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Your search keyword '"miR‐132"' showing total 8 results
Start Over Descriptor "miR‐132" Journal biochemical and biophysical research communications
8 results on '"miR‐132"'

1. Brown adipocyte-derived exosomal miR-132-3p suppress hepatic Srebf1 expression and thereby attenuate expression of lipogenic genes

Author

Eiichi Araki, Tatsuya Yoshizawa, Yoshifumi Sato, Yuichi Kariba, Kazuya Yamagata, and Tomonori Tsuyama

Subjects
0301 basic medicine, Male, Biophysics, Regulator, Down-Regulation, Biology, Exosomes, Biochemistry, Exosome, 03 medical and health sciences, miR-132, chemistry.chemical_compound, Norepinephrine, 0302 clinical medicine, microRNA, Gene expression, Brown adipose tissue, medicine, Animals, Neurotransmitter, Molecular Biology, Cells, Cultured, Lipogenesis, Cell Biology, Microvesicles, Cell biology, Up-Regulation, Mice, Inbred C57BL, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Adipocytes, Brown, chemistry, Liver, 030220 oncology & carcinogenesis, Sterol Regulatory Element Binding Protein 1
Abstract

Recent evidence has revealed a novel signaling mechanism through which brown adipose tissue (BAT)-derived exosomal microRNAs (miRNAs) influence hepatic gene expression. Here, we uncover neuronal control of these miRNAs and identify exosomal miR-132-3p as a regulator of hepatic lipogenesis under cold stress conditions. Norepinephrine, a sympathetic nervous system neurotransmitter mediating cold-induced BAT activation, altered the composition of brown adipocyte (BAC)-derived exosomal miRNAs; among them, miR-132-3p was significantly induced. The isolated BAC-derived exosomes suppressed expression of hepatic Srebf1, a predicted target of miR-132-3p. In an indirect co-culture system, BACs suppressed expression of hepatic Srebf1 and its target lipogenic genes; this effect was not seen with miR-132-3p-inhibited BACs. Srebf1 was experimentally validated as an miR-132-3p target. Cold stimuli consistently induced miR-132-3p expression in BAT and attenuated Srebf1 expression in the liver. Our results suggest that BAT-derived exosomal miR-132-3p acts as an endocrine factor that regulates hepatic lipogenesis for cold adaptation.

Published
2020

2. Na+–Ca2+ exchanger targeting miR-132 prevents apoptosis of cardiomyocytes under hypoxic condition by suppressing Ca2+ overload

Author

Hyang-Hee Seo, Jiyun Lee, Chang Yeon Lee, Seahyoung Lee, Soonchang Hong, Eunhyun Choi, Sung-Man Kim, Ki-Chul Hwang, and Kyung-Jong Yoo

Subjects
Programmed cell death, Biophysics, Apoptosis, Caspase 3, Biology, Real-Time Polymerase Chain Reaction, Biochemistry, Sodium-Calcium Exchanger, Toxicology, miR-132, microRNA, medicine, Animals, Myocytes, Cardiac, Molecular Biology, Cells, Cultured, Ca2 overload, Cell Biology, Hypoxia (medical), Rats, Cell biology, MicroRNAs, Calcium, medicine.symptom, Intracellular
Abstract

During ischemia-reperfusion (IR) injury of the heart, Ca(2+) overload occurs, leading to cardiomyocyte dysfunction and eventual cell death by apoptosis. Since preventing Ca(2+) overload during IR injury has been reported to protect cardiomyocytes, interrupting Ca(2+) signaling cascades leading to Ca(2+) overload may exert protective effect on cardiomyocytes under hypoxic condition. One of the key regulators of the intracellular Ca(2+) level during IR injury is Na(+)-Ca(2+) exchanger 1 (NCX1), whose down-regulation during IR injury conferred protection of heart. In the present study, we examined whether down-regulation of NCX1 using exogenous microRNA ameliorates apoptosis of cardiomyocytes under hypoxic condition. Here, we identified miR-132 as a novel microRNA targeting the NCX1, whose expression increased during hypoxia. Delivery of miR-132 suppressed the increase of intracellular Ca(2+) in cardiomyocytes under hypoxia, and the expressions of apoptotic molecules, such as Bax, cytochrome C, and caspase 3, and the number of apoptotic cells were also decreased by exogenous miR-132 treatment. These results suggest the potential of miR-132 as an effective therapeutic agent against IR damage to heart by preventing Ca(2+) overload during hypoxic condition and warrant further studies to validate its anti-apoptotic effect in vivo.

Published
2015
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3. MiR-132 regulates osteogenic differentiation via downregulating Sirtuin1 in a peroxisome proliferator-activated receptor β/δ-dependent manner

Author

Da Liu, Cai-ru Wang, Kai Gong, Jingsong Zhou, Liao Dongfa, Xianming Pan, and Bo Qu

Subjects
0301 basic medicine, medicine.medical_specialty, BALB 3T3 Cells, Cellular differentiation, Phosphatase, Biophysics, Peroxisome proliferator-activated receptor, Down-Regulation, Biochemistry, 03 medical and health sciences, miR-132, Mice, Downregulation and upregulation, Sirtuin 1, Osteogenesis, Internal medicine, medicine, Animals, Receptor, Molecular Biology, PPAR-beta, chemistry.chemical_classification, Osteoblasts, biology, Gene Expression Regulation, Developmental, Cell Differentiation, Cell Biology, Cell biology, PPAR gamma, MicroRNAs, 030104 developmental biology, Endocrinology, chemistry, biology.protein, Ectopic expression
Abstract

MicroRNAs (miRNAs) play significant roles in multiple diseases by regulating the expression of their target genes. Type 2 diabetes mellitus (T2DM) is a chronic endocrine and metabolic disease with complex mechanisms. T2DM can result in diabetic osteoporosis (DO), which is characterized by bone loss, decreased bone mineral density and increased bone fractures. The promotion of osteogenic differentiation of osteoblasts is an effective way to treat osteoporosis. In the present study, high glucose (HG) and free fatty acids (FFA) were employed to mimic T2DM in MC3T3-E1 cells. To induce osteogenic differentiation, MC3T3-E1 cells were cultured in osteogenic medium. The results showed that osteogenic differentiation was significantly suppressed by HG and FFA. We found that miR-132 expression was significantly upregulated and much higher in HG-FFA-induced cells than other selected miRNAs, indicating that miR-132 might play an important role in DO. Furthermore, overexpression of miR-132 markedly inhibited the expression of key markers of osteogenic differentiation and alkaline phosphatase (ALP) activity. Reciprocally, inhibition of miR-132 restored osteogenic differentiation, even under treatment with HG-FFA. We also showed that Sirtuin 1 (Sirt1) was one of the target genes of miR-132, whose expression was controlled by miR-132. Ectopic expression of Sirt1 reversed the decrease in osteogenic differentiation caused by miR-132 and HG-FFA. These results demonstrated the direct role of miR-132 in suppressing osteogenic differentiation through downregulating Sirt1. Moreover, we demonstrated that peroxisome proliferator-activated receptor β/δ (PPARβ/δ) was a downstream molecule of Sirt1, and its knockout by PPARβ/δ siRNA significantly abolished the promotive effects of Sirt1 on osteogenic differentiation, indicating that Sirt1 functioned in a PPARβ/δ-dependent manner. Taken together, we provide crucial evidence that miR-132 plays a key role in regulating osteogenic differentiation through Sirt1 in a PPARβ/δ-dependent manner, indicating that miR-132 and Sirt1-PPARβ/δ may act as potential therapeutic targets for T2DM-induced osteoporosis.

Published
2016

4. TGF-β induced miR-132 enhances the activation of TGF-β signaling through inhibiting SMAD7 expression in glioma cells

Author

Guo-Fei Li, Jian-Lei Zhang, Dong-Lin Zheng, Zhao-Hui Wang, Yan-Li Duan, and Qi-Shun Zhang

Subjects
Untranslated region, Male, Angiogenesis, Biophysics, medicine.disease_cause, Biochemistry, Cell Line, Smad7 Protein, miR-132, Transforming Growth Factor beta, Glioma, medicine, Humans, Molecular Biology, Chemistry, Brain Neoplasms, Brain, Cell Biology, medicine.disease, Cell biology, Gene Expression Regulation, Neoplastic, MicroRNAs, Biomarker (medicine), Female, Signal transduction, Carcinogenesis, Transforming growth factor, Signal Transduction
Abstract

Transforming growth factors β (TGF-β) pathway has been proven to play important roles in oncogenesis and angiogenesis of gliomas. MiR-132 might be related to TGF-β signaling pathway and high miR-132 expression was reported to be a biomarker of poor prognosis in patients diagnosed with glioma. However, the expression regulation way involved in TGF-β pathway and clinical significance of miR-132 have not been investigated in glioma cells. Here we reported that the mRNA level of miR-132 and TGF-β concentration were both increased in patients with brain glioma. Correlation analysis revealed that TGF-β concentration was positively correlated with mRNA level of miR-132. In addition, the mRNA level of miR-132 was up-regulated by TGF-β in a concentration-dependent and time-dependent manner. Furthermore, we found that miR-132 was involved in modulation of the TGF-β signaling pathway and down-regulation of SMAD7 expression by directly targeting the SMAD7 3'-UTR. MiR-132 was negatively correlated with SMAD7 in patients with brain glioma. Taken together, our results suggest that miR-132 could be stimulated by TGF-β and might enhance the activation of TGF-β signaling through inhibiting SMAD7 expression in glioma cells. These findings contribute to a better understanding of the mechanism of the activation of TGF-β signaling by miR-132.

Published
2015

5. MiR-132 regulates osteogenic differentiation via downregulating Sirtuin1 in a peroxisome proliferator-activated receptor β/δ-dependent manner.

Author

Gong K, Qu B, Liao D, Liu D, Wang C, Zhou J, and Pan X

Subjects
Animals, BALB 3T3 Cells, Cell Differentiation physiology, Down-Regulation physiology, Gene Expression Regulation, Developmental physiology, Mice, Osteoblasts cytology, MicroRNAs metabolism, Osteoblasts pathology, Osteogenesis physiology, PPAR gamma metabolism, PPAR-beta metabolism, Sirtuin 1 metabolism
Abstract

MicroRNAs (miRNAs) play significant roles in multiple diseases by regulating the expression of their target genes. Type 2 diabetes mellitus (T2DM) is a chronic endocrine and metabolic disease with complex mechanisms. T2DM can result in diabetic osteoporosis (DO), which is characterized by bone loss, decreased bone mineral density and increased bone fractures. The promotion of osteogenic differentiation of osteoblasts is an effective way to treat osteoporosis. In the present study, high glucose (HG) and free fatty acids (FFA) were employed to mimic T2DM in MC3T3-E1 cells. To induce osteogenic differentiation, MC3T3-E1 cells were cultured in osteogenic medium. The results showed that osteogenic differentiation was significantly suppressed by HG and FFA. We found that miR-132 expression was significantly upregulated and much higher in HG-FFA-induced cells than other selected miRNAs, indicating that miR-132 might play an important role in DO. Furthermore, overexpression of miR-132 markedly inhibited the expression of key markers of osteogenic differentiation and alkaline phosphatase (ALP) activity. Reciprocally, inhibition of miR-132 restored osteogenic differentiation, even under treatment with HG-FFA. We also showed that Sirtuin 1 (Sirt1) was one of the target genes of miR-132, whose expression was controlled by miR-132. Ectopic expression of Sirt1 reversed the decrease in osteogenic differentiation caused by miR-132 and HG-FFA. These results demonstrated the direct role of miR-132 in suppressing osteogenic differentiation through downregulating Sirt1. Moreover, we demonstrated that peroxisome proliferator-activated receptor β/δ (PPARβ/δ) was a downstream molecule of Sirt1, and its knockout by PPARβ/δ siRNA significantly abolished the promotive effects of Sirt1 on osteogenic differentiation, indicating that Sirt1 functioned in a PPARβ/δ-dependent manner. Taken together, we provide crucial evidence that miR-132 plays a key role in regulating osteogenic differentiation through Sirt1 in a PPARβ/δ-dependent manner, indicating that miR-132 and Sirt1-PPARβ/δ may act as potential therapeutic targets for T2DM-induced osteoporosis., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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6. TGF-β induced miR-132 enhances the activation of TGF-β signaling through inhibiting SMAD7 expression in glioma cells.

Author

Wang ZH, Zhang QS, Duan YL, Zhang JL, Li GF, and Zheng DL

Subjects
Brain metabolism, Brain Neoplasms metabolism, Cell Line, Female, Glioma metabolism, Humans, Male, MicroRNAs metabolism, Signal Transduction, Brain Neoplasms genetics, Gene Expression Regulation, Neoplastic, Glioma genetics, MicroRNAs genetics, Smad7 Protein genetics, Transforming Growth Factor beta metabolism
Abstract

Transforming growth factors β (TGF-β) pathway has been proven to play important roles in oncogenesis and angiogenesis of gliomas. MiR-132 might be related to TGF-β signaling pathway and high miR-132 expression was reported to be a biomarker of poor prognosis in patients diagnosed with glioma. However, the expression regulation way involved in TGF-β pathway and clinical significance of miR-132 have not been investigated in glioma cells. Here we reported that the mRNA level of miR-132 and TGF-β concentration were both increased in patients with brain glioma. Correlation analysis revealed that TGF-β concentration was positively correlated with mRNA level of miR-132. In addition, the mRNA level of miR-132 was up-regulated by TGF-β in a concentration-dependent and time-dependent manner. Furthermore, we found that miR-132 was involved in modulation of the TGF-β signaling pathway and down-regulation of SMAD7 expression by directly targeting the SMAD7 3'-UTR. MiR-132 was negatively correlated with SMAD7 in patients with brain glioma. Taken together, our results suggest that miR-132 could be stimulated by TGF-β and might enhance the activation of TGF-β signaling through inhibiting SMAD7 expression in glioma cells. These findings contribute to a better understanding of the mechanism of the activation of TGF-β signaling by miR-132., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Published
2015
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7. MiR-132 prohibits proliferation, invasion, migration, and metastasis in breast cancer by targeting HN1.

Author

Zhang ZG, Chen WX, Wu YH, Liang HF, and Zhang BX

Subjects
3' Untranslated Regions, Animals, Breast Neoplasms pathology, Cell Cycle Proteins, Cell Line, Tumor, Cell Movement genetics, Cell Proliferation genetics, Disease Progression, Female, Gene Expression Regulation, Neoplastic, Heterografts, Humans, Lung Neoplasms genetics, Lung Neoplasms metabolism, Lung Neoplasms secondary, Mice, Mice, Nude, Microtubule-Associated Proteins, Neoplasm Invasiveness genetics, Nuclear Proteins, Breast Neoplasms genetics, Breast Neoplasms metabolism, MicroRNAs genetics, MicroRNAs metabolism, Nerve Tissue Proteins genetics, Nerve Tissue Proteins metabolism, RNA, Neoplasm genetics, RNA, Neoplasm metabolism
Abstract

Accumulating evidence indicates that miRNAs play critical roles in tumorigenesis and cancer progression. This study aims to investigate the role and the underlying mechanism of miR-132 in breast cancer. Here, we report that miR-132 is significantly down-regulated in breast cancer tissues and cancer cell lines. Additional study identifies HN1 as a novel direct target of miR-132. MiR-132 down-regulates HN1 expression by binding to the 3' UTR of HN1 transcript, thereby, suppressing multiple oncogenic traits such as cancer cell proliferation, invasion, migration and metastasis in vivo and in vitro. Overexpression of HN1 restores miR-132-suppressed malignancy. Importantly, higher HN1 expression is significantly associated with worse overall survival of breast cancer patients. Taken together, our data demonstrate a critical role of miR-132 in prohibiting cell proliferation, invasion, migration and metastasis in breast cancer through direct suppression of HN1, supporting the potential utility of miR-132 as a novel therapeutic strategy against breast cancer., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Published
2014
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8. USF-1 inhibition protects against oxygen-and-glucose-deprivation-induced apoptosis via the downregulation of miR-132 in HepG2 cells.

Author

Wang R, Liang H, Li H, Dou H, Zhang M, Baobuhe, Du Z, Gao M, and Wang R

Subjects
Down-Regulation, Hep G2 Cells, Humans, Promoter Regions, Genetic, RNA, Small Interfering genetics, Apoptosis, Glucose metabolism, MicroRNAs genetics, Oxygen metabolism, RNA Interference, Upstream Stimulatory Factors genetics
Abstract

Upstream stimulatory factor 1 (USF-1) is an important transcription factor that participates in glucose metabolism and tumorigenesis. The aim of the current study was to explore the regulatory mechanism of USF-1 in HepG2 cells exposed to oxygen and glucose deprivation (OGD). After the establishment of the OGD model in HepG2 cells, we determined that the cells treated with OGD exhibited a high apoptotic rate and that the introduction of siRNA against USF-1 protected the cells from OGD-induced apoptosis. The miRNA microarray results demonstrated that a set of miRNAs were deregulated in the cells transfected with USF-1 siRNA, and the set of downregulated miRNAs included a novel miRNA, miR-132. Further analyses indicated that miR-132 overexpression inhibits the protective roles of USF-1 siRNA in OGD-induced apoptosis. We also identified several binding sites for USF-1 in the miR-132 promoter. The silencing of USF-1 resulted in a reduction in miR-132 expression, and USF-1 overexpression increased the expression of this miRNA. Our study indicated that the silencing of USF-1 plays protective roles in OGD-induced apoptosis through the downregulation of miR-132, which indicates that the silencing of USF-1 may be a therapeutic strategy for the promotion of cancer cell survival under OGD conditions., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Published
2014
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