Publications by authors named "Mohammad Mehdi Banoei"

18 Publications

  • Page 1 of 1

Metabolomic and metallomic profile differences between Veterans and Civilians with Pulmonary Sarcoidosis.

Sci Rep 2019 12 20;9(1):19584. Epub 2019 Dec 20.

Section of Pulmonary, Miami VA Healthcare System, Miami, FL, USA.

Sarcoidosis is a disorder characterized by granulomatous inflammation of unclear etiology. In this study we evaluated whether veterans with sarcoidosis exhibited different plasma metabolomic and metallomic profiles compared with civilians with sarcoidosis. A case control study was performed on veteran and civilian patients with confirmed sarcoidosis. Proton nuclear magnetic resonance spectroscopy (H NMR), hydrophilic interaction liquid chromatography mass spectrometry (HILIC-MS) and inductively coupled plasma mass spectrometry (ICP-MS) were applied to quantify metabolites and metal elements in plasma samples. Our results revealed that the veterans with sarcoidosis significantly differed from civilians, according to metabolic and metallomics profiles. Moreover, the results showed that veterans with sarcoidosis and veterans with COPD were similar to each other in metabolomics and metallomics profiles. This study suggests the important role of environmental risk factors in the development of different molecular phenotypic responses of sarcoidosis. In addition, this study suggests that sarcoidosis in veterans may be an occupational disease.
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http://dx.doi.org/10.1038/s41598-019-56174-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925242PMC
December 2019

An A10398G mitochondrial DNA alteration is related to increased risk of breast cancer, and associates with Her2 positive receptor.

Mitochondrial DNA A DNA Mapp Seq Anal 2020 01 4;31(1):11-16. Epub 2019 Dec 4.

Department of Medical Genetic, National Institute for Genetic Engineering and Biotechnology, Tehran, Iran.

Breast cancer is the most common malignancy and the second leading cause of cancer deaths among women worldwide after lung cancer. Mitochondria play a central role in the regulation of cellular function, metabolism, and cell death in cancer cells. We aim to examine the mitochondrial polymorphisms of complex I in association with breast cancer in an Iranian cohort.This experimental study includes 53 patients with breast cancer and 35 healthy control patients. In addition, tumor-adjacent normal breast tissue was obtained from each patient. The DNA of the tissue cells was extracted and analyzed for complex I mutations using a PCR sequencing method. Our results show 94 mtDNA complex I variants in tumor tissues. A10398G was the most prevalent polymorphism and strongly correlated with Her2 receptor in tumor tissue samples. Mitochondrial DNA (mtDNA) mutations have been widely linked to the etiology of numerous disorders. The mtDNA mutations screening on A10398G along with other mutations might provide insight on the role of mitochondrial mutations in breast cancer.
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http://dx.doi.org/10.1080/24701394.2019.1695788DOI Listing
January 2020

Metabolomics and Biomarker Discovery in Traumatic Brain Injury.

J Neurotrauma 2018 08;35(16):1831-1848

2 Departments of Critical Care Medicine, Medicine and Biochemistry and Molecular Biology, University of Calgary , Calgary, Alberta, Canada .

Traumatic brain injury (TBI) is one of the leading causes of disability and mortality worldwide. The TBI pathogenesis can induce broad pathophysiological consequences and clinical outcomes attributed to the complexity of the brain. Thus, the diagnosis and prognosis are important issues for the management of mild, moderate, and severe forms of TBI. Metabolomics of readily accessible biofluids is a promising tool for establishing more useful and reliable biomarkers of TBI than using clinical findings alone. Metabolites are an integral part of all biochemical and pathophysiological pathways. Metabolomic processes respond to the internal and external stimuli resulting in an alteration of metabolite concentrations. Current high-throughput and highly sensitive analytical tools are capable of detecting and quantifying small concentrations of metabolites, allowing one to measure metabolite alterations after a pathological event when compared to a normal state or a different pathological process. Further, these metabolic biomarkers could be used for the assessment of injury severity, discovery of mechanisms of injury, and defining structural damage in the brain in TBI. Metabolic biomarkers can also be used for the prediction of outcome, monitoring treatment response, in the assessment of or prognosis of post-injury recovery, and potentially in the use of neuroplasticity procedures. Metabolomics can also enhance our understanding of the pathophysiological mechanisms of TBI, both in primary and secondary injury. Thus, this review presents the promising application of metabolomics for the assessment of TBI as a stand-alone platform or in association with proteomics in the clinical setting.
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http://dx.doi.org/10.1089/neu.2017.5326DOI Listing
August 2018

Visfatin level in patients with colorectal adenoma.

Med J Islam Repub Iran 2016 24;30:320. Epub 2016 Jan 24.

Medical Student, Department of Surgery, Tehran University of Medical Sciences, Tehran, Iran.

Background: Visfatin is an adipocytokine secreted by visceral adipose tissue. It has been shown that adipocytokines may contribute to the induction of carcinogens and progression of tumors. Previously, we found a significant increase in the visfatin serum level in colorectal cancer patients. Herein, we investigated if this cytokine increases in patients with colorectal adenoma as a precursor of colorectal cancer.

Methods: In this case-control analytic study, a total of 34 patients diagnosed with colorectal adenoma and 35 disease-free controls were included. Adenomas were also categorized based on their location within the colon. Visfatin serum levels were measured in all cases and controls using enzyme- linked immunosorbent assay kits. In order to compare visfatin levels between groups a twotailed t-test was considered. Pearson correlation was also used to assess the relationship between visfatin levels and other measured variables.

Results: Patients included 18 male (53%) and 16 female (47%) with a mean±SD age of 48.3±10.96 years and controls were 18 male (51%) and 17 female (49%) with a mean±SD age of 51.6±12.52 years. There were no significant difference in terms of the visfatin level between the two groups (6.7±3.01 ng/ml for patients and 6.8±2.49 ng/ml for controls, p>0.05). Except for a significant correlation between the BMI and visfatin level (p=0.041), no other correlation was detected. We found no significant difference between the levels of visfatin in each location of adenoma comparing the healthy controls (p>0.05 in all comparisons). There was no statistical difference between the locations groups in terms of visfatin level as well (p>0.05).

Conclusion: Visfatin serum level does not significantly increase in patients with colorectal adenoma. Site of adenoma within the colon or rectum does not seem to play an important role in this regard as well.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4898872PMC
July 2016

Plasma metabolomic profile in fibrosing pulmonary sarcoidosis.

Sarcoidosis Vasc Diffuse Lung Dis 2016 Mar 29;33(1):29-38. Epub 2016 Mar 29.

University of Illinois at Chicago.

Background: There is no known marker to screen patients with sarcoidosis to determine the risk of progression to pulmonary fibrosis. We aimed to identify potential noninvasive biomarkers for early detection of pulmonary fibrosing sarcoidosis.

Methods: A case-control study was performed on African Americans with confirmed sarcoidosis included 31 subjects with pulmonary fibrosis vs. 36 without pulmonary fibrosis. Plasma samples were analyzed by liquid chromatography-mass spectrum. Multivariate statistical analysis models were developed in a training set based on 50 age- and sex-matched samples to identify metabolites involved in the discrimination. Principal component analysis and orthogonal partial least squares-discriminant (OPLS) analysis coupled to the most influential variables were used to derive significant metabolic discriminations.

Results: Of the datasets from 171 feature peaks, 14 features including p-coumaroylagmatine and palmitoylcarnitine showed significant differences between fibrosing and non-fibrosing pulmonary sarcoidosis (p = 0.001). OPLS analysis presented clear separation between two groups with an acceptable goodness of fit (R(2) = 0.522) and predictive power (Q(2)=0.322). Discriminating metabolites involved collagen pathway metabolites especially those in the arginine-proline pathway.

Conclusions: Metabolomics can provide a useful tool to detect pulmonary fibrosis in patients with sarcoidosis. Two discriminating metabolites, p-coumaroylagmatine and palmitoylcarnitine may be potential markers for fibrosing pulmonary sarcoidosis.
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March 2016

Reply: Metabolomics and Mycobacterial Disease: Don't Forget the Bioinformatics.

Ann Am Thorac Soc 2016 Jan;13(1):142-3

3 University of Illinois at Chicago Chicago, Illinois.

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http://dx.doi.org/10.1513/AnnalsATS.201510-711LEDOI Listing
January 2016

Metabolomics: Applications and Promise in Mycobacterial Disease.

Ann Am Thorac Soc 2015 Sep;12(9):1278-87

4 Division of Pulmonary and Critical Care Medicine, University of Illinois at Chicago, Chicago, Illinois.

Until recently, the study of mycobacterial diseases was trapped in culture-based technology that is more than a century old. The use of nucleic acid amplification is changing this, and powerful new technologies are on the horizon. Metabolomics, which is the study of sets of metabolites of both the bacteria and host, is being used to clarify mechanisms of disease, and can identify changes leading to better diagnosis, treatment, and prognostication of mycobacterial diseases. Metabolomic profiles are arrays of biochemical products of genes in their environment. These complex patterns are biomarkers that can allow a more complete understanding of cell function, dysfunction, and perturbation than genomics or proteomics. Metabolomics could herald sweeping advances in personalized medicine and clinical trial design, but the challenges in metabolomics are also great. Measured metabolite concentrations vary with the timing within a condition, the intrinsic biology, the instruments, and the sample preparation. Metabolism profoundly changes with age, sex, variations in gut microbial flora, and lifestyle. Validation of biomarkers is complicated by measurement accuracy, selectivity, linearity, reproducibility, robustness, and limits of detection. The statistical challenges include analysis, interpretation, and description of the vast amount of data generated. Despite these drawbacks, metabolomics provides great opportunity and the potential to understand and manage mycobacterial diseases.
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http://dx.doi.org/10.1513/AnnalsATS.201505-279PSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626905PMC
September 2015

Association of genetic variations in the mitochondrial D-loop with β-thalassemia.

Mitochondrial DNA A DNA Mapp Seq Anal 2016 05 18;27(3):1693-6. Epub 2014 Sep 18.

a Department of Medical Genetics , Special Medical Center , Tehran , Islamic Republic of Iran .

Beta-thalassemia, one of the most common single-gene disorders, is the result of reduced or absent production of β-globin chains. Patients with β-thalassemia show weak genotype-phenotype correlations. Mitochondrial DNA polymorphisms are a potential source for different physiological and pathological characteristics and have been found to be associated as genetic modifiers with various pathophysiologies, including cancers and neurodegenerative diseases. A group of 35 patients with β-thalassemia was investigated for the presence of mtDNA D-loop polymorphisms in comparison with 504 normal controls. We found four mtDNA D-loop polymorphisms at nucleotides 16,069C > T, 16,189T > C, 16,319G > A, and 16,519T > C that showed significant differences between patients and normal subjects. There is no strong proof for the association of these polymorphisms with β-thalassemia. It is hypothesized that iron overload or its effects on sequestration of calcium or zinc can lead to oxidative stress and ROS production inside the mitochondria. Therefore, possible accompanying of mtDNA polymorphisms with β-thalassemia disease may complicate the genotype-phenotype correlation and could affect the clinical outcomes in the patients.
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http://dx.doi.org/10.3109/19401736.2014.958730DOI Listing
May 2016

Beta-Thalassemia in Iran: new insight into the role of genetic admixture and migration.

ScientificWorldJournal 2012 18;2012:635183. Epub 2012 Dec 18.

Department of Animal Science, Faculty of Agriculture, Ferdowsi University of Mashhad, Mashhad, Iran.

Iran with an area of 1.648 million km(2) is located between the Caspian Sea and the Persian Gulf. The Iranian population consists of multiethnic groups that have been influenced by various invasions and migration throughout history. Studies have revealed the presence of more than 47 different β-globin gene mutations responsible for β-Thalassemia in Iran. This paper is an attempt to study the origin of β-Thalassemia mutations in different parts of Iran. Distribution of β-Thalassemia mutations in Iran shows different patterns in different areas. β-Thalassemia mutations have been a reflection of people and area in correlation with migration and origin of ancestors. We compared the frequencies of β-globin mutations in different regions of Iran with those derived from neighboring countries. The analysis provided evidence of complementary information about the genetic admixture and migration of some mutations, as well as the remarkable genetic classification of the Iranian people and ethnic groups.
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http://dx.doi.org/10.1100/2012/635183DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539370PMC
June 2013

Generation and bioenergetic analysis of cybrids containing mitochondrial DNA from mouse skeletal muscle during aging.

Nucleic Acids Res 2010 Apr 18;38(6):1913-21. Epub 2009 Dec 18.

Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.

Mitochondrial respiratory chain defects have been associated with various diseases and normal aging, particularly in tissues with high energy demands including skeletal muscle. Muscle-specific mitochondrial DNA (mtDNA) mutations have also been reported to accumulate with aging. Our understanding of the molecular processes mediating altered mitochondrial gene expression to dysfunction associated with mtDNA mutations in muscle would be greatly enhanced by our ability to transfer muscle mtDNA to established cell lines. Here, we report the successful generation of mouse cybrids carrying skeletal muscle mtDNA. Using this novel approach, we performed bioenergetic analysis of cells bearing mtDNA derived from young and old mouse skeletal muscles. A significant decrease in oxidative phosphorylation coupling and regulation capacity has been observed with cybrids carrying mtDNA from skeletal muscle of old mice. Our results also revealed decrease growth capacity and cell viability associated with the mtDNA derived from muscle of old mice. These findings indicate that a decline in mitochondrial function associated with compromised mtDNA quality during aging leads to a decrease in both the capacity and regulation of oxidative phosphorylation.
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http://dx.doi.org/10.1093/nar/gkp1162DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847227PMC
April 2010

Mitochondrial tRNALeu/Lys and ATPase 6/8 gene variations in spinocerebellar ataxias.

Neurodegener Dis 2009 5;6(1-2):16-22. Epub 2008 Nov 5.

Research and Sciences Campus, Azad University, Tehran, Iran.

Background: The spinocerebellar ataxias (SCA) comprise a heterogeneous group of severe late-onset neurodegenerative diseases that are promoted by the expansion of a tandem-arrayed DNA sequence that modifies the primary structure of the protein.

Methods: Genomic DNA of 20 patients affected with SCAs was extracted from peripheral blood and screened for deletions in mitochondrial DNA (mtDNA). Sequencing of tRNA(Leu), tRNA(Lys), cytochrome oxidase II, ATPase 6/8 and NADH dehydrogenase I (NDI) genes belonging to mtDNA from patients with SCAs was also carried out to detect the presence of variations.

Results: We identified cytosine-adenine-guanine (CAG) trinucleotide repeat expansions in 20 patients. Seven of these patients had at least one nucleotide change in mtDNA. In such cases, 5 nucleotide variations resulted in amino acid changes with two novel variations T8256G and G9010A.

Conclusion: SCA patients showed high levels of mtDNA variations in lymphocytes. It can be proposed that the SCA gene proteins (Ataxins) are involved in the complicated intracellular mechanisms that affect cellular organelles and their components, such as the mitochondrial genome. The instability of CAG repeats in polyglutamine diseases such as SCAs and Huntington's disease might be a causative factor in mtDNA variation or possible damage.
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http://dx.doi.org/10.1159/000170885DOI Listing
February 2009

An A8296G mutation in the MT-TK gene of a patient with epilepsy - a disease-causing mutation or rare polymorphism?

Neurol Neurochir Pol 2008 May-Jun;42(3):263-6

Shahrekord University, Shahrekord, Iran.

Mitochondrial DNA (mtDNA) mutations are an important cause of human diseases. mtDNA could be considered a candidate modifying factor in neurodegenerative disorders. A homoplasmic A8296G mutation was detected in a 24-year-old patient with idiopathic generalized epilepsy. The A8296G mutation in the mitochondrial DNA MT-TK gene has been associated with severe mitochondrial diseases. The pathogenicity of this mutation or its association with a specific disease is unclear. This mutation has already been reported exclusively as well as together with other mutations during trials of mtDNA. As in this case, the mutation was homoplasmic and there were no clinical findings in other family members. We suggest that this mutation is a rare polymorphism or may be a pathogenic mutation in combination with other mutations outside of the MT-TK gene.
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November 2008

Variation of DAT1 VNTR alleles and genotypes among old ethnic groups in Mesopotamia to the Oxus region.

Hum Biol 2008 Feb;80(1):73-81

Medical Genetic Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.

Variation of a VNTR in the DAT1 gene in seven ethnic groups of the Middle East was used to infer the history and affinities of these groups. The populations consisted of Assyrian, Jewish, Zoroastrian, Armenian, Turkmen, and Arab peoples of Iran, Iraq, and Kuwait. Three hundred forty subjects from these seven ethnic groups were screened for DAT1. DAT1 VNTR genotyping showed 3, 6, 7, 8, 9, 10, 11, and 12 alleles in the samples. Analysis of these data revealed differentiation and relationship among the populations. In this region, which covers an area of 2-2.5 million km2, the influence of geography and especially of linguistic characteristics has had potentially major effects on differentiation. Religion also has played a major role in imposing restrictions on some ethnic groups, who as a consequence have maintained their community. Overall, these ethnic groups showed greater heterogeneity compared to other populations.
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http://dx.doi.org/10.3378/1534-6617(2008)80[73:VODVAA]2.0.CO;2DOI Listing
February 2008

Investigation of tRNA(Leu/Lys) and ATPase 6 genes mutations in Huntington's disease.

Cell Mol Neurobiol 2008 Nov 2;28(7):933-8. Epub 2008 Apr 2.

Science & Research Unit, Azad University, Tehran, Iran.

Huntington disease (HD) is a genetically dominant condition caused by expanded CAG repeats which code for glutamine in the HD gene product, huntingtin. Huntingtin is expressed in almost all tissues, so abnormalities outside the brain can also be expected. Involvement of nuclei and mitochondria in HD pathophysiology has been suggested. In fact mitochondrial dysfunction is reported in brains of patients suffering from HD. The tRNA gene mutations are one of hot spots that can cause mitochondrial disorders. In this study, possible mitochondrial DNA (mtDNA) damage was evaluated by screening for mutations in the tRNA(leu/lys) and ATPase 6 genes of 20 patients with HD, using PCR and automated DNA sequencing. Mutations including an A8656G mutation in one patient were observed, which may be causal to the disease. Understanding the role of mitochondria in the pathogenesis of neurodegenerative diseases could potentially be important for the development of therapeutic strategies in HD.
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http://dx.doi.org/10.1007/s10571-008-9261-6DOI Listing
November 2008

Do mitochondrial DNA haplogroups play a role in susceptibility to tuberculosis?

Respirology 2007 Nov;12(6):823-7

National Institute for Genetic Engineering and Biotechnology, Tehran, Iran.

Background And Objectives: Mitochondrial DNA has a unique role in ATP production and subsequent mitochondrial reactive oxygen species (ROS) production in eukaryotic cells and there is a potential role for ROS and oxygen burst against Mycobacterium tuberculosis, an intracellular pathogen. This study aimed to determine whether the frequency of different mitochondrial haplogroups was significantly different in patients with tuberculosis (TB) compared with a normal population.

Methods: Mitochondrial DNA haplogroups M, N, J and K were studied by PCR-restriction fragment length polymorphism and sequencing. Cases were 54 patients with confirmed smear positive pulmonary TB. Controls were 256 healthy persons.

Results: There were no statistically significant differences between those with TB and the control group.

Conclusions: There was no statistically significant association between mtDNA haplogroups and the presence of TB infection.
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http://dx.doi.org/10.1111/j.1440-1843.2007.01163.xDOI Listing
November 2007

Huntington's disease and mitochondrial DNA deletions: event or regular mechanism for mutant huntingtin protein and CAG repeats expansion?!

Cell Mol Neurobiol 2007 Nov 20;27(7):867-75. Epub 2007 Oct 20.

Department of Medical Genetics, National Institute of Genetic Engineering and Biotechnology, PO Box 14155-6343, Tehran, Iran.

The mitochondrial DNA (mtDNA) may play an essential role in the pathogenesis of the respiratory chain complex activities in neurodegenerative disorders such as Huntington's disease (HD). Research studies were conducted to determine the possible levels of mitochondrial defect (deletion) in HD patients and consideration of interaction between the expanded Huntingtin gene as a nuclear gene and mitochondria as a cytoplasmic organelle. To determine mtDNA damage, we investigated deletions based in four areas of mitochondrial DNA, in a group of 60 Iranian patients clinically diagnosed with HD and 70 healthy controls. A total of 41 patients out of 60 had CAG expansion (group A). About 19 patients did not show expansion but had the clinical symptoms of HD (group B). MtDNA deletions were classified into four groups according to size; 9 kb, 7.5 kb, 7 kb, and 5 kb. We found one of the four-mtDNA deletions in at least 90% of samples. Multiple deletions have also been observed in 63% of HD patients. None of the normal control (group C) showed mtDNA deletions. The sizes or locations of the deletions did not show a clear correlation with expanded CAG repeat and age in our samples. The study presented evidence that HD patients had higher frequencies of mtDNA deletions in lymphocytes in comparison to the controls. It is thus proposed that CAG repeats instability and mutant Htt are causative factor in mtDNA damage.
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http://dx.doi.org/10.1007/s10571-007-9206-5DOI Listing
November 2007

Diversity and relationship between Iranian ethnic groups: human dopamine transporter gene (DAT1) VNTR genotyping.

Am J Hum Biol 2007 Nov-Dec;19(6):821-6

Department of Medical Genetics, National Institute for Genetic Engineering and Biotechnology, Tehran, Iran.

The 40-bp VNTR polymorphism in the 3' untranslated region of the human DAT1 (dopamine transporter 1) was analyzed in the Iranian ethnic groups in order to examine the influence of geographical and linguistic affiliation on the genetic affinities among the Iranian population. A total of 449 subjects belonging to nine ethnic groups from the Iranian population were included in the study. The screening of 898 chromosomes showed five alleles (6, 7, 8, 9, 10, and 11), of which allele 10 revealed the highest frequency in most regions. Allele 8 was predominant in one ethnicity and occurred more frequently in the center of Iran. This study shows that the DAT1 distribution in Iran has a different pattern from those in other studies, which can contribute to an understanding of differentiation and diversity of Iranian ethnic groups. This polymorphism could represent the genetic diversity among the various ethnic groups of Iran.
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http://dx.doi.org/10.1002/ajhb.20647DOI Listing
January 2008