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1.
Braz. j. med. biol. res ; 52(7): e8381, 2019. tab, graf
Article in English | LILACS | ID: biblio-1011592

ABSTRACT

Experiments were conducted to determine if the follicle-stimulating hormone (FSH) receptor binding inhibitor (FRBI) impacts the expression levels of AT-rich interactive domain-containing protein 1A (ARID1A) and phosphatase and tensin homolog (PTEN) in ovaries and blood, as well as expressions of follicle-stimulating hormone cognate receptor (FSHR) gene and proteins. Mice in FRBI-10, FRBI-20, FRBI-30, and FRBI-40 groups were intramuscularly injected with 10, 20, 30, and 40 mg FRBI/kg, respectively, for five consecutive days. Western blotting and qRT-PCR were utilized to determine expression levels of ARID1A and PTEN proteins and mRNAs. Serum ARID1A and PTEN concentrations of the FRBI-40 group were higher than the control group (CG) and FSH group (P<0.05). FSHR mRNA levels of FRBI-20, FRBI-30, and FRBI-40 groups were lower than that of CG and FSH groups on day 15 (P<0.05 or P<0.01). Expression levels of FSHR proteins of FRBI-30 and FRBI-40 groups were lower than those of CG and FSH groups (P<0.05). Levels of ARID1A and PTEN proteins of the FRBI-30 group were greater than CG on days 20 and 30 (P<0.05). FRBI doses had significant positive correlations to levels of ARID1A and PTEN proteins. Additionally, ARID1A and PTEN had negative correlations to FSHR mRNAs and proteins. A high dose of FRBI could promote the expression levels of ARID1A and PTEN proteins in ovarian tissues. FRBI increased serum concentrations of ARID1A and PTEN. However, FRBI depressed expression levels of FSHR mRNAs and proteins in mouse ovaries.


Subject(s)
Animals , Female , Rabbits , Ovarian Neoplasms/metabolism , Receptors, FSH/antagonists & inhibitors , Nuclear Proteins/blood , DNA-Binding Proteins/metabolism , PTEN Phosphohydrolase/blood , Follicle Stimulating Hormone/metabolism , Phosphorylation , Transcription Factors , Nuclear Proteins/metabolism , Transcriptional Activation/genetics , Up-Regulation , Blotting, Western , DNA-Binding Proteins/blood , PTEN Phosphohydrolase/metabolism , Real-Time Polymerase Chain Reaction
2.
Braz. j. med. biol. res ; 51(12): e7574, 2018. graf
Article in English | LILACS | ID: biblio-974257

ABSTRACT

Bone fracture is a common medical condition, which may occur due to traumatic injury or disease-related conditions. Evidence suggests that microRNAs (miRNAs) can regulate osteoblast differentiation and function. In this study, we explored the effects and mechanism of miR-221 on the growth and migration of osteoblasts using MC3T3-E1 cells. The expression levels of miR-221 in the different groups were measured by qRT-PCR. Then, miR-221 mimic and inhibitor were transfected into MC3T3-E1 cells, and cell viability and migration were measured using the CCK-8 assay and the Transwell migration assay. Additionally, the expression levels of differentiation-related factors (Runx2 and Ocn) and ZFPM2 were measured by qRT-PCR. Western blot was used to measure the expression of cell cycle-related proteins, epithelial-mesenchymal transition (EMT)-related proteins, ZFPM2, and Wnt/Notch, and Smad signaling pathway proteins. miR-221 was significantly up-regulated in the patients with lumbar compression fracture (LCM) and trochanteric fracture (TF). miR-221 promoted ALP, Runx2, and OPN expressions in MC3T3-E1 cells. miR-221 overexpression significantly increased cell proliferation, migration, differentiation, and matrix mineralization, whereas suppression of miR-221 reversed these effects. Additionally, the results displayed that ZFPM2 was a direct target gene of miR-221, and overexpression of ZFPM2 reversed the promoting effects of miR-221 overexpression on osteoblasts. Mechanistic study revealed that overexpression of miR-221 inactivated the Wnt/Notch and Smad signaling pathways by regulating ZFPM2 expression. We drew the conclusions that miR-221 overexpression promoted osteoblast proliferation, migration, and differentiation by regulation of ZFPM2 expression and deactivating the Wnt/Notch and Smad signaling pathways.


Subject(s)
Humans , Animals , Rabbits , Cell Differentiation/physiology , Cell Movement/physiology , MicroRNAs/physiology , Cell Proliferation/physiology , DNA-Binding Proteins/physiology , Fractures, Bone/blood , Osteoblasts/physiology , Reference Values , Transcription Factors/blood , Cell Survival/physiology , Blotting, Western , Analysis of Variance , 3T3 Cells , MicroRNAs/blood , DNA-Binding Proteins/blood
3.
Arch. endocrinol. metab. (Online) ; 61(5): 455-459, Sept.-Oct. 2017. tab, graf
Article in English | LILACS | ID: biblio-887598

ABSTRACT

ABSTRACT Objective To investigate serum nesfatin-1 levels at 24-28 weeks of pregnancy in women newly diagnosed with gestational diabetes and determine the association of nesfatin-1 with several metabolic parameters. Subjects and methods Forty women newly diagnosed with gestational diabetes at 24-28 weeks of pregnancy and 30 healthy pregnant women matched in age and gestational week were included in this cross-sectional study. Serum nesfatin-1 levels were analyzed using ELISA, and the relationship between nesfatin-1 and several metabolic parameters were assessed. Results Serum nesfatin-1 levels were found to be lower in women with gestational diabetes compared to the pregnant women in the control sample (p = 0.020). Multiple linear regression analysis revealed that nesfatin-1 was lower in participants with gestational diabetes independently from gestational age, BMI, HOMA-IR, fasting plasma glucose, and age. In correlation analysis, the only variable that was found to have a statistically significant correlation with nesfatin-1 was gestational age (p = 0.015, r = 0.30). Conclusion Lower nesfatin-1 levels in women with gestational diabetes compared to the control group at 24-28 weeks of gestation draws attention to nesfatin-1 levels in gestational diabetes and motivates further research in this area.


Subject(s)
Humans , Female , Pregnancy , Adult , Calcium-Binding Proteins/blood , Diabetes, Gestational/blood , DNA-Binding Proteins/blood , Nerve Tissue Proteins/blood , Enzyme-Linked Immunosorbent Assay , Biomarkers/blood , Body Mass Index , Case-Control Studies , Cross-Sectional Studies , Fasting/blood , Gestational Age , Diabetes, Gestational/diagnosis , Nucleobindins , Glucose Tolerance Test
4.
Bulletin of High Institute of Public Health [The]. 2007; 37 (3): 655-669
in English | IMEMR | ID: emr-112220

ABSTRACT

Association between the angiotensinogen gene [M235T] and pre-eclampsia has been confirmed in recent studies. Pre-eclampsia is a complication of pregnancy characterized by increased vascular resistance, higher blood pressure, proteinuria and oedema that appear in the second and third trimester of pregnancy. This study aimed at investigating the relationship between M235T gene polymorphism and pregnant women with different forms of pre-eclampsia. One hundred and fifteen pre-eclamptic women and 100 normal control group were recruited and evaluated for the frequency of M235T mutation using polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP]. A positive association was found between maternal age over 35 years [OR = 6.67; CI: 2.09-23.59], previous family history of hypertension [OR = 3.01; CI: 1.18-7.66], previous pre-eclampsia [OR = 7.44; CI: 2.47-22.42], history of reproductive losses [OR = 53.98; CI: 3.23-90.88], fetal anomalies [OR = 8.4; CI: 1.06-180.33], and pre-eclampsia. The frequency of heterozygous carriers of M235T mutation in pre-eclampsia [19.1%] was higher than that in control [14%] but the difference was statistically non-significant. Also, the frequency of M235T mutation was higher in mild pre-eclampsia women [63.6%] compared to women with severe pre-eclampsia [36.4%], however this was statistically non-significant. This study revealed that the frequency of M235T mutation was higher within women with mild pre-eclampsia


Subject(s)
Humans , Female , Angiotensinogen , Polymorphism, Genetic , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , DNA-Binding Proteins/blood , Nuclear Proteins/blood , Pregnancy
5.
Indian J Lepr ; 1988 Jul; 60(3): 363-73
Article in English | IMSEAR | ID: sea-55221

ABSTRACT

In the present work we report our studies on IgG separated from the serum of lepromatous patients and non-lepromatous leprosy cases using Laser Raman Spectroscopy. Striking spectral changes in LL cases have been observed in the following special regions: (a) the amide I and III, (b) the S-S and C-S stretching (c) the skeletal bending and (d) skeletal stretching regions. These changes indicate a decrease in the amount of beta-structure and a transition towards alpha-helical conformation.


Subject(s)
DNA-Binding Proteins/blood , Humans , Immunoglobulin G/analysis , Lasers , Leprosy, Lepromatous/blood , Mass Spectrometry , Protein Conformation , Stereoisomerism
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