scholarly journals Sex-based differences in myocardial infarction-induced kidney damage following cigarette smoking exposure: more renal protection in premenopausal female mice

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Nada J. Habeichi ◽  
Ali Mroueh ◽  
Abdullah Kaplan ◽  
Rana Ghali ◽  
Hiam Al-Awassi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cigarette Smoking ◽  
Tissue Growth ◽  
Kidney Damage ◽  
Female Group ◽  
Male Mice ◽  
Renal Protection ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Female Mice ◽  
The Impact

Abstract The impact of cigarette smoking (CS) on kidney homeostasis in the presence of myocardial infarction (MI) in both males and females remains poorly elucidated. C57BL6/J mice were exposed to 2 weeks of CS prior to MI induction followed by 1 week of CS exposure in order to investigate the impact of CS on kidney damage in the presence of MI. Cardiac hemodynamic analysis revealed a significant decrease in ejection fraction (EF) in CS-exposed MI male mice when compared with the relative female subjects, whereas cardiac output (CO) comparably decreased in CS-exposed MI mice of both sexes. Kidney structural alterations, including glomerular retraction, proximal convoluted tubule (PCT) cross-sectional area, and total renal fibrosis were more pronounced in CS-exposed MI male mice when compared with the relative female group. Although renal reactive oxygen species (ROS) generation and glomerular DNA fragmentation significantly increased to the same extent in CS-exposed MI mice of both sexes, alpha-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) significantly increased in CS-exposed MI male mice, only. Metabolically, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide riboside-1 (NMRK-1) substantially increased in CS-exposed MI female mice only, whereas sirtuin (SIRT)-1 and SIRT-3 substantially decreased in CS-exposed MI male mice compared with their relative female group. Additionally, renal NAD levels significantly decreased only in CS-exposed MI male mice. In conclusion, MI female mice exhibited pronounced renal protection following CS when compared with the relative male groups.

Abstract 390: The Absence of Abcg5 Abcg8 Reveals a Sexually Dimorphic Adaption to Impaired Biliary Cholesterol Secretion

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Jianing Li ◽  
Ailing Ji ◽  
Ryan E Temel ◽  
Deneys R van der Westhuyzen ◽  
Gregory A Graf
Keyword(s):  
Alternative Pathway ◽  
Male Mice ◽  
Biliary Cholesterol ◽  
Female Mice ◽  
Cholesterol Excretion ◽  
Biliary Cholesterol Secretion ◽  
Cholesterol Secretion ◽  
The Impact ◽  
Sterol Excretion ◽  
Secretion Rates

Objective: The ABCG5 ABCG8 (G5G8) sterol transporter is the primary mechanism for biliary cholesterol secretion, but mice maintain fecal sterol excretion in its absence. The mechanism by which mice maintain sterol excretion in the absence of this pathway is not known. Transintestinal cholesterol excretion (TICE) is an alternative pathway to hepatobiliary secretion. We investigated the impact of G5G8 deficiency on TICE in the absence of Sitosterolemia. Methods and Results: We compared both hepatobiliary and transintestinal cholesterol excretion rates in wild-type (WT) and G5G8 deficient mice of both sexes. WT and G5G8 were maintained on a plant-sterol free diet from the time of weaning to prevent the development of secondary phenotypes associated with Sitosterolemia. Biliary and intestinal cholesterol secretion rates were determined by biliary diversion with simultaneous perfusion of the proximal 10 cm of the small bowel. Among WT mice, biliary cholesterol secretion was greater in female mice compared to males. Conversely, male mice exhibited greater rates of TICE than females. As expected, WT mice had higher biliary cholesterol secretion rates than their G5G8 deficient littermates. However, the decline in biliary cholesterol secretion was far less in male mice compared to females in the absence of G5G8. In female mice, the absence of G5G8 resulted in a two-fold increase in TICE, whereas males were unaffected. Conclusion: Female mice are more dependent upon the biliary pathway for cholesterol excretion, whereas males are more dependent upon TICE. G5G8 independent pathways are present for both biliary and intestinal cholesterol secretion. Female and male mice differ in their adaptation to G5G8 deficiency in order to maintain fecal sterol excretion.

scholarly journals Chronic Repeated Predatory Stress Induces Resistance to Quinine Adulteration of Ethanol in Male Mice

2019 ◽  
Author(s):  
Gladys A. Shaw ◽  
Maria Alexis M. Bent ◽  
Kimaya R. Council ◽  
A. Christian Pais ◽  
Ananda Amstadter ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Open Field ◽  
Traumatic Event ◽  
Drinking Behavior ◽  
Specific Pattern ◽  
Male Mice ◽  
Female Mice ◽  
Drinking Response ◽  
Field Mice ◽  
The Impact

AbstractBackgroundTrauma related psychiatric disorders, such as posttraumatic stress disorder (PTSD), and alcohol use disorder (AUD) are highly comorbid illnesses that separately present an opposing, sex-specific pattern, with increased prevalence of PTSD in females and increased prevalence of AUD diagnoses in males. Likewise, PTSD is a risk factor in the development of AUD, with conflicting data on the impact of sex in the comorbid development of both disorders. Because the likelihood of experiencing more than one traumatic event is high, we aim to utilize chronic repeated predatory stress (CRPS) to query the extent to which sex interacts with CRPS to influence alcohol consumption, or cessation of consumption.MethodsMale (n=16) and female (n=15) C57BL/6J mice underwent CRPS or daily handling for two weeks during adolescence (P35-P49) and two weeks during adulthood (P65-P79). Following the conclusion of two rounds of repeated stress, behavior was assessed in the open field. Mice subsequently underwent a two-bottle choice intermittent ethanol access (IEA) assessment (P90-131) with the options of 20% ethanol or water. After establishing drinking behavior, increasing concentrations of quinine were added to the ethanol to assess the drinking response to adulteration of the alcohol.ResultsCRPS increased fecal corticosterone concentrations and anxiety-like behaviors in the open field in both male and female mice as compared to control mice that had not been exposed to CRPS. Consistent with previous reports, we observed a sex difference in alcohol consumption such that females consumed more ethanol per gram of body mass than males. In addition, CRPS reduced alcohol aversion in male mice such that higher concentrations of quinine were necessary to reduce alcohol intake as compared to control mice. CRPS did not alter alcohol-related behaviors in female mice.ConclusionCollectively, we demonstrate that repeated CRPS can induce anxiety-like behavior in both sexes but selectively influences the response to ethanol adulteration in males.

scholarly journals Jak1/Stat3 Activation Alters Phosphate Metabolism Independently of Sex and Extracellular Phosphate Levels

2021 ◽  
pp. 1-9
Author(s):  
Nicole Gehring ◽  
Carla Bettoni ◽  
Carsten A. Wagner ◽  
Isabel Rubio-Aliaga
Keyword(s):  
Signaling Pathway ◽  
Mineral Metabolism ◽  
Janus Kinase ◽  
Phosphate Metabolism ◽  
Male Mice ◽  
Male And Female ◽  
Female Mice ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
The Impact

<b><i>Introduction:</i></b> Phosphate homeostasis is regulated by a complex network involving the parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and calcitriol acting on several organs including the kidney, intestine, bone, and parathyroid gland. Previously, we showed that activation of the Janus kinase 1 (Jak1)-signal transducer and activator of transcription 3 (Stat3) signaling pathway leads to altered mineral metabolism with higher FGF23 levels, lower PTH, and higher calcitriol levels. Here, we investigated if there are sex differences in the role of Jak1/Stat3 signaling pathway on phosphate metabolism and if this pathway is sensitive to extracellular phosphate alterations. <b><i>Methods:</i></b> We used a mouse model (<i>Jak1</i><sup>S645P+/−</sup>) that resembles a constitutive activating mutation of the Jak1/Stat3 signaling pathway in humans and analyzed the impact of sex on mineral metabolism parameters. Furthermore, we challenged <i>Jak1</i><sup>S645P+/−</sup> male and female mice with a high (1.2% w/w) and low (0.1% w/w) phosphate diet and a diet with phosphate with organic origin with lower bioavailability. <b><i>Results:</i></b> Female mice, as male mice, showed higher intact FGF23 levels but no phosphaturia, and higher calcitriol and lower PTH levels in plasma. A phosphate challenge did not alter the effect of Jak1/Stat3 activation on phosphate metabolism for both genders. However, under a low phosphate diet or a diet with lower phosphate availability, the animals showed a tendency to develop hypophosphatemia. Moreover, male and female mice showed similar phosphate metabolism parameters. The only exception was higher PTH levels in male mice than those in females. <b><i>Discussion/Conclusion:</i></b> Sex and extracellular phosphate levels do not affect the impact of Jak1/Stat3 activation on phosphate metabolism.

scholarly journals Effects of litter size and subsequent gold-thioglucose-induced obesity on adipose tissue weight, distribution and cellularity in male and female mice: an age study

1988 ◽  
Vol 59 (3) ◽  
pp. 519-533 ◽  
Author(s):  
Jennifer L. Roberts ◽  
Frances M. Whittington ◽  
Michael Enser
Keyword(s):  
Litter Size ◽  
Tissue Growth ◽  
Male Mice ◽  
Newborn Mice ◽  
Small Litter ◽  
Male And Female ◽  
Cell Numbers ◽  
Female Mice ◽  
Gold Thioglucose ◽  
Large Litter

1. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning mice were fed ad lib. At 13 weeks of age some mice from large litters received gold thioglucose (GTG: 600 mg/kg intraperitoneally) to induce hyperphagia, and mice were killed at 13, 19·5, 26, 39 and 52 weeks.2. Total carcass lipid and the size and number of adipocytes in the inguinal subcutaneous, genital, perirenal and mesenteric depots were determined.3. Mice, both male and female, raised in small litters were heavier and had more carcass fat at all ages than mice raised in large litters. After GTG-treatment mice from large litters were heavier and fatter than mice raised in small litters.4. Fat distribution between the depots was related to carcass lipid content and not to treatment. The order of depot development was subcutaneous, parametrial, perirenal and mesenteric in females and epididymal, subcutaneous, perirenal and mesenteric in males. At 13 weeks the depots in males were more developed than those in females.5. Litter size had no effect on adipocyte volume in female mice at 13 weeks but by 52 weeks small-litter mice had larger cells in all depots and more cells in the parametrial and perirenal depots.6. Male mice from small litters had bigger cells at 13 weeks in all depots compared with males from large litters but by 52 weeks no significant differences remained. Greater numbers of cells were present only in the perirenal and mesenteric depots of small-litter males at some ages.7. Depots of GTG-treated large-litter female mice had larger cells than those of small-litter females, while a similar number of cells was found by 52 weeks in all but the perirenal depot, which had significantly more cells.8. GTG treatment of male mice from large litters also caused bigger cells than in small-litter mice, and an increased depot cell number at earlier ages in all but the epididymal depot. By 52 weeks cell numbers were similar in depots from small-litter and GTG-treated large-litter mice, except for the epididymal depot from the latter which had fewer cells.9. Increases in cell numbers with age in different depots occurred independently of existing cell mean volume and even of tissue growth, suggesting the presence of an in-built chronology, at least in older mice.10. We suppose that the differences in response to the level of preweaning nutrition in males and females result from a greater effect on the hypothalamic appetite centre in the latter. Whereas the cellular changes in large-litter males occur in the late-developing depots and are reversed naturally with time, those in the large-litter females are more extensive and require induction of hyperphagia for reversal.

scholarly journals Chronic Mild Stress Causes Bone Loss via an Osteoblast-Specific Glucocorticoid-Dependent Mechanism

Endocrinology ◽  
2017 ◽  
Vol 158 (6) ◽  
pp. 1939-1950 ◽  
Author(s):  
Holger Henneicke ◽  
Jingbao Li ◽  
Sarah Kim ◽  
Sylvia J. Gasparini ◽  
Markus J. Seibel ◽  
...  
Keyword(s):  
Bone Loss ◽  
Chronic Stress ◽  
Structural Parameters ◽  
Chronic Mild Stress ◽  
Bone Resorption Marker ◽  
Mild Stress ◽  
Male Mice ◽  
Female Mice ◽  
Glucocorticoid Signaling ◽  
The Impact

Abstract Chronic stress and depression are associated with alterations in the hypothalamic–pituitary–adrenal signaling cascade and considered a risk factor for bone loss and fractures. However, the mechanisms underlying the association between stress and poor bone health are unclear. Using a transgenic (tg) mouse model in which glucocorticoid signaling is selectively disrupted in mature osteoblasts and osteocytes [11β-hydroxysteroid-dehydrogenase type 2 (HSD2)OB-tg mice], the present study examines the impact of chronic stress on skeletal metabolism and structure. Eight-week-old male and female HSD2OB-tg mice and their wild-type (WT) littermates were exposed to chronic mild stress (CMS) for the duration of 4 weeks. At the endpoint, L3 vertebrae and tibiae were analyzed by micro–computed tomography and histomorphometry, and bone turnover was measured biochemically. Compared with nonstressed controls, exposure to CMS caused an approximately threefold increase in serum corticosterone concentrations in WT and HSD2OB-tg mice of both genders. Compared with controls, CMS resulted in loss of vertebral trabecular bone mass in male WT mice but not in male HSD2OB-tg littermates. Furthermore, both tibial cortical area and area fraction were reduced in stressed WT but not in stressed HSD2OB-tg male mice. Osteoclast activity and bone resorption marker were increased in WT males following CMS, features absent in HSD2OB-tg males. Interestingly, CMS had little effect on vertebral and long-bone structural parameters in female mice. We conclude that in male mice, bone loss during CMS is mediated via enhanced glucocorticoid signaling in osteoblasts (and osteocytes) and subsequent activation of osteoclasts. Female mice appear resistant to the skeletal effects of CMS.

scholarly journals Acute Exposure to Cigarette Smoking Followed by Myocardial Infarction Aggravates Renal Damage in an In Vivo Mouse Model

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Firas Kobeissy ◽  
Abdullah Shaito ◽  
Abdullah Kaplan ◽  
Lama Baki ◽  
Hassan Hayek ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cigarette Smoking ◽  
Mouse Model ◽  
Renal Dysfunction ◽  
Renal Damage ◽  
Smooth Muscle Actin ◽  
Tissue Growth ◽  
Mrna Levels ◽  
Protein Levels

Cigarette smoking (S) is a risk factor for progressive chronic kidney disease, renal dysfunction, and renal failure. In this study, the effect of smoking on kidney function was investigated in a mouse model of myocardial infarction (MI) using 4 groups: control (C), smoking (S), MI, and S+MI. Histological analysis of S+MI group showed alterations in kidney structure including swelling of the proximal convoluted tubules (PCTs), thinning of the epithelial lining, focal loss of the brush border of PCTs, and patchy glomerular retraction. Molecular analysis revealed that nephrin expression was significantly reduced in the S+MI group, whereas sodium-hydrogen exchanger-1 (NHE-1) was significantly increased, suggesting altered glomerular filtration and kidney functions. Moreover, S+MI group, but not S alone, showed a significant increase in the expression of connective tissue growth factor (CTGF) and fibrotic proteins fibronectin (FN) and α-smooth muscle actin (SMA), in comparison to controls, in addition to a significant increase in mRNA levels of IL-6 and TNF-α inflammatory markers. Finally, reactive oxygen species (ROS) production was significantly accentuated in S+MI group concomitant with a significant increase in NOX-4 protein levels. In conclusion, smoking aggravates murine acute renal damage caused by MI at the structural and molecular levels by exacerbating renal dysfunction.

scholarly journals Cigarette Smoke Extract-Induced Oxidative Stress and Fibrosis-Related Genes Expression in Orbital Fibroblasts from Patients with Graves’ Ophthalmopathy

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Hui-Chuan Kau ◽  
Shi-Bei Wu ◽  
Chieh-Chih Tsai ◽  
Catherine Jui-Ling Liu ◽  
Yau-Huei Wei
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Tissue Growth ◽  
Graves Ophthalmopathy ◽  
Genes Expression ◽  
The Impact ◽  
Orbital Fibroblasts

Cigarette smoking is the most important risk factor for the development or deterioration of Graves’ ophthalmopathy. Smoke-induced increased generation of reactive oxygen species may be involved. However, it remains to be clarified how orbital fibroblasts are affected by cigarette smoking. Our study demonstrated that Graves’ orbital fibroblasts have exaggerated response to cigarette smoke extract challenge along with increased oxidative stress, fibrosis-related genes expression, especially connective tissue growth factor, and intracellular levels of transforming growth factor-β1 and interleukin-1β. The findings obtained in this study provide some clues for the impact of cigarette smoking on Graves’ ophthalmopathy and offer a theoretical basis for the potential and rational use of antioxidants in treating Graves’ ophthalmopathy.

Effects of Neonatal Caffeine Administration on Vessel Reactivity in Adult Mice

2020 ◽  
Author(s):  
Ajay Pratap Singh ◽  
Praveen Chandrasekharan ◽  
Sylvia Gugino ◽  
Sara Berkelhamer ◽  
Huamei Wang ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Systemic Blood Pressure ◽  
Systemic Hypertension ◽  
Male Mice ◽  
Treated Male ◽  
Female Mice ◽  
Adult Mice ◽  
Specific Effects ◽  
Lower Body Weight ◽  
The Impact

Abstract Objective The effects of neonatal caffeine therapy in adults born preterm are uncertain. We studied the impact of neonatal caffeine on systemic blood pressure, vessel reactivity, and response to stress in adult mice. Study Design Mice pups were randomized to caffeine (20 mg/kg/d) or saline by intraperitoneal injection for 10 days after birth. We performed tail-cuff BP (8/12 weeks), urinary 8-hydroxydeoxyguanosine and fecal corticosterone (14 weeks), and vessel reactivity in aortic rings (16 weeks) in adult mice. Results No differences were noted in systolic, diastolic, and mean blood pressures between the two groups at 8 and 12 weeks of age. However, norepinephrine-induced vasoconstriction was substantially higher in aortic rings in CAF-treated male mice. More significant vasodilator responses to nitric oxide donors in aortic rings in female mice may suggest gender-specific effects of caffeine. Female mice exposed to caffeine had significantly lower body weight over-time. Caffeine-treated male mice had substantially higher fecal corticosterone and urinary 8-hydroxydeoxyguanosine at 14 weeks, suggestive of chronic stress. Conclusion We conclude sex-specific vulnerability to the heightened vascular tone of the aorta in male mice following neonatal caffeine therapy. Altered vessel reactivity and chronic stress in the presence of other risk factors may predispose to the development of systemic hypertension in adults born preterm.

scholarly journals Girls gone wild: Social isolation induces hyperactivity and exploration in aged female mice

2020 ◽  
Author(s):  
D. Gregory Sullens ◽  
Kayla Gilley ◽  
Kendall Jensen ◽  
Melanie J. Sekeres
Keyword(s):  
Social Isolation ◽  
Early Life ◽  
Elevated Plus Maze ◽  
Late Life ◽  
Young Female ◽  
Affective Behavior ◽  
Male Mice ◽  
Female Mice ◽  
Plus Maze ◽  
The Impact

ABSTRACTThe likelihood of experiencing social isolation increases later in life, particularly for females. It remains unknown how late-life social isolation impacts cognition and affective behavior in aged mice. We assessed the impact of late-life social isolation in 18-month old female mice. One month of single-housing did not lead to robust depressive-like symptomology, altered social interaction behavior, or sensitivity to context fear acquisition or memory. Rather, isolation increased hyperactivity and exploration, and reduced anxiety-like behavior in the open field and elevated plus maze, findings that have been similarly observed in young female and male mice following early-life isolation. These findings suggest that hyperactivity is a robust behavior following social isolation across the lifespan.

scholarly journals Impact of formate supplementation on body weight and plasma amino acids

2020 ◽  
Author(s):  
Sandeep Dhayade ◽  
Matthias Pietzke ◽  
Robert Wiesheu ◽  
Jacqueline Tait-Mulder ◽  
Dimitris Athineos ◽  
...  
Keyword(s):  
Amino Acids ◽  
Body Weight ◽  
Immune Cell ◽  
Sodium Formate ◽  
The Body ◽  
Control Group ◽  
Male Mice ◽  
Female Mice ◽  
Cell Counts ◽  
The Impact

AbstractCurrent nutritional recommendations are focused on energy, fat, carbohydrate, protein and vitamins. Less attention has been paid to the nutritional demand of one-carbon units for nucleotide and methionine synthesis. Here we investigate the impact of sodium formate supplementation as a nutritional intervention to increase the dietary intake of one-carbon units. A cohort of six female and six male mice received 125 mM sodium formate in the drinking water for three months. A control group of another six female and six male mice was also followed up for the same period of time. Tail vein blood samples were collected once a month and profiled with a haematology Analyser. At the end of the study blood and tissues were collected for metabolomics analysis and immune cell sorting. Formate supplementation has no significant physiological effect on male mice. Formate supplementation has no significant effect on the immune cell counts during the intervention or at the end of the study in either gender. In female mice however, the body weight and spleen wet-weight were significantly increased by formate supplementation, while the blood plasma levels of amino acids were decreased. Formate supplementation also increased the frequency of probiotic bacteria in the stools of female mice. We conclude that formate supplementation induces physiological changes in female mice.

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