scholarly journals Estrogens and female developing brain: two sides of the coin

2021 ◽  
pp. 8-12
Author(s):  
A.G. Reznikov
Keyword(s):  
Physiological Role ◽  
Perinatal Period ◽  
Protective Role ◽  
Postnatal Period ◽  
Neuroendocrine System ◽  
Developing Brain ◽  
Individual Development ◽  
Potential Hazard ◽  
Female Brain

The review highlights current views and hypotheses on the pathogenetic role of natural and xenoestrogens in the disorders of programming of neuroendocrine regulation of reproduction, alaptation, and various forms of instinctive behavior (reproductive, eating, parental, etc.) in the perinatal period of development of the female brain. Catecholestrogens, which are formed in the brain as a result of sequential metabolic conversions of testosterone, are involved in exogenous or endogenous androgen-induced defeminization of hypothalamic control of ovulation in early female ontogenesis. In the research on female animals with a knocked out gene of alpha-fetoprotein, the protective role of this protein against the possible pathogenic effect of placental estrogens on the developing brain of female fetuses was proved. The damaging effect of phytoestrogens (genistein, coumestrol) in the early postnatal period on the formation of ovulatory cycles has been shown. Evidence from studies in rodents and other animal species, supported by clinical observations, indicate the potential damaging effect of exposure to low levels of environmental xenoestrogens on the developing brain, in particular on its sexual differentiation and the hypothalamic-pituitary-adrenal axis. The potential hazard of the perinatal exposure to low doses of bisphenol A for the formation of estrogen receptors in the hypothalamus and amygdala of the female brain, sexual behavior and ovulation is discussed. Special attention is paid to the possible physiological role of natural estrogens in the formation of the female neuroendocrine system during puberty. It was concluded that in the early stages of female life, estrogens play a different role in the programming of the neuroendocrine system and behavior, depending on the period of individual development.

The role of PCSK9 in infectious diseases.

2021 ◽  
Vol 28 ◽  
Author(s):  
Laura Magnasco ◽  
Chiara Sepulcri ◽  
Roberta Maria Antonello ◽  
Stefano Di Bella ◽  
Laura Labate ◽  
...  
Keyword(s):  
Infectious Diseases ◽  
Malaria Infection ◽  
Bacterial Infections ◽  
Viral Infections ◽  
Physiological Role ◽  
Protective Role ◽  
Loss Of Function ◽  
Pcsk9 Inhibition ◽  
Sepsis And Septic Shock

Background: In recent years, many aspects of the physiological role of PCSK9 have been elucidated, particularly regarding its role in lipid metabolism, cardiovascular risk, and its role in innate immunity. Increasing evidence is available about the involvement of PCSK9 in the pathogenesis of viral infections, mainly HCV, and the regulation of host response to bacterial infections, primarily sepsis and septic shock. Moreover, the action of PCSK9 has been investigated as a crucial step in the pathogenesis of malaria infection and disease severity. Objective: This paper aims to review the available published literature on the role of PCSK9 in a wide array of infectious diseases. Conclusion: Besides the ongoing investigation on PCSK9 inhibition among HIV-infected patients to treat HIV- and ART-related hyperlipidemia, preclinical studies indicate how PCSK9 is involved in reducing the replication of HCV. Interestingly, high plasmatic PCSK9 levels have been described in patients with sepsis. Moreover, a protective role of PCSK9 inhibition has also been proposed against dengue and SARS-CoV-2 viral infections. Finally, a loss of function in the PCSK9-encoding gene has been reported to reduce malaria infection mortality.

scholarly journals Circadian Clock and OxInflammation: Functional Crosstalk in Cutaneous Homeostasis

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Elena Frigato ◽  
Mascia Benedusi ◽  
Anna Guiotto ◽  
Cristiano Bertolucci ◽  
Giuseppe Valacchi
Keyword(s):  
Circadian Clock ◽  
Redox Homeostasis ◽  
Physiological Role ◽  
Protective Role ◽  
Circadian System ◽  
Circadian Disruption ◽  
Cellular Damage ◽  
Lifestyle Risk Factors

Circadian rhythms are biological oscillations that occur with an approximately 24 h period and optimize cellular homeostasis and responses to environmental stimuli. A growing collection of data suggests that chronic circadian disruption caused by novel lifestyle risk factors such as shift work, travel across time zones, or irregular sleep-wake cycles has long-term consequences for human health. Among the multiplicity of physiological systems hypothesized to have a role in the onset of pathologies in case of circadian disruption, there are redox-sensitive defensive pathways and inflammatory machinery. Due to its location and barrier physiological role, the skin is a prototypical tissue to study the influence of environmental insults induced OxInflammation disturbance and circadian system alteration. To better investigate the link among outdoor stressors, OxInflammation, and circadian system, we tested the differential responses of keratinocytes clock synchronized or desynchronized, in an in vitro inflammatory model exposed to O3. Being both NRF2 and NF-κB two key redox-sensitive transcription factors involved in cellular redox homeostasis and inflammation, we analyzed their activation and expression in challenged keratinocytes by O3. Our results suggest that a synchronized circadian clock not only facilitates the protective role of NRF2 in terms of a faster and more efficient defensive response against environmental insults but also moderates the cellular damage resulting from a condition of chronic inflammation. Our results bring new insights on the role of circadian clock in regulating the redox-inflammatory crosstalk influenced by O3 and possibly can be extrapolated to other pollutants able to affect the oxinflammatory cellular processes.

Lung hyaluronan during development: a quantitative and morphological study

1991 ◽  
Vol 260 (5) ◽  
pp. H1449-H1454 ◽  
Author(s):  
S. J. Allen ◽  
E. Gunnar Sedin ◽  
A. Jonzon ◽  
A. F. Wells ◽  
T. C. Laurent
Keyword(s):  
Morphological Study ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Late Gestation ◽  
Visceral Pleura ◽  
Predominant Role ◽  
Neonatal Lung ◽  
Important Constituent ◽  
Migrating Cells

Hyaluronan, an important constituent of developmental interstitium in fetal lungs, mediates cell-to-cell interactions and thereby directs migrating cells. Furthermore, because of the polyionic nature of the molecule, hyaluronan forms open, hydrated matrices that provide channels for migrating cells. This hydrated matrix undergoes contraction before birth. However, continued growth of the lung in the perinatal period requires newly synthesized hyaluronan. This study's purpose was to elucidate the changes in lung hyaluronan concentration and distribution in the perinatal period. We studied rabbits at days -6, -4, -2, -1, 0, +2, and +4 with respect to term, as well as adult rabbits. We found that hyaluronan concentration was highest in the youngest fetuses studied [682 +/- 115 micrograms/g dry wt (means +/- SD)]. However, hyaluronan concentration decreased to 129 +/- 12 micrograms/g dry wt just before birth then returned to 366 +/- 111 micrograms/g dry wt at day +4; these values were similar to adult values. We found hyaluronan staining decreased during late gestation, particularly in the interalveolar region. In the postnatal period, hyaluronan staining increased in the visceral pleura and, to a lesser extent, beneath the epithelium of the bronchioles. Hyaluronan did not reaccumulate in the interalveolar region in the postnatal period. Our data suggest a change in the predominant role of lung hyaluronan during the perinatal period. Before term, hyaluronan facilitates morphogenesis. However, hyaluronan's major role in neonatal lung is most likely in regulation of fluid balance in interstitium.

scholarly journals Adiponectin, the controversial hormone

2007 ◽  
Vol 10 (10A) ◽  
pp. 1145-1150 ◽  
Author(s):  
Marta Garaulet ◽  
Juan J Hernández-Morante ◽  
Fátima Pérez de Heredia ◽  
Francisco J Tébar
Keyword(s):  
Insulin Resistance ◽  
Plasma Concentrations ◽  
Physiological Role ◽  
Protective Role ◽  
Mechanisms Of Action ◽  
Acid Protein ◽  
Related Proteins ◽  
Contradictory Data ◽  
Amino Acid Protein

AbstractObjectiveTo discuss present knowledge about adiponectin hormone.DesignReview of existing literature.Setting and resultsAdiponectin is one of the most interesting cytokines associated with obesity, although its physiological role remains to be fully clarified. Adiponectin is a 247-amino acid protein that contains four differentiable domains. Contrary to most adipose-related cytokines, adiponectin levels are surprisingly lower in obese than in lean humans. Women have been found to have significantly higher adiponectin plasma concentrations than men. Further research is needed in order to identify new polymorphisms which contribute to explain the potential role of adiponectin in obesity and related pathologies.Considering the anti-inflammatory properties of adiponectin and the fact that it is negatively associated with adiposity, this cytokine could be one of the links between obesity and inflammation. The main mechanisms of action of adiponectin are directed to a protective role against atherogenic and insulin resistance processes. Research has revealed interesting new functions far beyond metabolism, such as immunity, cancer and bone formation.Contrary to all adipose-related proteins, adiponectin decreases with obesity. Most of the contradictory data surrounding adiponectin are related to plasma values and their relationship with body fat, gender differences and insulin resistance. There are important confounding results regarding the mechanisms of action and functions of adiponectin, especially in relation to insulin resistance and inflammation.

scholarly journals Chorioamnionitis Precipitates Perinatal Alterations of Heme-Oxygenase-1 (HO-1) Homeostasis in the Developing Rat Brain

2021 ◽  
Vol 22 (11) ◽  
pp. 5773
Author(s):  
Maide Ozen ◽  
Yuma Kitase ◽  
Vikram Vasan ◽  
Christopher Burkhardt ◽  
Sindhu Ramachandra ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Iron Homeostasis ◽  
Mononuclear Cells ◽  
Developmental Regulation ◽  
Perinatal Period ◽  
Postnatal Period ◽  
Heme Oxygenase 1 ◽  
Perinatal Brain Injury ◽  
The Brain

Chorioamnionitis (CHORIO), placental insufficiency, and preterm birth are well-known antecedents of perinatal brain injury (PBI). Heme-oxygenase-1 (HO-1) is an important inducible enzyme in oxidative and inflammatory conditions. In the brain, HO-1 and the iron regulatory receptor, transferrin receptor-1 (TfR1), are known to be involved in iron homeostasis, oxidative stress, and cellular adaptive mechanisms. However, the role of HO pathway in the pathophysiology of PBI has not been previously studied. In this study, we set out to define the ontogeny of the HO pathway in the brain and determine if CHORIO changed its normal developmental regulation. We also aimed to determine the role of HO-1/TfR1 in CHORIO-induced neuroinflammation and peripheral inflammation in a clinically relevant rat model of PBI. We show that HO-1, HO-2, and TfR1 expression are developmentally regulated in the brain during the perinatal period. CHORIO elevates HO-1 and TfR1 mRNA expression in utero and in the early postnatal period and results in sustained increase in HO-1/TfR1 ratios in the brain. This is associated with neuroinflammatory and peripheral immune phenotype supported by a significant increase in brain mononuclear cells and peripheral blood double negative T cells suggesting a role of HO-1/TfR1 pathway dysregulation in CHORIO-induced neuroinflammation.

Ecdysteroid Titres during Autonomous Metamorphosis in a Dermestid Beetle

1980 ◽  
Vol 35 (11-12) ◽  
pp. 1066-1080 ◽  
Author(s):  
Jean-Paul Delbecque ◽  
Karel Sláma
Keyword(s):  
Larval Instar ◽  
Physiological Role ◽  
Head Capsule ◽  
Neuroendocrine System ◽  
The Body ◽  
Cervical Region ◽  
Good Survival ◽  
Physiological Concentration ◽  
Prothoracic Glands

The larvae of Dermestes maculatus are able to undergo several moults in complete absence of the cephalic and prothoracic neuroendocrine system, showing thus spontaneous metamorphosis. Measurements of ecdysteroid contents by radioimmunoassay methods have revealed distinctive larval, prepupal and pupal ecdysteroid peaks, as found in other species where development requires frequent stimulation by the centrally produced hormones. Mass fragmentographic analysis has indicated that more than 80% of the ecdysteroids detected by the radioimmunoassay during the peaks consists of ecdysterone. The prothoracic glands (PG) of D. maculatus larvae are located in the head capsule and in the cervical region. They can be separated from the body by neck-ligation. Only the larval peak of ecdysterone can be correlated with PG function. The prepupal and pupal peaks of ecdysterone are not produced by the central neuroendocrine system. The isolated abdominal fragments of larvae and pupae positively produce ecdysteroids in the course of their independent development, but this synthesis has been subnormal and occasionally delayed in time. In contrast, the isolated thoracic fragments produce well synchronized peaks of ecdysterone and this does not depend on the PG. It thus appears that some thoracic tissue other than PG is able to maintain the physiological concentration of ecdysterone by means of a concentration-dependent feed-back mechanism. Due to spontaneous metamorphosis and extremely good survival we have succeeded to induce in this species: a) premature formation of the prepupal cycle of ecdysterone synthesis in the penultimate larval instar by ligation; b) inhibition and delay of the prepupal peak by means of juvenoid treatments; c) reappearance of the prepupal peak in the inhibited “permanent larvae” by exogenous administration of ecdysterone, or; d) modification of the pupal peak by a qualitatively new pupal-pupal one after juvenoid treatments. These experimental transformations of the ecdysterone peaks have suggested that the kind and nature of the peaks are closely related to nature and stage of the ontogenetic development. We therefore believe that the process of larval-pupal reprogramming has occurred in this species long before the increase of ecdysterone titer in the body. Both the prepupal and pupal peaks do not represent a cause but they show to be rather consequences of the developmental programming. Further features associated with possible physiological role of ecdysteroids in insect development have been briefly discussed.

scholarly journals Protective Role of Galanin during Chemically Induced Inflammation in Zebrafish Larvae

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 99
Author(s):  
Natalia Nowik ◽  
Anna Przyborowska ◽  
Waldemar Sienkiewicz ◽  
Piotr Podlasz
Keyword(s):  
Pathological Condition ◽  
Protective Role ◽  
Neuroendocrine System ◽  
Biological Processes ◽  
Zebrafish Larvae ◽  
Chemically Induced ◽  
Enhanced Expression ◽  
The Central Nervous System ◽  
Endocrine Axis

During a pathological condition, many different systems are involved in the response of an affected organism. Galanin is considered to be a neuropeptide that plays an important role in the central nervous system; however, it is involved in many other biological processes, including the immune response. During our studies, we showed that galanin became upregulated in zebrafish larvae when exposed to copper sulfate. Moreover, the presence of normal levels of galanin, administration of a galanin analog NAX 5055 or galanin overexpression led to lowered lateral line damage and enhanced expression of inflammatory markers compared to the knockout larvae. The results showed that the neuroendocrine system acts multifunctionally and should be considered as a part of the complex neuro–immune–endocrine axis.

scholarly journals The Protective Role of Erythropoietin in the Developing Brain

10.5772/27859 ◽  
2012 ◽  
Author(s):  
Marco Sifringer ◽  
Angela M. ◽  
Stefanie Endesfelder ◽  
Clarissa von ◽  
Ivo Bendix ◽  
...  
Keyword(s):  
Protective Role ◽  
Developing Brain

scholarly journals Delineating the Requirement for the Borrelia burgdorferi Virulence Factor OspC in the Mammalian Host

2006 ◽  
Vol 74 (6) ◽  
pp. 3547-3553 ◽  
Author(s):  
Philip E. Stewart ◽  
Xiaohui Wang ◽  
Dawn M. Bueschel ◽  
Dawn R. Clifton ◽  
Dorothee Grimm ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Physiological Role ◽  
Surface Protein ◽  
Protective Role ◽  
Innate Immune ◽  
Myeloid Differentiation ◽  
Mammalian Host ◽  
Mammalian Infection ◽  
Deficient Mice

ABSTRACT We previously demonstrated that outer surface protein C (OspC) of Borrelia burgdorferi is essential for establishing mammalian infection. However, the role of OspC in mammalian infection is unknown. Here, we report experiments designed to distinguish between two models of OspC function in the mammalian host: (i) OspC fulfills an essential physiological role for growth and host adaptation or (ii) OspC provides a protective role for evasion of components of the innate immune response. We found that a B. burgdorferi ospC mutant, previously demonstrated to be noninfectious in both immunocompetent and SCID mice, could survive in the relatively immune-privileged environment of dialysis membrane chambers implanted within the peritoneum of a rat. The ospC mutant also adapts to the mammalian environment, as determined by the protein profiles of the chamber-cultivated spirochetes. Therefore, OspC does not appear to provide a physiological function for the survival of B. burgdorferi within the mammalian host. The second model, evasion of the innate immune system, was tested by assessing the infectivity of the ospC mutant in mice deficient for myeloid differentiation protein 88 (MyD88). Recent studies have shown that B. burgdorferi is prevented from reaching high cell numbers in the mammalian host by MyD88-dependent signaling pathways. The ospC mutant was incapable of infecting MyD88-deficient mice, suggesting that the role of OspC cannot be related solely to evasion of MyD88-mediated innate immunity. These results reiterate the importance of OspC in mammalian infection and eliminate simple models of function for this enigmatic protein.

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