Mechanisms Of Sexual Dimorphism Research Articles

Mechanisms of sexual dimorphism in the pathogenesis of sarcomas

Sarcomas of non-genital organs affect women 1.5–3 times less often than men. The mechanism of such dimorphism is studied at various levels, mainly in the field of influence on the pathogenesis of sex hormones and their receptors, the effect of which is significantly related to the histogenesis of the tumor, its localization, the mechanism of malignant transformation and the stage of progression. Sex hormone receptors are often found in the early stages of tumor development and are lost during progression. At the same time, the expression of the same receptors in tumors of different histogenesis sometimes correlates with the opposite prognosis of the disease and sensitivity to hormonal therapy. For example, in uterine leiomyosarcomas, the expression of estrogen and androgen receptors correlates with a better prognosis and greater effectiveness of therapy, and in osteo- and fibrosarcomas, vice versa. Estrogens stimulate proliferation of osteosarcoma cells, and androgens that of rhabdomyosarcoma and small round cell tumor, which growth is inhibited by antiandrogens used in the treatment of prostate cancer. In this regard, when trying to include a hormonal component in a therapeutic complex, an individual study of the hormonal sensitivity of the tumor is necessary. One of the methodological approaches to this could be testing a culture of tumor cells from surgical material for sensitivity to agonists/antagonists of hormonal receptors separately and in combination with chemotherapy drugs.

Sex-specific transcription and DNA methylation landscapes of the Asian citrus psyllid, a vector of huanglongbing pathogens.

The relationship of DNA methylation and sex-biased gene expression is of high interest, it allows research into mechanisms of sexual dimorphism and the development of potential novel strategies for insect pest control. The Asian citrus psyllid, Diaphorina citri Kuwayama, is a major vector for the causative agents of Huanglongbing (HLB), which presents an unparalleled challenge to citrus production worldwide. Here, we identify the X chromosome of D. citri and investigate differences in the transcription and DNA methylation landscapes between adult virgin males and females. We find a large number of male-biased genes on the autosomes and a depletion of such on the X chromosome. We have also characterised the methylome of D. citri, finding low genome-wide levels, which is unusual for an hemipteran species, as well as evidence for both promoter and TE methylation. Overall, DNA methylation profiles are similar between the sexes but with a small number of differentially methylated genes found to be involved in sex differentiation. There also appears to be no direct relationship between differential DNA methylation and differential gene expression. Our findings lay the groundwork for the development of novel epigenetic-based pest control methods, and given the similarity of theD. citri methylome to some other insect species, these methods could be applicable across agricultural insect pests.

Sexual dimorphism in functional pain syndromes.

Injury-free pain conditions, defined as functional pain syndromes, are more prevalent and more disabling in women. Mechanisms of sexual dimorphism in functional pain are now emerging from preclinical studies, suggesting an opportunity to advance the development of sex-specific therapies that may improve treatment of pain in women.

24. Sexual dimorphism in the placenta

There is a sexual dimorphism in pregnancy outcomes with male fetuses generally being at higher risk for adverse outcomes. The underlying physiologic mechanisms likely involve sexual dimorphism in placental function given the role of the placenta in directing both maternal metabolic and cardiovascular changes in gestation and fetal growth and development. Gene expression in the human placenta is sexually dimorphic and is affected by maternal inflammatory status, diet and fatty acids in a sex-dependent manner. We find increased markers of inflammation, hypoxia and apoptotic cell death in the placenta with preeclampsia compared to normotensive pregnancies but with sexual dimorphism as TNFa, Il-6, Il-8, HIF1a, apoptotic markers and DNA binding of the NFkB p65 transcription factor are significantly higher, but the angiogenic marker VEGF significantly lower, in male vs female preeclamptic placentas. Obesity and gestational diabetes are associated with increased placental inflammation and oxidative and nitrative stress, increased miR-210 expression and consequent decreased trophoblast respiration, altered autophagic responses and altered antioxidant defenses, however all of which occur in a sexually dimorphic manner. In trophoblast from a female, but not a male, placenta TNF stimulates the NFkBp50 pathway to increase miR210 expression which in turn depresses mitochondrial respiration. Interestingly miR210 expression is significantly higher in placenta from a female vs a male fetus across all birthweight centiles with the difference being greatest in placentas of large for gestational age fetuses. The mechanisms of sexual dimorphism in placenta with preeclampsia, obesity or GDM and the range of functional effects remain to be elucidated; however evidence links sex differences to gonadal steroids. Placental levels of aromatase, the rate-limiting enzyme converting androgens to estrogens, are higher in placentas of preeclamptic women with female vs male fetuses and aromatase can be downregulated by TNF α , hypoxia, insulin and leptin, factors which mirror placental conditions with maternal obesity.

Involvement of WNK1-mediated potassium channels in the sexual dimorphism of blood pressure

Potassium homeostasis plays an essential role in the control of blood pressure. It is unknown, however, whether potassium balance is involved in the gender-associated blood pressure differences. We therefore investigated the possible mechanism of sexual dimorphism in blood pressure regulation by measuring the blood pressure, plasma potassium, renal actions of potassium channels and upstream regulator in male and female mice. Here we found that female mice exhibited lower blood pressure and higher plasma K+ level as compared to male littermates. Western blot analyses of mouse kidney extract revealed a significant decrease in renal outer medullary potassium (ROMK) channel expression, while large-conductance Ca2+-activated K+ (BK) channel and Na-K-2Cl cotransporter (NKCC2) as well as the upstream regulator with-no-lysine kinase 1 (WNK1) enhanced in female mice under normal condition. Surprisingly, both dietary K+ loading and K+ depletion eliminated the differences in plasma K+ and blood pressure between females and males, and the differences of renal K+ channels and WNK1 also attenuated in both groups of mice. These findings indicated the existence of a close correlation between K+ homeostasis and sex-associated blood pressure. Moreover, the differential regulation of ROMK, BK-α and NKCC2 between female and male mice, at least, were partly mediated via WNK1 pathway, which may contribute to the sexual dimorphism of plasma K+ and blood pressure control.

Characterization and sexual dimorphic expression of Cytochrome P450 genes in the hypothalamic–pituitary–gonad axis of yellow catfish

Yellow catfish (Pelteobagrus fulvidraco) is an important freshwater fish species in China. In particular, an all-male population has been commercially produced for the males grow faster than females. However, the molecular mechanisms underlying sexual dimorphism of body size and sex differentiation are still unclear in yellow catfish. This study attempts to characterize and analyze the expression of Cytochrome P450 (CYP) family members that have been shown to play an important role in sex differentiation and metabolism in teleosts. A total of 25 CYP genes were identified from our transcriptomes by 454 pyrosequencing and Solexa sequencing, including 17 genes with complete open reading frame (ORF). Phylogenetic analyses were conducted to compare these genes with their counterparts from other teleosts. In the tissues of hypothalamic–pituitary–gonad (HPG) axis, most of the genes were expressed at uniform level in both sexes. However, multiple CYP genes displayed sexual dimorphic expression, such as cyp2AD, cyp4b, cyp8a, cyp11b2, cyp17a and cyp27a expressed at higher level in testis than in ovary, whereas cyp2g, cyp7a, cyp8b, cyp19a1a and cyp26a expressed at higher level in ovary than in testis. The expression response of six CYP genes in ovary was also assessed after 17α-methyltestosterone (MT) treatment. Testis-biased expressed cyp11b2 and cyp17a were significantly up-regulated, while cyp11a and cyp19a1a were reduced in ovary after MT treatment. Our work is helpful for understanding molecular evolution of CYP genes in vertebrates and the mechanism of sexual dimorphism in teleosts.

Sex, sex steroids, and diabetic cardiomyopathy: making the case for experimental focus

More than three decades ago, the Framingham study revealed that cardiovascular risk is elevated for all diabetics and that this jeopardy is substantially accentuated for women in particular. Numerous studies have subsequently documented worsened cardiac outcomes for women. Given that estrogen and insulin exert major regulatory effects through common intracellular signaling pathways prominent in maintenance of cardiomyocyte function, a sex-hormone:diabetic-disease interaction is plausible. Underlying aspects of female cardiovascular pathophysiology that exaggerate cardiovascular diabetic risk may be identified, including increased vulnerability to coronary microvascular disease, age-dependent impairment of insulin-sensitivity, and differential susceptibility to hyperglycemia. Since Framingham, considerable progress has been made in the development of experimental models of diabetic disease states, including a diversity of genetic rodent models. Ample evidence indicates that animal models of both type 1 and 2 diabetes variably recapitulate aspects of diabetic cardiomyopathy including diastolic and systolic dysfunction, and cardiac structural pathology including fibrosis, loss of compliance, and in some instances ventricular hypertrophy. Perplexingly, little of this work has explored the relevance and mechanisms of sexual dimorphism in diabetic cardiomyopathy. Only a small number of experimental studies have addressed this question, yet the prospects for gaining important mechanistic insights from further experimental enquiry are considerable. The case for experimental interrogation of sex differences, and of sex steroid influences in the aetiology of diabetic cardiomyopathy, is particularly compelling-providing incentive for future investigation with ultimate therapeutic potential.

Sexual Dimorphism on Growth Hormone Secretion after Oral Glucose Administration

Sexual dimorphism of GH secretion is unclear in humans. There is evidence that oral glucose (OG) administration initially decreases and subsequently stimulates GH secretion. Our aim was to study fasting GH concentrations and their response to OG administration in obese and healthy women and men, in order to elucidate the mechanism of sexual dimorphism of GH secretion and the possible contribution of ghrelin. We selected 33 women and 11 men as obese and healthy subjects. After an overnight fast, 75 g of oral glucose were administered; glucose, insulin, ghrelin, and PYY1-36 were obtained at baseline and during 300 min. Fasting GH (μg/l) was higher in women than men; 1.3 ± 0.3 vs. 0.2 ± 0.1, p=0.009, for women and men, respectively. The area under the curve between 0 and 150 min (AUC) of GH (μg/l · min) was higher in women than men; 98.2 ± 25.9 vs. 41.5 ± 28.6, p=0.002, for women and men, respectively. The AUC of total ghrelin (pg/ml · min, mean ± SEM) between 0 and 150 min was borderline and significantly higher in women than men; 128 562.3 ± 8 335.9 vs. 98 839.1 ± 7 668.6, p=0.069, for women and men, respectively. Several initial time points were higher in women than men. Glucose, insulin, and PYY1-36 were similar in women and men after OG. There were significant correlations between indices of post-oral glucose GH and ghrelin secretion. Fasting and initial GH secretion is higher in women than men, in contrast to peak and late GH secretion, which is similar in both cases. Sexual dimorphism in the regulation of GH secretion probably involves ghrelin.

Hormonal Organization and Activation: Evolutionary Implications and Questions

Event Abstract Back to Event Hormonal Organization and Activation: Evolutionary Implications and Questions Elizabeth Adkins-Regan1* 1 Cornell University, Psychology/Neurobiology and Behavior, United States Comparative endocrinology is a fascinating field of science in part because it can integrate ultimate and proximate causation. Research on sexual dimorphism and sexual differentiation has excellent potential for this kind of integration. Vertebrate comparative endocrinologists have made many important discoveries about the role of genes and sex steroid hormones in the organization and activation of sexually differentiated behavior, brain function, anatomy and physiology. In addition to taxonomically general principles and conserved features, there is also striking diversity in sexual differentiation processes. Much of the evolutionary basis of this diversity (its phylogenetic history and adaptive functions) is not well understood. A set of questions is raised to illustrate this point, with an emphasis on mechanisms of sexual dimorphism in body size and ornamentation, sexual differentiation of avian behavior, and the puzzle of the phylogeny of vertebrate sex determining mechanisms. Applying tree thinking and other concepts from evolutionary biology to developmental and adult mechanisms holds promise for eventually answering some of these questions. Keywords: evolution, Hormonal organization, Japanese quail, phylogeny, sex determination, sex steroid hormones, sexual differentiation, sexual dimorphism Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Plenary Topic: Sex determination and differentiation Citation: Adkins-Regan E (2011). Hormonal Organization and Activation: Evolutionary Implications and Questions. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00102 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 01 Aug 2011; Published Online: 09 Aug 2011. * Correspondence: Prof. Elizabeth Adkins-Regan, Cornell University, Psychology/Neurobiology and Behavior, Ithaca, New York, 14850, United States, er12@cornell.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Elizabeth Adkins-Regan Google Elizabeth Adkins-Regan Google Scholar Elizabeth Adkins-Regan PubMed Elizabeth Adkins-Regan Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Monomorphism, male-male competition, and mechanisms of sexual dimorphism

Monomorphism, male-male competition, and mechanisms of sexual dimorphism

Role of the gonads in sex differentiation of growth hormone-releasing hormone and somatostatin neurons in the mouse hypothalamus during postnatal development

We clarify the mechanism of sexual dimorphism of growth hormone releasing hormone (GHRH) neurons in the arcuate nucleus (ARC) and somatostatin (SS) neurons in periventricular nucleus (PeN), by studying the role of the gonads during the neonatal period and after puberty using immunohistochemical and morphometric methods. As in our previous works the numbers of ARC GHRH-ir and PeN SS-ir neurons were significantly greater in adult normal male (NM) mice than in adult normal female (NF) mice. Adult female mice that were ovariectomized neonatally (NOF) increased the expression of GHRH-ir neurons to the male pattern, but adult female mice ovariectomized after puberty (APO) did not change. Adult male mice castrated neonatally and after puberty (NCM and APC, respectively) were not significantly different from NM mice. However, NCT male mice, which were castrated neonatally and transplanted with ovary just before puberty, showed a significantly reduced number of GHRH-ir neurons compared with NCM mice, but no significant difference from NM and NF mice. On the other hand, the PeN SS-ir neuron expression in NCM mice and APC mice showed a significant reduction compared with NM mice, but no significant difference from NF mice. The number of PeN SS-ir neurons in NOF increased to match that of NM mice. Our results suggest that the presence of the ovary during postnatal life inhibits the development of ARC GHRH-ir neurons. The presence of the testis during postnatal life may stimulate the development of PeN SS-ir neurons, while the presence of the ovary during neonatal period may inhibit the development of PeN SS-ir neurons; the presence of ovary after puberty does not inhibit.

Possible underlying mechanisms of sexual dimorphism in the immune response, fact and hypothesis.

It is a confirmed fact that in females both the humoral and cell mediated immune response is more active than in males. A large amount of information supports the view that hormones of the endocrine system are intimately involved in this immunological dimorphism. Such hormones include the gonadal steroids, the adrenal glucocorticoids, growth hormone (GH) and prolactin (Prl) from the pituitary, thymic hormones, and substances generated by activated lymphocytes. It is suggested that a complex medley of these hormonal interactions effect both developing lymphocytes within the microenvironment and regulate adult effector cells. The most important of these hormonal interactions leading to immunological dimorphism are the effects elicited by estrogen (E) elaborated at elevated levels from the female ovary after puberty. Elevated E leads to basal GH secretion, increased Prl, and increased thymosin release, all of which are hypothesized to effect lymphocyte development and stimulate adult T- and B-cell function in females. Interactions of hormonal regulatory axes involving the hypothalamus, pituitary, gonads, adrenals, and thymus are also thought to be involved. Factors elaborated by activated immune cells including IL-1 and IL-2 may also play a role in down regulation of these responses. Finally, genetic components are also considered pertinent especially under conditions of pathological disequilibrium leading to autoimmune disease. While the benefits provided by immunological dimorphism are still not entirely clarified, since sex hormones are intimately involved in immunological regulation it is quite possible that the increased immune response in females allows them to compensate for the increased physiological stress which accompanies reproduction. The final outcome would thus be the assurance of reproductive success of the species.

Sexually dimorphic muscles in the forelimb of the Japanese toad, Bufo japonicus.

During the breeding season, male anurans display clasping behavior by holding females with their forelimbs. This behavior is peculiar to males, and may require specializations in forelimb musculature. The present study revealed that five kinds of forelimb muscles were heavier in the male Japanese toad than in the female: the flexor carpi radialis (FCR), the flexor antibrachii medialis caput superius (FAMsup), the abductor indicis longus (AIL), the extensor carpi radialis caput superius (ECRsup), and the flexor antibrachii lateralis superficialis caput superius (FALSsup). In addition, one breast muscle, the coracoradialis (CR), was also heavier in males than in females. A quantitative analysis of muscle fibers processed for myosin ATPase activity showed that, in such "sexually dimorphic muscles" of the female, both fast (twitch) and slow (tonic) muscle fibers were of smaller diameter than in other forelimb muscles of both sexes (all male muscles plus "nondimorphic muscles" of the female). Moreover, both types of fibers were less numerous than in the corresponding muscles of the male. These results suggest that the "sexually dimorphic muscles" are used especially for clasping by the male and are degenerative or subnormal in the female. Slow muscle fibers were neither peculiar to, nor abundant in, these clasping muscles, although they may well be necessary for tonic and prolonged contractions of the forelimb muscles during clasping. The mechanism of sexual dimorphism may be a direct action of androgens on clasping muscles or an indirect action on clasping muscles via the innervating motoneurons.