12 results on '"Xia Xiong"'
Search Results
2. The influence of benzoyl peroxide on skin microbiota and the epidermal barrier for acne vulgaris
- Author
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Lin Zhou, Lingna Chen, Xueping Liu, Yukun Huang, Yong Xu, Xia Xiong, and Yongqiong Deng
- Subjects
Drug Combinations ,Young Adult ,Treatment Outcome ,Benzoyl Peroxide ,Microbiota ,RNA, Ribosomal, 16S ,Acne Vulgaris ,Humans ,Dermatologic Agents ,Dermatology ,General Medicine ,Gels - Abstract
The disordered skin microbiome has been reported to contribute to the pathogenesis of acne vulgaris, for which benzoyl peroxide (BPO) has long been recommended as the first-line therapy. However, there are no data regarding the effect of BPO treatment on skin microbiota and the epidermal barrier in young adults with acne vulgaris. Thirty-three patients with acne vulgaris and 19 healthy controls were enrolled in the study. All patients received topical treatment with BPO 5% gel for 12 weeks. The epidermal barrier was analyzed at baseline and after treatment. Microbial diversity was analyzed using a high-throughput sequencing approach targeting the V3-V4 region of 16S rRNA genes. After receiving treatment with BPO, patients had significant improvement in their Global Acne Grading System (GAGS) score, porphyrin, and red areas (p 0.05), and the presence of sebum, stratum corneum hydration (SCH), and transepidermal water loss (TEWL) increased (p 0.05). When compared with baseline, microbial diversity was significantly reduced after treatment, as calculated by the goods coverage (p = 0.0017), Shannon (p = 0.0094), and Simpson (p = 0.0017) diversity indices. The prevalence of the genus Cutibacterium (before treatment: 5.64 [3.50, 7.78] vs. after treatment: 2.43 [1.81, 3.05], p = 0.011) was significantly reduced after treatment while Staphylococcus (before treatment: 43.80 [36.62, 50.98] vs. after treatment: 53.38 [44.88, 61.87], p = 0.075) tended to increase. The abundance of Staphylococcus was negatively associated with SCH (p = 0.008, r = -0.286). Despite its contribution to an improved GAGS score, BPO treatment for acne vulgaris may reduce microbial diversity and damage the epidermal barrier.
- Published
- 2022
3. Nrf2 Overexpression for the Protective Effect of Skin-Derived Precursors against UV-Induced Damage: Evidence from a Three-Dimensional Skin Model
- Author
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Qirong Lei, Li Xian, Dehai Xian, Jing Song, Jixiang Xu, Jianqiao Zhong, and Xia Xiong
- Subjects
Keratinocytes ,0301 basic medicine ,Aging ,Article Subject ,NF-E2-Related Factor 2 ,Ultraviolet Rays ,Apoptosis ,medicine.disease_cause ,Biochemistry ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,chemistry.chemical_compound ,Organ Culture Techniques ,0302 clinical medicine ,medicine ,Humans ,LY294002 ,Photosensitivity Disorders ,lcsh:QH573-671 ,Protein kinase B ,Cells, Cultured ,PI3K/AKT/mTOR pathway ,Skin ,chemistry.chemical_classification ,Reactive oxygen species ,lcsh:Cytology ,Chemistry ,Stem Cells ,Cell Biology ,General Medicine ,Fibroblasts ,Cytoprotection ,Up-Regulation ,Cell biology ,Oxidative Stress ,030104 developmental biology ,030220 oncology & carcinogenesis ,Photoprotection ,Reactive Oxygen Species ,Heme Oxygenase-1 ,Oxidative stress ,Research Article ,Signal Transduction - Abstract
Background. Skin photodamage is associated with ultraviolet- (UV-) induced reactive oxygen species (ROS) overproduction and nuclear factor erythroid 2-related factor 2 (Nrf2) inactivation. In our previous study, skin-derived precursors (SKPs) were shown to ameliorate a UV-induced damage in mice, probably through Nrf2 activation and ROS scavenging. Objective. To clarify the mechanism underlying the photoprotective effect of SKPs against UV-induced damage in a three-dimensional (3D) skin model. Methods. The Nrf2 gene in SKPs was modified using lentiviral infection, and 3D skin models were reconstructed with keratinocytes and fibroblasts on the basis of type I collagen. Subsequently, these models were divided into the following six groups: normal, model, overexpressed, control, silenced, and negative control groups. Prior to irradiation, respective SKPs were injected into the last four groups. Next, all groups except the normal group were exposed to UVA+UVB. Lastly, the pathological and molecular-biological techniques were employed to determine the parameters. Additionally, LY294002, a PI3K inhibitor, was used to investigate the roles of PI3K/Akt and Nrf2/hemeoxygenase-1 (HO-1) in SKP photoprotection. Results. Normal 3D skin models appeared as milky-white analogs with a clear, well-arranged histological structure. After the skin was exposed to irradiation, it exhibited cell swelling and a disorganized structure and developed nuclear condensation with numerous apoptotic cells. The expressions of cellular protective genes and Nrf2/HO-1/PI3K/Akt proteins remarkably decreased, which were accompanied by increased oxidative stress and decreased antioxidants (P<0.05). However, these phenomena were reversed by nrf2-overexpressing SKPs. The 3D skin in the overexpressed group showed mild swelling, neatly arranged cells, and few apoptotic cells. Cellular protective genes and Nrf2/HO-1/PI3K/Akt proteins were highly expressed, and the oxidative biomarkers were remarkably ameliorated (P<0.05). Nevertheless, the expression of these proteins decreased after LY294002 pretreatment regardless of SKP treatment or not. Meanwhile, there were increases in both UV-induced apoptotic cells and ROS level accompanied with SOD and GPX decrease in the presence of LY294002. Conclusions. Evidence from the 3D skin model demonstrates that the protection of SKPs against UV-mediated damage is primarily via the PI3K/Akt-mediated activation of the Nrf2/HO-1 pathway, indicating that SKPs may be a promising candidate for the treatment of photodermatoses.
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- 2019
4. Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses
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Rui Lai, Jianqiao Zhong, Lingyu Yang, Dehai Xian, Jing Song, and Xia Xiong
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0301 basic medicine ,Aging ,Angiogenesis ,Review Article ,Fibroblast growth factor ,Skin Diseases ,Biochemistry ,Neovascularization ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Humans ,lcsh:QH573-671 ,Thrombospondin ,Angiostatin ,Neovascularization, Pathologic ,lcsh:Cytology ,business.industry ,Proteolytic enzymes ,Cell Biology ,General Medicine ,Vascular endothelial growth factor ,Oxidative Stress ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,Cancer research ,medicine.symptom ,Endostatin ,business ,Oxidation-Reduction - Abstract
Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.
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- 2019
5. The Landscape of Interactions between Hypoxia-Inducible Factors and Reactive Oxygen Species in the Gastrointestinal Tract
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Yirui Shao, Yulong Yin, Kexing Wang, Ruilin Huang, Jian Zhou, Zhiliang Tan, Xia Xiong, Lijun Zou, Hongnan Liu, Gang Liu, and Ming Qi
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Aging ,Cell signaling ,Gastrointestinal Diseases ,Oxidative phosphorylation ,Review Article ,Biochemistry ,Immunity ,Animals ,Humans ,chemistry.chemical_classification ,Reactive oxygen species ,Gastrointestinal tract ,QH573-671 ,Chemistry ,Cell Biology ,General Medicine ,Hypoxia-Inducible Factor 1, alpha Subunit ,Cell Hypoxia ,Oxygen tension ,Cell biology ,Gastrointestinal Tract ,Oxidative Stress ,Hypoxia-inducible factors ,Reactive Oxygen Species ,Cytology ,Homeostasis ,Signal Transduction - Abstract
The gastrointestinal tract (GT) is the major organ involved in digestion, absorption, and immunity, which is prone to oxidative destruction by high levels of reactive oxygen species (ROS) from luminal oxidants, such as food, drugs, and pathogens. Excessive ROS will lead to oxidative stresses and disrupt essential biomolecules, which also act as cellular signaling molecules in response to growth factors, hormones, and oxygen tension changes. Hypoxia-inducible factors (HIFs) are critical regulators mediating responses to cellular oxygen tension changes, which are also involved in energy metabolism, immunity, renewal, and microbial homeostasis in the GT. This review discusses interactions between HIF (mainly HIF-1α) and ROS and relevant diseases in the GT combined with our lab’s work. It might help to develop new therapies for gastrointestinal diseases associated with ROS and HIF-1α.
- Published
- 2021
6. Emerging Perspective: Role of Increased ROS and Redox Imbalance in Skin Carcinogenesis
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Dehai Xian, Jing Song, Jianqiao Zhong, Xia Xiong, and Rui Lai
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0301 basic medicine ,Aging ,Programmed cell death ,Skin Neoplasms ,Cell ,Review Article ,Gene mutation ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Humans ,lcsh:QH573-671 ,integumentary system ,business.industry ,lcsh:Cytology ,Cell Biology ,General Medicine ,Epigenome ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Cancer research ,Skin cancer ,Signal transduction ,Carcinogenesis ,business ,Reactive Oxygen Species ,Oxidation-Reduction ,Oxidative stress - Abstract
Strategies to battle malignant tumors have always been a dynamic research endeavour. Although various vehicles (e.g., chemotherapeutic therapy, radiotherapy, surgical resection, etc.) are used for skin cancer management, they mostly remain unsatisfactory due to the complex mechanism of carcinogenesis. Increasing evidence indicates that redox imbalance and aberrant reactive oxygen species (ROS) are closely implicated in the oncogenesis of skin cancer. When ROS production goes beyond their clearance, excessive or accumulated ROS could disrupt redox balance, induce oxidative stress, and activate the altered ROS signals. These would damage cellular DNA, proteins, and lipids, further leading to gene mutation, cell hyperproliferation, and fatal lesions in cells that contribute to carcinogenesis in the skin. It has been known that ROS-mediated skin carcinogenesis involves multiple ways, including modulating related signaling pathways, changing cell metabolism, and causing the instability of the genome and epigenome. Nevertheless, the exact role of ROS in skin cancer has not been thoroughly elucidated. In spite of ROS inducing skin carcinogenesis, toxic-dose ROS could trigger cell death/apoptosis and, therefore, may be an efficient therapeutic tool to battle skin cancer. Considering the dual role of ROS in the carcinogenesis and treatment of skin cancer, it would be essential to clarify the relationship between ROS and skin cancer. Thus, in this review, we get the related data together to seek the connection between ROS and skin carcinogenesis. Besides, strategies basing on ROS to fight skin cancer are discussed.
- Published
- 2019
7. miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42/β-Catenin Signaling
- Author
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Hong-Yan Zhang, Li-Xia Xiong, Qing-Yun Huang, Jing Duan, Wen Ding, Xiangtong Lu, Xian-Ling Qian, Jun Li, Xing-Hua Xiao, and Lin-Chen Lv
- Subjects
0301 basic medicine ,endocrine system ,lcsh:RC648-665 ,Cell division ,Article Subject ,Endocrine and Autonomic Systems ,Cell growth ,business.industry ,Endocrinology, Diabetes and Metabolism ,Stimulation ,CDC42 ,lcsh:Diseases of the endocrine glands. Clinical endocrinology ,Cell biology ,Blot ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Endocrinology ,Downregulation and upregulation ,Cell culture ,030220 oncology & carcinogenesis ,microRNA ,Medicine ,business ,Research Article - Abstract
Background. Diabetes is a progressive metabolic disease characterized by hyperglycemia. Functional impairment of islet β cells can occur to varying degrees. This impairment can initially be compensated for by proliferation and metabolic changes of β cells. Cell division control protein 42 (Cdc42) and the microRNA (miRNA) miR-29 have important roles in β-cell proliferation and glucose-stimulated insulin secretion (GSIS), which we further explored using the mouse insulinoma cell line MIN6. Methods. Upregulation and downregulation of miR-29a and Cdc42 were accomplished using transient transfection. miR-29a and Cdc42 expression was detected by real-time PCR and western blotting. MIN6 proliferation was detected using a cell counting kit assay. GSIS under high-glucose (20.0 mM) or basal-glucose (5.0 mM) stimulation was detected by enzyme-linked immunosorbent assay. The miR-29a binding site in the Cdc42 mRNA 3′-untranslated region (UTR) was determined using bioinformatics and luciferase reporter assays. Results. miR-29a overexpression inhibited proliferation (P<0.01) and GSIS under high-glucose stimulation (P<0.01). Cdc42 overexpression promoted proliferation (P<0.05) and GSIS under high-glucose stimulation (P<0.05). miR-29a overexpression decreased Cdc42 expression (P<0.01), whereas miR-29a downregulation increased Cdc42 expression (P<0.01). The results showed that the Cdc42 mRNA 3′-UTR is a direct target of miR-29a in vitro. Additionally, Cdc42 reversed miR-29a-mediated inhibition of proliferation and GSIS (P<0.01). Furthermore, miR-29a inhibited β-catenin expression (P<0.01), whereas Cdc42 promoted β-catenin expression (P<0.01). Conclusion. By negatively regulating Cdc42 and the downstream molecule β-catenin, miR-29a inhibits MIN6 proliferation and insulin secretion.
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- 2019
8. Proanthocyanidins against Oxidative Stress: From Molecular Mechanisms to Clinical Applications
- Author
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Rui Lai, Lingyu Yang, Dehai Xian, Jianqiao Zhong, Xia Xiong, and Jing Song
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0301 basic medicine ,DNA repair ,lcsh:Medicine ,Review Article ,Mitochondrion ,medicine.disease_cause ,General Biochemistry, Genetics and Molecular Biology ,Pathogenesis ,03 medical and health sciences ,In vivo ,medicine ,Animals ,Humans ,Proanthocyanidins ,chemistry.chemical_classification ,Reactive oxygen species ,General Immunology and Microbiology ,lcsh:R ,food and beverages ,General Medicine ,In vitro ,Oxidative Stress ,030104 developmental biology ,Biochemistry ,chemistry ,Chronic Disease ,Signal transduction ,Oxidative stress ,Signal Transduction - Abstract
Proanthocyanidins (PCs) are naturally occurring polyphenolic compounds abundant in many vegetables, plant skins (rind/bark), seeds, flowers, fruits, and nuts. Numerousin vitroandin vivostudies have demonstrated myriad effects potentially beneficial to human health, such as antioxidation, anti-inflammation, immunomodulation, DNA repair, and antitumor activity. Accumulation of prooxidants such as reactive oxygen species (ROS) exceeding cellular antioxidant capacity results in oxidative stress (OS), which can damage macromolecules (DNA, lipids, and proteins), organelles (membranes and mitochondria), and whole tissues. OS is implicated in the pathogenesis and exacerbation of many cardiovascular, neurodegenerative, dermatological, and metabolic diseases, both through direct molecular damage and secondary activation of stress-associated signaling pathways. PCs are promising natural agents to safely prevent acute damage and control chronic diseases at relatively low cost. In this review, we summarize the molecules and signaling pathways involved in OS and the corresponding therapeutic mechanisms of PCs.
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- 2018
9. Pruritus: Progress toward Pathogenesis and Treatment
- Author
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Jing Song, Dehai Xian, Jianqiao Zhong, Xia Xiong, Rui Lai, and Lingyu Yang
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0301 basic medicine ,medicine.medical_specialty ,lcsh:Medicine ,Review Article ,General Biochemistry, Genetics and Molecular Biology ,Pathogenesis ,030207 dermatology & venereal diseases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Chinese traditional ,medicine ,Humans ,Cutaneous symptom ,Medicine, Chinese Traditional ,skin and connective tissue diseases ,General Immunology and Microbiology ,integumentary system ,business.industry ,Pruritus ,lcsh:R ,General Medicine ,Dermatology ,body regions ,030104 developmental biology ,chemistry ,Itching ,medicine.symptom ,business ,Histamine ,Signal Transduction - Abstract
Pruritus, the most common cutaneous symptom, is widely seen in many skin complaints. It is an uncomfortable feeling on the skin and sometimes impairs patients’ quality of life. At present, the specific mechanism of pruritus still remains unclear. Antihistamines, which are usually used to relieve pruritus, ineffectively work in some patients with itching. Recent evidence has suggested that, apart from histamine, many mediators and signaling pathways are involved in the pathogenesis of pruritus. Various therapeutic options for itching correspondingly have been developed. In this review, we summarize the updated pathogenesis and therapeutic strategies for pruritus.
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- 2018
10. Therapeutic Hotline. Oral allicin in the treatment of Behcet's disease through attenuating oxidative stress: A pilot study in 20 patients with mucocutaneous lesions
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Dehai Xian, Jianqiao Zhong, Xia Xiong, and Junxiang Liu
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Adult ,Male ,medicine.medical_specialty ,Time Factors ,Scoring system ,Antioxidant ,medicine.medical_treatment ,Mucocutaneous zone ,Administration, Oral ,Pilot Projects ,Dermatology ,Behcet's disease ,Disease ,medicine.disease_cause ,Severity of Illness Index ,Gastroenterology ,Antioxidants ,Young Adult ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Effective treatment ,Disulfides ,Oral Ulcer ,Ulcer ,Aged ,Allicin ,business.industry ,Behcet Syndrome ,Remission Induction ,General Medicine ,Middle Aged ,Sulfinic Acids ,medicine.disease ,Surgery ,Oxidative Stress ,Treatment Outcome ,chemistry ,030220 oncology & carcinogenesis ,Female ,Genital Diseases, Male ,business ,Genital Diseases, Female ,Biomarkers ,030217 neurology & neurosurgery ,Oxidative stress - Abstract
Behcet's disease (BD) involves oxidative stress (OS) aggression and imbalanced oxidant/antioxidant status. Owing to its antioxidant property, allicin is proposed for treating BD. In this study, we aimed to investigate the efficacy and safety of allicin on patients with BD with mucocutaneous involvement. Twenty patients with active BD were treated with allicin for 12 weeks and followed up to 16 weeks. A clinical manifestations index and scoring system was the primary technique for efficacy evaluation at baseline and Week 4, 12, 16. The secondary efficacy variables were OS-related biomarkers determined at first and final visit. Side effects were assessed at each visit. By the end of study, 18 patients completed the trail. Allicin was effective in decreasing ulcer and cutaneous parameters (p
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- 2016
11. The Evaluation of Music Teaching in Colleges and Universities Based on Machine Learning
- Author
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Xia Xiongjun and Danmeng Lv
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Mathematics ,QA1-939 - Abstract
With the implementation of the strategic policy of rejuvenating the country through science and education, many innovative and practical teaching concepts and teaching models have been comprehensively developed. This breaks the backward teaching mode of traditional teaching activities. With the development of science and technology and Internet technology, deep learning is widely used in the field of education. Music teachers in colleges and universities constantly update their teaching methods and comprehensively use a variety of methods to carry out in-depth teaching in the classroom, and strive to stimulate students’ learning Interest and enthusiasm, and comprehensively enhance students’ music aesthetic ability. This article uses decision tree algorithms, support vector machines, Bayesian theory, and random forest four different classification techniques to evaluate the student curriculum evaluation dataset. Classification experiment: through the analysis of the experimental results, the performance of the four classifier models was compared, and the data showed the difference in accuracy, precision, recall, and F1 value of the four classifiers. At the same time, each of the classifier models was analyzed. This article verifies the effectiveness of machine learning models in curriculum evaluation and higher education mining, the importance of evaluation features.
- Published
- 2022
- Full Text
- View/download PDF
12. miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42/β-Catenin Signaling
- Author
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Jing Duan, Xian-Ling Qian, Jun Li, Xing-Hua Xiao, Xiang-Tong Lu, Lin-Chen Lv, Qing-Yun Huang, Wen Ding, Hong-Yan Zhang, and Li-Xia Xiong
- Subjects
Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
Background. Diabetes is a progressive metabolic disease characterized by hyperglycemia. Functional impairment of islet β cells can occur to varying degrees. This impairment can initially be compensated for by proliferation and metabolic changes of β cells. Cell division control protein 42 (Cdc42) and the microRNA (miRNA) miR-29 have important roles in β-cell proliferation and glucose-stimulated insulin secretion (GSIS), which we further explored using the mouse insulinoma cell line MIN6. Methods. Upregulation and downregulation of miR-29a and Cdc42 were accomplished using transient transfection. miR-29a and Cdc42 expression was detected by real-time PCR and western blotting. MIN6 proliferation was detected using a cell counting kit assay. GSIS under high-glucose (20.0 mM) or basal-glucose (5.0 mM) stimulation was detected by enzyme-linked immunosorbent assay. The miR-29a binding site in the Cdc42 mRNA 3′-untranslated region (UTR) was determined using bioinformatics and luciferase reporter assays. Results. miR-29a overexpression inhibited proliferation (P
- Published
- 2019
- Full Text
- View/download PDF
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