamts1−/− mice failed to undergo normal lymphatic vascular development. Treatment of Adamts1 null mice with eCG significantly increased the number and size of ovarian lymphatic vessels, however, the vessels were still smaller and fewer in number than wildtypes. These combined results indicate that the ovarian lymphatic system develops in response to hormonal signals, which promote folliculogenesis, through induction of lymphangiogenic factors in granulosa cells; as well as involving Adamts1-dependent mechanisms. This study is the first demonstration of the novel principle of hormonal regulation of lymphangiogenesis in any tissue and suggests a requirement for functional lymphatics during normal folliculogenesis. In addition our results inform the elucidation of the tightly regulated processes that control fluid dynamics and immune cell surveillance within reproductive tissues.

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Surfactant protein C: hormonal control of SP-C mRNA levels in vitro

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1992.262.6.l684 ◽

1992 ◽

Vol 262 (6) ◽

pp. L684-L687 ◽

Cited By ~ 6

Author(s):

S. V. Veletza ◽

K. V. Nichols ◽

I. Gross ◽

H. Lu ◽

D. W. Dynia ◽

...

Keyword(s):

Hormonal Regulation ◽

Protein C ◽

Cdna Probe ◽

Surfactant Protein ◽

Hormonal Control ◽

Mrna Levels ◽

Cyclic Monophosphate ◽

Surfactant Protein C ◽

Dose Dependent Increase ◽

Dose Dependent

We have studied hormonal regulation of the surfactant protein C (SP-C) in fetal 18-dah rat lung explants. SP-C mRNA was detected in Northern blots with a specific rat SP-C cDNA probe and quantified by densitometry. Treatment of the explants with dexamethasone resulted in a dose-dependent increase of the SP-C mRNA level. Transcriptional assays have shown that the regulation of SP-C mRNA by dexamethasone involves a transcriptional step. Administration of the cAMP analogues, 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) or dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), produced a dose-dependent increase of SP-C mRNA levels, with maximum stimulation observed at 200 microM. The thyroid hormone T3 had no effect on SP-C mRNA levels, whether administered alone or in combination with dexamethasone. Variation in the effects of the above hormones on three surfactant protein mRNAs, SP-A, SP-B and SP-C, indicates that the hormonal regulation of the surfactant proteins is a complex process and that each gene is, in part, differentially regulated.

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Hormonal control of postnatal development of corticosteroid-binding globulin

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1981.240.4.e402 ◽

1981 ◽

Vol 240 (4) ◽

pp. E402-E406 ◽

Cited By ~ 2

Author(s):

J. D'Agostino ◽

S. J. Henning

Keyword(s):

Postnatal Development ◽

Hormonal Regulation ◽

Binding Capacity ◽

Postnatal Period ◽

Hormonal Control ◽

Early Postnatal Period ◽

Daily Administration ◽

Rat Pups ◽

Corticosteroid Binding Globulin ◽

Thyroxine Replacement

The hormonal regulation of the ontogenic rise in serum corticosteroid-binding globulin (CBG) has been studied in the rat. Pups received daily injections of estrogens (either estradiol, estrone, or diethylstilbesterol, each at 0.05 microgram/g body wt) or thyroxine (0.1 microgram/g body wt) on postnatal days 2-7. When CBG binding capacity was determined on day 8, only the thyroxine-injected pups were found to have elevated CBG. This effect of thyroxine on CBG binding capacity was further studied by daily administration of the hormone (0.1 microgram.g body wt-1.day-1) between postnatal days 5-12. This caused a precocious rise in serum CBG, with CBG values 6- to 38-fold higher than euthyroid controls on days 8, 10, and 12. Conversely, in pups made hypothyroid by administration of propylthiouracil, the normal ontogenic increase in CBG was suppressed. Thyroxine replacement resulted in the reappearance of the CBG rise. These results suggest that the developmental rise in the binding capacity of CBG is independent of estradiol and estrone and instead is elicited by the rising concentrations of circulating thyroxine that normally occur in the early postnatal period.

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Characterization, expression, and hormonal control of a thymic beta 2-adrenergic receptor

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1994.267.5.e718 ◽

1994 ◽

Vol 267 (5) ◽

pp. E718-E731 ◽

Cited By ~ 8

Author(s):

B. Marchetti ◽

M. C. Morale ◽

P. Paradis ◽

M. Bouvier

Keyword(s):

Hormonal Regulation ◽

Adrenergic Receptor ◽

Radioligand Binding ◽

Hormonal Control ◽

Sex Steroid ◽

Rat Tissues ◽

Female Rat ◽

Adrenergic Agonists ◽

Binding Studies ◽

Beta 2

In the present study, we have characterized the beta 2-adrenergic receptor (beta 2-AR)-adenosine 3',5'-cyclic monophosphate (cAMP) system of the rat thymus gland and examined the hormonal regulation of the thymic beta 2-AR gene expression under physiological or pharmacological conditions accompanied by marked alterations of the sex steroid hormone milieu. We report here that membrane preparations of female rat thymic tissue contain iodocyanopindolol binding sites that exhibit pharmacological properties typical of a beta-AR. Detailed analysis by computer modeling of the binding potencies of a large series of beta 1- and beta 2-adrenergic agonists and antagonists revealed predominantly the beta 2-AR subtype (78%) in rat thymus. This inference from radioligand binding studies was corroborated functionally by the rank order of potencies of a series of adrenergic agonists to stimulate the production of cAMP. Northern blot analysis, using a human beta 2-AR cDNA as a probe, revealed the presence of a mRNA of 2.3 kb, which is consistent with the size of the beta 2-AR mRNA found in other rat tissues. Physiological regulation of specific beta 2-AR in the rat thymus was indicated by significant increases in both receptor concentration and steady-state levels of beta 2-AR mRNA during the diestrous 2 and proestrous phases of the rat estrous cycle and pregnancy, whereas castration sharply reduced beta 2-AR numbers and transcript levels within the thymus. The modulation of the thymic beta 2-AR-cAMP signaling system by the preexisting sex steroid milieu, coupled with the sex-dependent adrenergic modulation of thymic cell-mediated immune response, may contribute to the various sex-related alterations in immune responsiveness and could play a role in sexually related immune disorders.

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Nutrient and hormonal regulation of pyruvate kinase gene expression

Biochemical Journal ◽

10.1042/bj3370001 ◽

1998 ◽

Vol 337 (1) ◽

pp. 1-11 ◽

Cited By ~ 77

Author(s):

Kazuya YAMADA ◽

Tamio NOGUCHI

Keyword(s):

Pyruvate Kinase ◽

Hormonal Regulation ◽

Regulatory Elements ◽

Glycolytic Enzyme ◽

Hormonal Control ◽

Nuclear Factor ◽

Alternative Promoters ◽

Kinase Gene ◽

Flanking Region ◽

Nuclear Factor 1

Mammalian pyruvate kinase (PK), a key glycolytic enzyme, has two genes named PKL and PKM, which produce the L- and R-type isoenzymes by means of alternative promoters, and the M1-and M2-types by mutually exclusive alternative splicing respectively. The expression of these genes is tissue-specific and under developmental, dietary and hormonal control. The L-type isoenzyme (L-PK) gene contains multiple regulatory elements necessary for regulation in the 5´ flanking region, up to position -170. Both L-II and L-III elements are required for stimulation of L-PK gene transcription by carbohydrates such as glucose and fructose, although the L-III element is itself responsive to carbohydrates. The L-II element is also responsible for the gene regulation by polyunsaturated fatty acids. Nuclear factor-1 proteins and hepatocyte nuclear factor 4, which bind to the L-II element, may also be involved in carbohydrate and polyunsaturated fatty acid regulation of the L-PK gene respectively. However, the L-III-element-binding protein that is involved in carbohydrate regulation remains to be clarified, although involvement by an upstream stimulating factor has been proposed. Available evidence suggests that the carbohydrate signalling pathway to the L-PK gene includes a glucose metabolite, possibly glucose 6-phosphate or xylulose 5-phosphate, as well as phosphorylation and dephosphorylation mechanisms. In addition, at least five regulatory elements have been identified in the 5´ flanking region of the PKM gene up to position -279. Sp1-family proteins bind to two proximal elements, but the binding of proteins to other elements have not yet been clarified. Glucose may stimulate the transcription of the PKM gene via hexosamine derivatives. Sp1 may be involved in this regulation via its dephosphorylation, although the carbohydrate response element has not been determined precisely in the PKM gene. Thus glucose stimulates transcription of the PKM gene by the mechanism which is probably different from the L-PK gene.

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