Autoradiogaphic investigation of cell proliferation in the adrenal cortex of castrated female rats under the influence of oestradiol

1984 ◽  
Vol 40 (12) ◽  
pp. 1384-1385 ◽  
Author(s):  
H. Ueberberg ◽  
H. -G. Muff ◽  
G. Trieb
1961 ◽  
Vol 38 (1) ◽  
pp. 50-58 ◽  
Author(s):  
N. E. Borglin ◽  
L. Bjersing

ABSTRACT Oestriol (oestra-1,3,5(10)-triene-3,16α,17β-triol) is a weakly oestrogenic substance which, however, in contrast to what was formerly believed, is of physiological significance. Its effect is localized largely to the uterine cervix and vagina. Clinical experience argues both for and against an effect on the pituitary gland. This investigation is concerned with the morphological changes in the pituitary gland and adrenal cortex of gonadectomized male and female rats after the injection of oestriol. It was found that oestriol has the same type of action on these glands as other oestrogens, but under the experimental conditions used, this effect proved much weaker than that produced by oestradiol (oestra-1,3,5(10)-triene-3,17β-diol).


2009 ◽  
Vol 201 (1) ◽  
pp. 141-150 ◽  
Author(s):  
N David Åberg ◽  
Inger Johansson ◽  
Maria A I Åberg ◽  
Johan Lind ◽  
Ulf E Johansson ◽  
...  

IGF-I treatment has been shown to enhance cell genesis in the brains of adult GH- and IGF-I-deficient rodents; however, the influence of GH therapy remains poorly understood. The present study investigated the effects of peripheral recombinant bovine GH (bGH) on cellular proliferation and survival in the neurogenic regions (subventricular zone (SVZ), and dentate gyrus of the hippocampus), as well as the corpus callosum, striatum, parietal cortex, and piriform cortex. Hypopituitarism was induced in female rats by hypophysectomy, and the rats were supplemented with thyroxine and cortisone acetate. Subsequently, the rats received daily s.c. injections of bGH for either 6 or 28 days respectively. Following 5 days of peripheral bGH administration, the number of bromodeoxyuridine (BrdU)-positive cells was increased in the hippocampus, striatum, parietal cortex, and piriform cortex after 6 and 28 days. In the SVZ, however, BrdU-positive cells increased only after 28 days of bGH treatment. No significant change was observed in the corpus callosum. In the hippocampus, after 28 days of bGH treatment, the number of BrdU/NeuN-positive cells was increased proportionally to increase the number of BrdU-positive cells. 3H-thymidine incorporation in vitro revealed that 24 h of bGH exposure was sufficient to increase cell proliferation in adult hippocampal progenitor cells. This study shows for the first time that 1) peripheral bGH treatment increased the number of newborn cells in the adult brain and 2) bGH exerted a direct proliferative effect on neuronal progenitor cells in vitro.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Courtney Stewart ◽  
Aditya Panta ◽  
Taylor Branyan ◽  
Farida Sohrabji

Background: Post-stroke depression (PSD) occurs in one-third of stroke survivors, is more prevalent in women, and negatively impacts quality of life and recovery. Our previous work showed that acyclic middle-aged female rats display depressive behaviors after stroke, and IV treatment with mir363-3p attenuates these behaviors. Serotonin has been implicated in affective behaviors, and loss of this neurotransmitter is also associated with decreased neurogenesis in the hippocampus. The present study determined (a) whether stroke affected tryptophan, a gut metabolite, and precursor for serotonin, and cell proliferation in the hippocampus and (b) whether serum tryptophan levels and hippocampal cell proliferation was restored by mir363-3p. Methods: Ischemic stroke was induced by stereotaxic delivery of endothelin-1 to the MCA of middle-aged female rats. Animals received a single injection of mir363-3p or scrambled oligos 4h after stroke. Depressive-like behaviors were assessed by the Effort-based sucrose consumption test, Social Interaction and Forced Swim Test 3 months after stroke. Blood was collected at termination. Serum tryptophan levels were quantified by ELISA. Bacterial composition was analyzed by 16S sequencing of fecal samples. Ki67 immunohistochemistry was performed on brain tissue collected at termination and quantified within the dentate gyrus by two blind observers. Results: Animals subjected to stroke exhibited depressive-like behaviors and had decreased tryptophan levels as compared to sham treated animals. This is also accompanied by microbiota dysbiosis as measured by an elevated ratio of Firmicutes to Bacteroidetes. Mir363-3p treatment increased tryptophan levels as compared to scrambled controls and were no different from sham (non-stroke) animals. Moreover, miR363-3p treated rats exhibit a significantly more dentate gyrus-specific Ki67 expression a proliferation marker. Conclusions: Together, these data indicate that miR363-3p attenuates post stroke depression via a mechanism that prevents microbiota dysbiosis and increases hippocampal cell proliferation.


2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Zhoujun Liu ◽  
Yu Chen ◽  
Guofang Chen ◽  
Xiaodong Mao ◽  
Xiao Wei ◽  
...  

Purpose. Because thyroid hormones from the maternal thyroid glands are known to influence the growth, development, and metabolic functioning of offspring, we used a rat model to preliminarily investigate the effects of maternal hypothyroidism on glucose metabolism, pancreas cell proliferation, and insulin production in young male offspring and the possible underlying mechanisms. Methods. Female rats were divided into a maternal hypothyroidism (MH) group, which received water containing 0.02% 6-propyl-2-thiouracil before and during pregnancy to induce hypothyroidism, and a control group which consumed tap water. Results. Our results showed that there were no differences of islets structure between the offspring from the two groups, but glucose metabolism was impaired with higher plasma glucose concentrations at 0 and 15 min in the OGTT in 8-week-old offspring of the MH group. From birth to 8 weeks, pancreatic TRβ1 and TRβ2 mRNA level declined significantly in MH offspring, accompanied by decreased Ki67 and insulin mRNA expression. Conclusions. Maternal hypothyroidism results in impaired pancreatic insulin synthesis and pancreatic cell proliferation in neonatal offspring and subsequent glucose intolerance in young offspring, which may be related to TRβ gene downregulation in the pancreas.


2018 ◽  
Vol 239 (2) ◽  
pp. 197-213 ◽  
Author(s):  
Marlise Guerrero Schimpf ◽  
María M Milesi ◽  
Enrique H Luque ◽  
Jorgelina Varayoud

In a previous work, we detected that postnatal exposure to a glyphosate-based herbicide (GBH) alters uterine development in prepubertal rats causing endometrial hyperplasia and increasing cell proliferation. Our goal was to determine whether exposure to low dose of a GBH during postnatal development might enhance the sensitivity of the uterus to an estrogenic treatment. Female Wistar pups were subcutaneously injected with saline solution (control) or GBH using the reference dose (2 mg/kg/day, EPA) on postnatal days (PND) 1, 3, 5 and 7. At weaning (PND21), female rats were bilaterally ovariectomized and treated with silastic capsules containing 17β-estradiol (E2, 1 mg/mL) until they were 2 months of age. On PND60, uterine samples were removed and processed for histology, immunohistochemistry and mRNA extraction to evaluate: (i) uterine morphology, (ii) uterine cell proliferation by the detection of Ki67, (iii) the expression of the estrogen receptors alpha (ESR1) and beta (ESR2) and (iv) the expression of WNT7A and CTNNB1. GBH-exposed animals showed increased luminal epithelial height and stromal nuclei density. The luminal and glandular epithelium were markedly hyperplastic in 43% of GBH-exposed animals. GBH exposure caused an increase in E2-induced cell proliferation in association with an induction of both ESR1 and ESR2. GBH treatment decreased membranous and cytoplasmic expression of CTNNB1 in luminal and glandular epithelial cells and increased WNT7A expression in the luminal epithelium. These results suggest that early postnatal exposure to a GBH enhances the sensitivity of the rat uterus to estradiol and induces histomorphological and molecular changes associated with uterine hyperplasia.


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