Time course of behavioral, physiological, and morphological changes after estradiol treatment of ovariectomized rats

Lactate dehydrogenase (LDH; EC 1.1.1.27), citrate synthase (CS; EC 4.1.3.7), and beta-hydroxyacyl-CoA-dehydrogenase (beta-OH-acyl-CoA-DH; EC 1.1.1.35) activities were determined in each of the three major cell types of rat uterus, i.e., epithelial, stromal, and smooth muscle, using quantitative microanalytical techniques. Adult ovariectomized rats were treated with 17-beta-estradiol to determine the time course and dose response (0.025-50 micrograms/300-g rat) effect of estrogen on enzyme activity of each type of uterine cell. The use of "oil well" and enzyme-cycling microtechniques to determine the time course and the dose responses of enzyme activity changes required microassays involving 1595 microdissected single cell specimens. Estradiol treatment increased epithelial LDH, CS and beta-OH-acyl-CoA-DH activity but had no effect on these enzymes in the stroma or in smooth muscle cells. The estradiol-stimulated peak enzyme activities on Day 4 in the intervention group are compared with those in the ovariectomized rat controls as follows: LDH, 44.5 +/- 3.5 vs 22.3 +/- 3.9; CS, 3.5 +/- 0.2 vs 1.5 +/- 0.6; beta-OH-acyl-CoA-H, 3.5 +/- 0.32 vs 2.2 +/- 0.2 (mean +/- standard deviation; mol/kg/hr). Stromal cell activities (LDH, 7.4 +/- 1.0; CS, 1.2 +/- 0.2; beta-OH-acyl-CoA-DH, 0.9 +/- 0.1) were significantly lower than epithelial cell levels and were similar to smooth muscle levels. Therefore, even in the ovariectomized animal epithelial cells have markedly higher metabolic activity compared with adjacent cells. The enzyme activities are expressed as moles of substrate reacting per kilogram of dry weight per hour. All three enzymes exhibited a 17-beta-estradiol-induced dose response between 0.025-0.15 micrograms/300-g rat. The three enzymes studied all had similar response patterns to estrogen. The effect of estradiol was restricted to epithelial cells, with enzyme activities increasing to maximal levels after approximately 96 hr of hormone treatment. This study therefore not only confirms the specific and differential metabolic responses of uterine cells to estradiol treatment, but clearly demonstrates that marked metabolic differences exist between epithelial cells and stromal or smooth muscle uterine cells.

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Time Course of Serum FSH Suppression in Ovariectomized Rats Injected with Porcine Follicular Fluid (Folliculostatin): Effect of Estradiol Treatment

Biology of Reproduction ◽

10.1095/biolreprod20.5.1093 ◽

1979 ◽

Vol 20 (5) ◽

pp. 1093-1098 ◽

Cited By ~ 20

Author(s):

Constance S. Campbell ◽

Neena B. Schwartz

Keyword(s):

Follicular Fluid ◽

Time Course ◽

Ovariectomized Rats ◽

Estradiol Treatment

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Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie ◽

10.1024/1422-4917/a000265 ◽

2014 ◽

Vol 42 (1) ◽

pp. 7-18 ◽

Cited By ~ 56

Author(s):

Jochen Seitz ◽

Katharina Bühren ◽

Georg G. von Polier ◽

Nicole Heussen ◽

Beate Herpertz-Dahlmann ◽

...

Keyword(s):

Anorexia Nervosa ◽

Cognitive Deficits ◽

Time Course ◽

Morphological Changes ◽

Meta Analysis ◽

Short Term ◽

Clinical Prognosis ◽

Qualitative Review ◽

Brain Changes ◽

The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

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Evaluation of cellular plasticity in the collecting duct during recovery from lithium-induced nephrogenic diabetes insipidus

AJP Renal Physiology ◽

10.1152/ajprenal.00152.2012 ◽

2013 ◽

Vol 305 (6) ◽

pp. F919-F929 ◽

Cited By ~ 35

Author(s):

Francesco Trepiccione ◽

Giovambattista Capasso ◽

Søren Nielsen ◽

Birgitte Mønster Christensen

Keyword(s):

Time Course ◽

Morphological Changes ◽

Collecting Duct ◽

Lithium Treatment ◽

Transition Element ◽

Type A ◽

Functional Markers ◽

Intercalated Cells ◽

Anion Exchanger 1 ◽

Principal Cells

The cellular morphology of the collecting duct is altered by chronic lithium treatment. We have previously shown that lithium increases the fraction of type-A intercalated cells and lowers the fraction of principal cells along the collecting duct. Moreover, type-A intercalated cells acquire a long-row distribution pattern along the tubules. In the present study, we show that these morphological changes reverse progressively after discontinuation of lithium and finally disappear after 19 days from lithium suspension. In this time frame we have identified for the first time, in vivo, a novel cellular type positive for both intercalated and principal cells functional markers, as recognized by colabeling with H+-ATPase/aquaporin-4 (AQP4) and anion exchanger-1 (AE-1)/AQP2 and Foxi1/AQP4. This cell type is mainly present after 6 days of lithium washout, and it disappears in parallel with the long-row pattern of the type-A intercalated cells. It usually localizes either in the middle or at the edge of the long-row pattern. Its ultrastructure resembles the intercalated cells as shown both by differential interference contrast and by electron microscopy. The time course of appearance, the localization along the collecting duct, and the ultrastructure suggest that the cells double labeled for principal and intercalated cells markers could represent a transition element driving the conversion of intercalated cells into principal cells.

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Resistance training and caloric restriction prevent systolic blood pressure rise by improving the nitric oxide effect on smooth muscle and morphological changes in the aorta of ovariectomized rats

PLoS ONE ◽

10.1371/journal.pone.0201843 ◽

2018 ◽

Vol 13 (8) ◽

pp. e0201843 ◽

Cited By ~ 1

Author(s):

Anderson Diogo de Souza Lino ◽

Daiana Vianna ◽

Jorge Camargo Oishi ◽

Markus Vinicius Campos Souza ◽

Leandro Dias Ruffoni ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Smooth Muscle ◽

Resistance Training ◽

Systolic Blood Pressure ◽

Caloric Restriction ◽

Morphological Changes ◽

Pressure Rise ◽

Ovariectomized Rats ◽

Blood Pressure Rise

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Abstract P502: Abnormal Myocyte Calcium Dynamics And The Resultant Contraction Band Formation Of The Rat Heart Under Irreversible Injury By Membrane Permeabilization

Circulation Research ◽

10.1161/res.129.suppl_1.p502 ◽

2021 ◽

Vol 129 (Suppl_1) ◽

Author(s):

Yuma Morishita ◽

Shoko Tamura ◽

Kentaro Mochizuki ◽

Yoshinori Harada ◽

Hideo Tanaka

Keyword(s):

Fluorescence Intensity ◽

High Frequency ◽

Time Course ◽

Morphological Changes ◽

Confocal Imaging ◽

Band Formation ◽

Contraction Band Necrosis ◽

Scanning Confocal Microscopy ◽

The Individual ◽

Contraction Band

Ca 2+ overload is a cardinal feature of cardiomyocyte injury, and its progression to irreversible state leads to cell death. However, unknowns are the precise spatiotemporal changes in the myocyte Ca 2+ dynamics and the relevant cell morphology of irreversibly injured hearts. On the hypothesis that myocytes exhibit high-frequency Ca 2+ waves and contraction band necrosis in saponin-permeabilized injured heart, we observed changes in the Ca 2+ dynamics and the relevant morphological changes in the subepicardial myocardium of the Fluo4-loaded rat hearts (n = 14) by rapid-scanning confocal microscopy (100 frames/s) under Langendorff perfusion with 0.3 mM Ca 2+ -Tyrode solution including 0.4 % saponin at 30°C. Also performed was confocal imaging of tetramethylrhodamine methyl ester (TMRM) fluorescence of the myocardium. Under quasi-quiescence of the heart after dissection of the SA node, individual myocytes barely exhibited spontaneous Ca 2+ waves, whereas after commencement of saponin perfusion high-frequency (118 ± 9.7 /min/cell, mean ± SEM) Ca 2+ waves (hereafter, “agonal waves”) emerged within 1 min, showing asynchronous, oscillatory contractions in the individual myocytes with a V prop of 124 ± 2.5 μm/s (n = 60). Subsequently, the waves gradually decreased in frequency with concomitant slowing of its decay time course, and eventually, disappeared in 6 min; myocytes exhibited high, static Fluo4-fluorescence intensity. Along with the progression of Ca 2+ overload by saponin, the TMRM fluorescence intensity was discretely lost in individual myocytes. The myocytes showing the agonal waves exhibited contraction bands, i.e., band-like aggregations of the actin fibers. Under mechanical arrest of the heart by 2,3-butanedione monoxime (20 mM), saponin still induced the agonal waves with a frequency of 253 ± 10.6 /cell/min and V prop of 118 ± 2.1 μm/s (n = 60); however, contraction bands were barely seen.In conclusion, irreversible myocyte injury by saponin provoked agonal Ca 2+ waves and oscillatory contractions indicating progressive Ca 2+ overload and the following mitochondrial damage, which may provide deeper insights into understanding the mechanism of contraction band necrosis.

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Estrogen modulates the recruitment of myelopoietic cell progenitors in rat through a stromal cell-independent mechanism involving apoptosis

Blood ◽

10.1182/blood.v87.7.2683.bloodjournal8772683 ◽

1996 ◽

Vol 87 (7) ◽

pp. 2683-2692 ◽

Cited By ~ 33

Author(s):

NK Shevde ◽

JW Pike

Keyword(s):

Estrogen Receptor ◽

Ovarian Function ◽

Morphological Changes ◽

Estrogen Treatment ◽

Ovariectomized Rats ◽

Terminal Deoxynucleotidyl Transferase ◽

Protective Effects ◽

Hematopoietic Stem

Loss of ovarian function leads to a significant increase in the number of bone-resorbing osteoclasts. Estrogen replacement is known to manifest bone protective effects in the treatment of postmenopausal osteoporosis. In the present study, we used ovariectomized rats to examine the effects of estrogen loss at the osteoclast progenitor colony forming unit-granulocyte macrophage (CFU-GM) level. A significant increase in CFU-GM number was observed as early as 7 days following ovariectomy, and correlated directly with an increase in the number of osteoclast-like cells generated in marrow cultures. The increase in CFU-GM following ovariectomy was abrogated in animals that received estrogen treatment in vivo. A similar suppressive effect was observed on CFU-GM number when ovariectomized rat marrow was treated with estrogen in vitro. This effect was blocked in the presence of the estrogen antihormone ICI 164,384. Thus, the data suggest the possibility that estrogen exerts a direct effect on osteoclast progenitors, and does so through the estrogen receptor-mediated mechanism. Ovariectomy also led to an increase in the early hematopoietic stem/progenitor cell population (Thy 1.1+ cells) as determined by FLOW cytometry methods. Morphological changes as well as terminal deoxynucleotidyl transferase assays revealed that estrogen treatment negated growth factor-induced proliferation of these early progenitors by promoting apoptosis. The cellular effects of estrogen in vitro together with the immunocytochemical detection of the estrogen receptor in these cells, strongly support the contention that in addition to osteoclast progenitors such as CFU-GM, earlier hematopoietic progenitors are also unique cellular targets for estrogen action.

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Hypoxia during pregnancy in rats leads to early morphological changes of atherosclerosis in adult offspring

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00440.2008 ◽

2009 ◽

Vol 296 (5) ◽

pp. H1321-H1328 ◽

Cited By ~ 34

Author(s):

Zhenhua Wang ◽

Ziyang Huang ◽

Guorong Lu ◽

Ling Lin ◽

Markus Ferrari

Keyword(s):

Morphometric Analysis ◽

Time Course ◽

Morphological Changes ◽

Adult Life ◽

Inflammatory Cells ◽

Prenatal Hypoxia ◽

Control Group ◽

Adult Offspring ◽

Sprague Dawley ◽

Maternal Hypoxia

Exposure to an adverse intrauterine environment increases the risk of cardiovascular disease later in adult life. However, the time course relationship between prenatal hypoxia and the onset of atherosclerosis in offspring remains unknown. The purpose of this study is to evaluate the role of reduced fetal oxygen supply on early development of atherogenesis in the adult offspring and further assess its susceptibility to sex-, hyperlipidemia-, and postnatal hypoxemia-related differences. Based on a 4 × 2 full factorial design consisting of four factors of maternal hypoxia, sex, hyperlipidemia, and postnatal hypoxemia, characteristics of growth were determined, and histopathological observation and morphometric analysis of the thoracic aortas were performed in Sprague-Dawley rat offspring. Intrauterine growth restriction, altered body shape at birth, and accelerated postnatal weight gain occurred in the maternal hypoxia group but did not occur in the control group. In 16-mo-old maternal hypoxia offspring, the thoracic aortas exhibited lesions similar to early events in atherosclerosis that involved impaired endothelial cells, thickening and fibration of intimas, infiltration of inflammatory cells to the subendothelial space, and migration and proliferation of vascular smooth muscle cells to the intima. In contrast, no detectable pathological changes were observed in the offspring without maternal hypoxia exposure. Morphometric analysis further demonstrated that prenatal hypoxia caused a significant thickening of intima ( P < 0.001) with a main effect of 5.5 μm, an approximately twofold increase compared with controls. In addition, there was a positive additive relationship between prenatal hypoxia and hyperlipidemia on the intimal thickness ( P < 0.05). There were no other main effects or interaction among these four factors. In summary, our results indicate that maternal hypoxia during pregnancy leads to early pathological appearances of atherogenesis in adult offspring. This effect was enhanced with hyperlipemia but was unaffected by postnatal hypoxia or sex.

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