alexa MicroRNA-150 Regulates Lipid Metabolism and Inflammatory Response | Open Access Journals
ISSN: 2167-0943
Journal of Metabolic Syndrome
Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

MicroRNA-150 Regulates Lipid Metabolism and Inflammatory Response

Nanlan Luo1, W. Timothy Garvey1,2, Da-Zhi Wang3 and Yuchang Fu1*
1Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294-3360, USA
2Birmingham VA Medical Center, Birmingham, AL 35233, USA
3Department of Cardiology, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Corresponding Author : Yuchang Fu
Department of Nutrition Sciences
The University of Alabama at Birmingham
Shelby Building/1213, 1825 University Boulevard
Birmingham, AL 35294-0012, USA
Tel: 205-996-4013
Fax: 205-996-5896
E-mail: yfu@uab.edu
Received October 23, 2013; Accepted November 15, 2013; Published November 22, 2013
Citation: Luo N, Garvey WT, Wang D-Z, Fu Y (2013) MicroRNA-150 Regulates Lipid Metabolism and Inflammatory Response. J Metabolic Synd 2:131. doi:10.4172/2167-0943.1000131
Copyright: © 2013 Luoa N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Metabolic Syndrome

Abstract

Background: MicroRNAs (miRNAs) have emerged as an important class of small molecules that regulate a spectrum of biological processes. However, their roles in the regulation of lipid metabolism and inflammatory response in metabolic syndrome are not completely known. To identify miRNAs and investigate how they are involved in lipid metabolism and inflammatory response in cells and animals and define the function and regulatory mechanism of these microRNAs.

Methods and results: We stimulated human THP-1 macrophages with oxLDL and found that one of the miRNAs, miR-150, strongly responded to the lipid accumulation and inflammatory response in these cells. Overexpression of miR-150 in macrophage cells resulted in an increase in lipid accumulation, accompanying with a high expression of several pro-inflammatory cytokines. Conversely, when miR-150 knockout mice were challenged with a high fat diet, these mice presented reduced whole body weight with less fat accumulation, improved systemic glucose tolerance and insulin sensitivity. The expression of pro-inflammatory cytokines in the insulin target adipose tissues was reduced in miR-150 null mice. We identified Adiponectin receptor 2 (AdipoR2) as a potential miR-150 target gene and suggested it may play an important role in miR-150-mediated lipid metabolism and inflammatory response.

Conclusions: These results uncovered novel functions for miR-150 in modulating lipid metabolism and inflammatory response by regulating genes linked to lipid accumulation and related inflammation and provided a firm mechanistic explanation with characterization and determination of critical miR-150 for its associations with the metabolic diseases. These studies will highly impact and benefit metabolic disease research both in vitro and in vivo

Keywords
Birth defects; Gene therapy; Molecular medicine
Introduction
Now a day’s congenital defect, birth defects, craniosynostosis (syndromic and nonsyndromic) craniofacial abnormalities developed day by day. Its etiopathogenesis still unclear. In our experience, Nonsyndromic Craniosynostosis (NSC) is more commonly encountered than Syndromic Craniosynostosis (SCS). Particularly, in these types of cases surgery is more essential. Otherwise infants are died, because of sutures and ossification of primary and secondary. In presentscenario developing of the molecular biology a new and very innovative consepts are coming to controlling these disease. The etiopathogenesis, neurocognitive impairment stated and we specifically observed in our day today experience in these diseases these infants are suffering in mutations (point, substitutional, deletion, addition, allelespecific, missense and haplotypes) [1].
This contributes to premature suture fusion. An idea germinating in these concepts in experimental observations to overcome this globally burden. We are trying to develop and targeting genetic therapy to prevent pathologically sutural fusion and at the same time other defects by birth [1]. TNFRSF11B plus Vitamin-D Deficiency in infancy was associating with severs JPD [2] which complicated by craniosynostosis. Panidornate treatment with Vitamin-D sufficiency can be effective therapy for the skeletal diseases. It caused by the OPJ deficiency form of JPD.
NEL-Like molecule 1 (Nell 1) is a patent osteogenic factor. It is associating with craniosynostosis. Adeno viruses are the most commonly used viral oesteogenesis. The lanti viruses can serve as ideal vectors for gene therapy for bone regeneration. Basically there are two lanti viral vectors (Lv NELL 1 and Lv BMP2). Researcher observed that these genes transfer in hADSCs may be a novel and potential approach for bone regeneration [3].
NELL 1 is able to promote the osteogenic differentiation. The hPDLSCs, may be related to the down regulation of MSX2 expression. Lentil transfection used during in vitro gene therapy for periodontal regeneration [4]. However Beare- Stevension cutis gyratra Syndrome (BSS) is a human genetic disorder. This corrected by skin and skull deformities. BSS is by mutations in the FGF Receptors (FGFR2). Molecular mechanisms that induce skin and skull abnormalities are remaining unclear.
We found that ligand-independent phosphorylation of FGFR2 and potential activation p38 signaling is mutant skin in calvarial tissues [5]. In our experience the pathogenic role for this activation lead to development of therapeutic strategy for BSS and related condition of acanthosis nigirinicans or craniosynostosis.
Gene environment interaction could not support a therapeutic intervention based on this interaction [6]. In our experience, sagittal synostosis is safely treated with endoscopic suturectomy and helmet therapy [7].
The molecular basis of HR-ALL is multi factorial effect its proved a new potential therapeutic approach which directly involved in JAK inhibition [8].
Noggin is also a potential inhibitor of bone formation with small suturectomy sites, which is useful in avoiding post operative resynostosis. Which may be useful an adjunct to traditional surgical intervention to treat the craniosynostosis [9].
Moreover, FGFR signaling and its cross talk with tyrosine kinase and immunoglobulin’s i, ii, iii, iv controlling skeletal cell fate. Pharmacologically we should target to correct the deformity of cell phenotype [10].
Materials and Methods
Successful gene therapy requires standardized techniques. Retroviruses are a class of viruses that having the ability to produce double-stranded DNA copies from their RNA genomes. Selected Copies of its Genome can be made to integrate into target chromosomes of host cells. Adenoviruses are another class of viruses with the capability of inserting their genetic material at a specific site of chromosome. A similarly Herpes simplex virus infects a particular cell type, neurons. HSV type I is very common pathogen, which causes cold sores. However, direct introduction of therapeutic DNA into target cells, is easier than others. Its application only in selected tissues requires large amounts of DNA. Non-viral approach involves the creation of an artificial lipid sphere with an aqueous core. Liposomes carry the therapeutic DNA and are capable to transmitting the DNA through the specific target cells membrane.
The process of the inserting therapeutic DNA into target cells by chemically linking the DNA to a molecule that binds to special receptors. When bound to receptors, the therapeutic DNA constructs are engulfed by cell membrane and transported inside the target cell. The difficulty arises in delivering these larger molecules to the nucleus of the target cell.
Results
Microarray technology reports suggested that the data confined globally in gene expression between regional dura mater underline fusing with patent sutures. Which play a major role in cranial suture biology [11].
Moreover, various cytokine signaling pathways are investigated and promising for the future development of potential alternative therapy to solve the disease like craniosynostosis and craniofacial deformity [12]. Microinjection techniques are developed newly cell membrane and intracellular dyes. The number of (RNA and DNA viral) constructs are delivering the genes to enhancing the solution of cell fate maps, cell lineage activities which are more approachable for human diseases.
TGF-beta also playing a role of different is forms to produce craniosynostosis the specific receptors, signaling pathways, animal models, expressions also helpful for normal and pathological sutures [13].
For improving collaborating with different clinical manifestations, centers, standardization, data collection and addressed should be the special priorities. We should focus team approach to solve this problem in near future for public health research and education for craniosynostosis/birth defects and other diseases [14].
Genetic counseling
Genetic counseling is a process to assist the parents and family. They should understand the nature of genetic disorder and its risk of transmission to subsequent siblings. The available options for prenatal diagnosis and medical termination of pregnancy are as follows.
Gene therapy in medical informatics
Gene therapy with replacement of abnormal gene is curative. But it is still in experimental stage. GT has been tried in patients with Adenosine Deaminase Deficiency (ADA) Duchenne Muscular Dystrophy (DMD), familial hypercholesterolemia and certain cancers. The aim is to replace the deactivate gene with the normal gene. This is done by using a viral or non-viral vector for introducing the normal functioning gene.
Discussion
Many inherited metabolic diseases will not require complete restoration of gene function for correcting important aspects of the disease phenotype. e.g. Parkinsonism, phenylketouria and other diseases. Pseudogene and transgenic expression are adequate (Table 1). In general view, both the significance of the role for somatic gene therapy and molecular mechanisms for its implementation have evolved dramatically now days (Table 2). Particularly, candidates have expanded from just single-gene disorders to include Cancer, AIDS, Birth Defects, Craniofacial deformities and atherosclerosis. Distinguished with another area of change is the expansion of the delivery system, which began retroviral vectors but now includes vectors based on adenovirus, Adeno-Associated Viruses (AAV), herpes virus, vaccine, and other agents are documented Non-viral systems such as liposomes, DNA-protein conjugates, and DNA-Protein-defective virus conjugates are also promising. Retroviral vectors have the major advantage that they integrate with the foreign DNA and permanently alter the recipient cell; But they have two major disadvantages namely requirement for dividing cells and they need to provide low-titer virus, which is relatively impractical for most in vivo approaches. In-contrast, adenovirus vectors can be offered as high titer and they have the ability to effect large number of cells in-vivo, but there is concern about toxic effects on infected cells, and the therapeutic effects is only transient. Both in-vivo and in-vitro results have been good. Gene therapy has so far been reported to be useful in few genetic disorders, including ADA deficiency and hypercholesterolemia. Many trials have been approved for many malignancies, AIDS, Cystic fibrosis, Gauchers Diseases, A Craniofacial defects (Table 3). As per the development of recent advancement like microarray, next generation sequencing, SSCP, SNPs, DDGE, RFLP, Bloting, karyotyping, ARMS, Direct sequencing, VNTRS, microsatellites and other molecular techniques are more helpful to developed these therapeutics.
In the present scenario it seems that this new form of therapy is far from routine bed side clinical application.
GT for single-gene disorders like syndromic and non-syndromic craniosynostosis diseases are still not well documented or progressed. Though it is highly promising and very serious threaten in near future. Researcher, Scientist, Clinicians, paramedic, Tissue Engineers should focus on developing therapy for these patients. Government and funding agencies should take necessary action for achieving this goal. Even suicide gene therapy is one of the most promising therapies to treat mesothelioma. A protein-producing gene is introduced that converts a non-toxic drug into one that can kill cancer cells. Cytokines are proteins that control and direct our immune response. It helps immune systems to an attack against cancer cells. Controlled gene expression, getting genes to their proper targets, preventing destruction of the gene, delivery methods, condition of the host and host immune response are some of the challenges facing genetherapy. Moreover, viruses, viral delivery methods, Liposome delivery, and targeted gene delivery in cellular level in-vitro and in-vivo need to be improved.
Side effects
Gene therapy and potential complications are including the long term effects of the treatment remain unknown. Though it has not yet been observed researchers have raised concern that healthy cells may also become infected by the modified viruses, which could possibly cause new diseases or lead to carcinogenesis.
Conclusion
It is hoped that molecular genetics techniques will be useful not only for diagnosis of disease, but for treatment as well. The normal gene may be introduced directly into the defective body organ i.e. in vivo or more often the process is achieved in vitro followed by its introduction into the patient. Another obstacle to genetherapy is the high cost involved. GT should always be monitored and instituted at centers with sufficient experience and expertise. In the absences of definite treatment modalities it appropriate to create awareness among clinicians regarding counseling and preventive strategies. Newer tools in medical informatics to provide e-learning, such as simulation, animation, and media may be exploited to provide better treatment and to foster future research.
References

 

Figures at a glance

Figure Figure Figure Figure
Figure 1 Figure 2 Figure 3 Figure 4

 

Figure Figure Figure
Figure 5 Figure 6 Figure 7
Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Relevant Topics

Recommended Conferences

Article Usage

  • Total views: 11607
  • [From(publication date):
    April-2014 - Jul 22, 2017]
  • Breakdown by view type
  • HTML page views : 7825
  • PDF downloads :3782
 
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

agrifoodaquavet@omicsonline.com

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

clinical_biochem@omicsonline.com

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

business@omicsonline.com

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

chemicaleng_chemistry@omicsonline.com

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

environmentalsci@omicsonline.com

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

engineering@omicsonline.com

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

generalsci_healthcare@omicsonline.com

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

genetics_molbio@omicsonline.com

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

immuno_microbio@omicsonline.com

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

omics@omicsonline.com

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

materialsci@omicsonline.com

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

mathematics_physics@omicsonline.com

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

medical@omicsonline.com

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

neuro_psychology@omicsonline.com

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

pharma@omicsonline.com

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

social_politicalsci@omicsonline.com

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version