scholarly journals Decreased Expression of Brg1 and β-Catenin in Nasal Epithelial Cells in CRSwNPs

2021 ◽  
Author(s):  
Yanli Tao ◽  
Huitao Zhu ◽  
Chengcheng Liu ◽  
Xiaoyan Sun ◽  
Tiejun Yuan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Expression Pattern ◽  
Complex Disease ◽  
Cell Structure ◽  
Disease Process ◽  
Chromatin Remodeling Complex ◽  
Cell Proliferation And Differentiation ◽  
Tnf Α ◽  
Proliferation And Differentiation

Abstract Background: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a pathophysiologically complex disease process characterized by chronic inflammation of the nose and epithelial cell structure remodeling. Objectives: Studies have shown that the chromatin remodeling complex subunit Brg1 can interact with β-catenin, which plays an important role in cell proliferation and differentiation. However, the role of Brg1 and β-catenin in epithelial cells of chronic rhinitis and sinusitis remains unclear. Material and Methods: We detected the expression level of Brg1 in CRSwNP by qPCR, and observed the expression pattern of Brg1 in CRSwNP by immunohistochemistry and immunofluorescence. HNEpC cells were used to detect the expression changes of the two proteins after TNF-α stimulation. Results: In our study, the expression levels of Brg1 and β-catenin are significantly decreased in nasal mucosa of CRSwNP patients. To our interest, we also observed expression decrease and expression pattern changes of Brg1 and β-catenin by stimulating HNEpCs cells with TNF-α. Conclusions: This study shows that the expression of Brg1 and β-catenin may be related to the development of CRSwNPs.Subject classification codes: include these here if the journal requires them

scholarly journals Epithelial c-jun and c-fos are temporally and spatially regulated by estradiol during neonatal rat oviduct differentiation

2004 ◽  
Vol 182 (2) ◽  
pp. 219-227 ◽  
Author(s):  
A Okada ◽  
Y Ohta ◽  
SL Brody ◽  
T Iguchi
Keyword(s):  
Cell Proliferation ◽  
Transcription Factors ◽  
Epithelial Cells ◽  
Neonatal Rat ◽  
Cellular Mechanisms ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Ciliated Epithelial Cells ◽  
The Relationship

Expression of transcription factors binding to the activating protein-1 (AP-1) site is induced by estrogens in association with epithelial proliferation in the uterus, but, in the oviduct, the relationship between cell proliferation and differentiation and AP-1 transcription factors is not well understood. In the developing rat oviduct, we found that proliferation and differentiation of epithelial cells were region-dependently regulated by 17beta-estradiol (E2). To determine the role of AP-1 transcription factors in the development of rat oviduct, we performed immunohistochemistry for epithelial c-jun and c-fos proteins in E2-untreated and -treated newborn rats. E2 increased the expression of c-jun and c-fos during proliferation of undifferentiated epithelial cells, but diminished both proteins during accelerated differentiation of ciliated epithelial cells. A pure estrogen receptor (ER) antagonist, ICI 182,780, inhibited changes in their expression during both cell proliferation and differentiation. Importantly, no reduction of c-jun was noted in the epithelial cells of the foxj1-deficient oviduct, which lacks cilia development. This study shows that c-jun and c-fos are regulated during epithelial cell proliferation and differentiation in a region-specific manner. This provides critical information for understanding the molecular and cellular mechanisms of the development of the neonatal oviduct.

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

scholarly journals Chandipura virus dysregulates the expression of hsa-miR-21-5p to activate NF-κB in human microglial cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Neha Pandey ◽  
Meghana Rastogi ◽  
Sunit K. Singh
Keyword(s):  
Expression Pattern ◽  
Case Fatality ◽  
Microglial Cells ◽  
Luciferase Assay ◽  
Western India ◽  
Cellular Mirnas ◽  
Over Expression ◽  
Chandipura Virus ◽  
Tnf Α

Abstract Background Chandipura virus (CHPV) is a negative single-stranded RNA virus of the Rhabdoviridae family. CHPV infection has been reported in Central and Western India. CHPV causes acute encephalitis with a case fatality rate of 70 % and mostly affects children below 15 years of age. CHPV infection in brain leads to neuronal apoptosis and activation of the microglial cells. The microRNAs (miRNAs) are small endogenous non-coding RNA that regulate the gene expression. Viral infections perturb the expression pattern of cellular miRNAs, which may in turn affect the expression pattern of downstream genes. This study aims to investigate hsa-miR-21-5p mediated regulation of PTEN, AKT, NF-ĸBp65, IL-6, TNF-α, and IL-1β, in human microglial cells during CHPV infection. Methods To understand the role of hsa-miR-21-5p in CHPV infection, the human microglial cells were infected with CHPV (MOI-0.1). Real-time PCR, western blotting, Luciferase assay, over-expression and knockdown techniques were used to understand the role of hsa-miR-21-5p in the regulation of PTEN, AKT and, NF-ĸBp65, IL-6, TNF-α, and IL-1β in this study. Results The hsa-miR-21-5p was found to be upregulated during CHPV infection in human microglial cells. This led to the downregulation of PTEN which promoted the phosphorylation of AKT and NF-ĸBp65. Over-expression of hsa-miR-21-5p led to the decreased expression of PTEN and promoted further phosphorylation of AKT and NF-ĸBp65 in human microglial cells. However, the inhibition of hsa-miR-21-5p using hsa-miR-21-5p inhibitor restored the expression. Conclusions This study supports the role of hsa-miR-21-5p in the regulation of pro-inflammatory genes in CHPV infected human microglial cells.

scholarly journals Identification of a microRNA signature in renal fibrosis: role of miR-21

2011 ◽  
Vol 301 (4) ◽  
pp. F793-F801 ◽  
Author(s):  
Abolfazl Zarjou ◽  
Shanzhong Yang ◽  
Edward Abraham ◽  
Anupam Agarwal ◽  
Gang Liu
Keyword(s):  
Epithelial Cells ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Response To Treatment ◽  
Tubular Epithelial Cells ◽  
Altered Expression ◽  
Tnf Α ◽  
Tgf Β1

Renal fibrosis is a final stage of many forms of kidney disease and leads to impairment of kidney function. The molecular pathogenesis of renal fibrosis is currently not well-understood. microRNAs (miRNAs) are important players in initiation and progression of many pathologic processes including diabetes, cancer, and cardiovascular disease. However, the role of miRNAs in kidney injury and repair is not well-characterized. In the present study, we found a unique miRNA signature associated with unilateral ureteral obstruction (UUO)-induced renal fibrosis. We found altered expression in UUO kidneys of miRNAs that have been shown to be responsive to stimulation by transforming growth factor (TGF)-β1 or TNF-α. Among these miRNAs, miR-21 demonstrated the greatest increase in UUO kidneys. The enhanced expression of miR-21 was located mainly in distal tubular epithelial cells. miR-21 expression was upregulated in response to treatment with TGF-β1 or TNF-α in human renal tubular epithelial cells in vitro. Furthermore, we found that blocking miR-21 in vivo attenuated UUO-induced renal fibrosis, presumably through diminishing the expression of profibrotic proteins and reducing infiltration of inflammatory macrophages in UUO kidneys. Our data suggest that targeting specific miRNAs could be a novel therapeutic approach to treat renal fibrosis.

An oligomer complementary to c-myc mRNA inhibits proliferation of HL-60 promyelocytic cells and induces differentiation

1988 ◽  
Vol 8 (2) ◽  
pp. 963-973
Author(s):  
J T Holt ◽  
R L Redner ◽  
A W Nienhuis
Keyword(s):  
Cell Growth ◽  
Protein Concentration ◽  
Myeloid Differentiation ◽  
Sequence Specificity ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Steady State Levels ◽  
Cell Growth And Differentiation ◽  
Antisense Oligomer

To study the role of a nuclear proto-oncogene in the regulation of cell growth and differentiation, we inhibited HL-60 c-myc expression with a complementary antisense oligomer. This oligomer was stable in culture and entered cells, forming an intracellular duplex. Incubation of cells with the anti-myc oligomer decreased the steady-state levels of c-myc protein by 50 to 80%, whereas a control oligomer did not significantly affect the c-myc protein concentration. Direct inhibition of c-myc expression with the anti-myc oligomer was associated with a decreased cell growth rate and an induction of myeloid differentiation. Related antisense oligomers with 2- to 12-base-pair mismatches with c-myc mRNA did not influence HL-60 cells. Thus, the effects of the antisense oligomer exhibited sequence specificity, and furthermore, these effects could be reversed by hybridization competition with another complementary oligomer. Antisense inhibition of a nuclear proto-oncogene apparently bypasses cell surface events in affecting cell proliferation and differentiation.

Questioning Role of Hypochloremia in Bronchopulmonary Dysplasia

PEDIATRICS ◽  
1986 ◽  
Vol 78 (6) ◽  
pp. 1173-1173
Author(s):  
JEFFREY M. PERLMAN ◽  
JEFF DAWSON
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Metabolic Alkalosis ◽  
Complex Disease ◽  
Disease Process ◽  
Control Group ◽  
Study Group

In Reply.— We appreciate the interest in our report published in Pediatrics (1986;77:212-216). The three letters raise similar questions, and in response we would like to make three points. First, including the two infants in the control group who died with the infants in the study group still resulted in significant differences between the two groups regarding duration of furosemide (Lasix) therapy, hypochloremia, or metabolic alkalosis (P > .001). Second (as noted in our discussion), bronchopulmonary dysplasia is a complex disease process.

scholarly journals The Role of the Hedgehog Pathway in Cholangiocarcinoma

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4774
Author(s):  
Giulia Anichini ◽  
Laura Carrassa ◽  
Barbara Stecca ◽  
Fabio Marra ◽  
Chiara Raggi
Keyword(s):  
Anticancer Agents ◽  
Cell Biology ◽  
Detailed Knowledge ◽  
Molecular Features ◽  
Cell Proliferation And Differentiation ◽  
Predominant Type ◽  
Proliferation And Differentiation ◽  
Cholangiocarcinoma Cell ◽  
Hh Signaling

Cholangiocarcinoma (CCA) is a poorly treatable type of cancer and, along with hepatocellular carcinoma (HCC), is the predominant type of primitive liver cancer in adults. The lack of understanding of CCA biology has slowed down the identification of novel targets and the development of effective treatments. While tumors share some general characteristics, detailed knowledge of specific features is essential for the development of effectively tailored therapeutic approaches. The Hedgehog (HH) signaling cascade regulates stemness biology, embryonal development, tissue homeostasis, and cell proliferation and differentiation. Its aberrant activation has been associated with a variety of solid and hematological human malignancies. Several HH-inhibiting compounds have been indeed developed as potential anticancer agents in different types of tumors, with Smoothened and GLI inhibitors showing the most promising results. Beside its well-established function in other tumors, findings regarding the HH signaling in CCA are still controversial. Here we will give an overview of the most important clinical and molecular features of cholangiocarcinoma, and we will discuss the available evidence of the crosstalk between the HH signaling pathway and the cholangiocarcinoma cell biology.

scholarly journals MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhuo-Ma Luoreng ◽  
Da-Wei Wei ◽  
Xing-Ping Wang
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Bovine Mammary Epithelial Cells ◽  
Tnf Α

AbstractMastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3′ untranslated region (3′ UTR) of the NKIRAS2, but not the 3′UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.

scholarly journals Mechanical Growth Factor Promotes FOXP3 Expression in Regulatory T Cells and Enhances Its Function in Treating Ankylosing Spondylitis

2021 ◽  
Author(s):  
Hongyu Qin ◽  
Shuangshuang Yuan ◽  
Hao Zeng ◽  
Hao Li ◽  
Jinsong Yang
Keyword(s):  
Ankylosing Spondylitis ◽  
Growth Factor ◽  
Bone Destruction ◽  
Foxp3 Expression ◽  
Treg Cells ◽  
Control Group ◽  
Related Factors ◽  
Cell Proliferation And Differentiation ◽  
Tnf Α ◽  
Proliferation And Differentiation

Abstract Objective: We aimed to verify whether mechanical growth factor (MGF) may be an effective target for treating ankylosing spondylitis. Methods: FOXP3 expression was measured in Treg cells from healthy male subjects administered MGF. A rat model of ankylosing spondylitis was established, and the level of ankylosing spondylitis-related factors (tumor necrosis factor [TNF]-α, interleukin [IL]-2, and IL-10) was measured. Results: We found that the proliferation and total number of Treg cells, as well as FOXP3 expression, significantly increased in the MGF-treated groups compared with those in the control. The level of inflammation, bone destruction, and new bone formation significantly decreased in rats treated with MGF compared with those in the control group. TNF-α expression significantly decreased, whereas the IL-2 and IL-10 levels significantly increased in the MGF group compared with those in the control. Conclusions: MGF may delay disease progression in ankylosing rats by inducing FOXP3 expression, promoting FOXP3+ Treg cell proliferation and differentiation, reducing TNF-α expression, and increasing IL-10 and IL-2 expression.

Role of miR-214 in biomaterial transplantation therapy for osteonecrosis

2021 ◽  
pp. 1-13
Author(s):  
Yuying Wang ◽  
Rui He ◽  
Anqi Yang ◽  
Rui Guo ◽  
Jie Liu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Formation ◽  
Bone Scaffold ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Marrow Mesenchymal Stem Cells ◽  
Transplantation Therapy ◽  
Cells Cultured ◽  
In Cells

BACKGROUND: The effectiveness and availability of conservative therapies for osteonecrosis of the femoral head (ONFH) are limited. Transplantation of bone marrow mesenchymal stem cells (BMSCs) combined with Bio-Oss, which is a good bone scaffold biomaterial for cell proliferation and differentiation, is a new potential therapy. Of note, the expression of miRNAs was significantly modified in cells cultured with Bio-Oss, and MiR-214 was correlated positively with osteonecrosis. Furthermore, miR-214 was upregulated in cells exposed to Bio-Oss. OBJECTIVE: To investigate whether targeting miR-214 further improves the transplantation effect. METHODS: We treated BMSCs with agomiR-214 (a miR-214 agonist), antagomiR-214 (a miR-214 inhibitor), or vehicle, followed by their transplantation into ONFH model rats. RESULTS: Histological and histomorphometric data showed that bone formation was significantly increased in the experimental groups (Bio-Oss and BMSCs treated with antagomiR-214) compared with other groups. CONCLUSIONS: miR-214 participates in the inhibition of osteoblastic bone formation, and the inhibition of miR-214 to bone formation during transplantation therapy with Bio-Oss combined with BMSCs for ONFH.

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