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Article: Unraveling molecular mechanism underlying biomaterial and stem cells interaction during cell fate commitment using high throughput data analysis

Sharifi, Erfan / Khazaei, Niusha / Kieran, Nicholas W. / Esfahani, Sahel Jahangiri / Mohammadnia, Abdulshakour / Yaqubi, Moein

Gene. 2022 Feb. 20, v. 812

2022

Abstract: Stem cell differentiation towards various somatic cells and body organs has proven to be an effective technique in the understanding and progression of regenerative medicine. Despite the advances made, concerns regarding the low efficiency of ... ...

Abstract	Stem cell differentiation towards various somatic cells and body organs has proven to be an effective technique in the understanding and progression of regenerative medicine. Despite the advances made, concerns regarding the low efficiency of differentiation and the remaining differences between stem cell products and their in vivo counterparts must be addressed. Biomaterials that mimic endogenous growth conditions represent one recent method used to improve the quality and efficiency of stem cell differentiation, though the mechanisms of this improvement remain to be completely understood. The effectiveness of various biomaterials can be analyzed through a multidisciplinary approach involving bioinformatics and systems biology tools. Here, we aim to use bioinformatics to accomplish two aims: 1) determine the effect of different biomaterials on stem cell growth and differentiation, and 2) understand the effect of cell of origin on the differentiation potential of multipotent stem cells. First, we demonstrate that the dimensionality (2D versus 3D) and the degradability of biomaterials affects the way that the cells are able to grow and differentiate at the transcriptional level. Additionally, according to transcriptional state of the cells, the particular cell of origin is an important factor in determining the response of stem cells to same biomaterial. Our data demonstrates the ability of bioinformatics to understand novel molecular mechanisms and context by which stem cells are most efficiently able to differentiate. These results and strategies can be used to suggest proper combinations of biomaterials and stem cells to achieve high differentiation efficiency and functionality of desired cell types.
Keywords	biocompatible materials ; cell differentiation ; cell growth ; genes ; medicine ; stem cells ; transcription (genetics)
Language	English
Dates of publication	2022-0220
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2021.146111
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: MiR-548k suppresses apoptosis in breast cancer cells by affecting PTEN/PI3K/AKT signaling pathway.

Yadollahi-Farsani, Mahtab / Amini-Farsani, Zeinab / Moayedi, Fatemeh / Khazaei, Niusha / Yaghoobi, Hajar

IUBMB life

2022 Volume 75, Issue 2, Page(s) 97–116

Abstract: Breast cancer is the most aggressive and fatal form of cancer among women globally. Although the role of some miRNAs that are often dysregulated in breast cancer has been deciphered, the regulatory function of others still remains unknown. The current ... ...

Abstract	Breast cancer is the most aggressive and fatal form of cancer among women globally. Although the role of some miRNAs that are often dysregulated in breast cancer has been deciphered, the regulatory function of others still remains unknown. The current study was aimed at determining the biological role and underlying mechanism of miR-548k in breast cancer. In this study, the significant overexpression of miR-548k in breast cancer tissues compared to adjacent normal tissues was confirmed. Also, bioinformatics analysis indicated that PTEN, as a negative regulator of PI3K/AKT signaling pathway, was a potential target of miR-548k, and its expression was downregulated in breast cancer tissues rather than normal tissues. Furthermore, the ectopic increase of miR-548k decreased the expression of PTEN in breast cancer, suggesting that PTEN is one of the potential downstream targets of miR-548k. Besides, functional analysis was conducted to assess the capability of miR-548k to alter apoptosis along with the changed expression levels of miR-548k in breast cancer cells. Based on this investigation, forced increase of miR-548k disrupted programmed cell death in MCF-7 cells. Apart from this, in silico study of miR-548 family supported its association with the main components of PI3K/Akt signaling pathway, opening a prospective research area in cancer therapy. In brief, suppression of PTEN partly mediated by miR-548k diminished apoptosis and promoted cell proliferation through PI3K/Akt pathway in breast cancer, suggesting a novel therapeutic axis, miR-548k/PTEN/ PI3K/Akt, for treatment of breast cancer in the future.
MeSH term(s)	Humans ; Female ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Breast Neoplasms/genetics ; Prospective Studies ; Signal Transduction/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Apoptosis/genetics ; Cell Proliferation/genetics ; Cell Line, Tumor ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; MicroRNAs ; PTEN protein, human (EC 3.1.3.67) ; PTEN Phosphohydrolase (EC 3.1.3.67)
Language	English
Publishing date	2022-12-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1492141-8
ISSN	1521-6551 ; 1521-6543
ISSN (online)	1521-6551
ISSN	1521-6543
DOI	10.1002/iub.2688
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Unraveling molecular mechanism underlying biomaterial and stem cells interaction during cell fate commitment using high throughput data analysis.

Sharifi, Erfan / Khazaei, Niusha / Kieran, Nicholas W / Esfahani, Sahel Jahangiri / Mohammadnia, Abdulshakour / Yaqubi, Moein

Gene

2021 Volume 812, Page(s) 146111

Abstract	Stem cell differentiation towards various somatic cells and body organs has proven to be an effective technique in the understanding and progression of regenerative medicine. Despite the advances made, concerns regarding the low efficiency of differentiation and the remaining differences between stem cell products and their in vivo counterparts must be addressed. Biomaterials that mimic endogenous growth conditions represent one recent method used to improve the quality and efficiency of stem cell differentiation, though the mechanisms of this improvement remain to be completely understood. The effectiveness of various biomaterials can be analyzed through a multidisciplinary approach involving bioinformatics and systems biology tools. Here, we aim to use bioinformatics to accomplish two aims: 1) determine the effect of different biomaterials on stem cell growth and differentiation, and 2) understand the effect of cell of origin on the differentiation potential of multipotent stem cells. First, we demonstrate that the dimensionality (2D versus 3D) and the degradability of biomaterials affects the way that the cells are able to grow and differentiate at the transcriptional level. Additionally, according to transcriptional state of the cells, the particular cell of origin is an important factor in determining the response of stem cells to same biomaterial. Our data demonstrates the ability of bioinformatics to understand novel molecular mechanisms and context by which stem cells are most efficiently able to differentiate. These results and strategies can be used to suggest proper combinations of biomaterials and stem cells to achieve high differentiation efficiency and functionality of desired cell types.
MeSH term(s)	Biocompatible Materials/pharmacology ; Cell Communication ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Gene Expression Profiling/methods ; Gene Expression Regulation/drug effects ; High-Throughput Nucleotide Sequencing ; Humans ; Regenerative Medicine ; Sequence Analysis, RNA ; Stem Cells/chemistry ; Stem Cells/cytology ; Stem Cells/drug effects
Chemical Substances	Biocompatible Materials
Language	English
Publishing date	2021-12-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2021.146111
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: HB-EGF Synthesized by CD4 T Cells Modulates Allergic Airway Eosinophilia by Regulating IL-5 Synthesis.

Farahnak, Soroor / Simon, Leora / McGovern, Toby K / Chen, Michael / Khazaei, Niusha / Martin, James G

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 203, Issue 1, Page(s) 39–47

Abstract: CD4 T cells express the epidermal growth factor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pathophysiological function. Therefore, we wished to elucidate the function of HB-EGF synthesized by CD4 T cells in the context of ...

Abstract	CD4 T cells express the epidermal growth factor (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pathophysiological function. Therefore, we wished to elucidate the function of HB-EGF synthesized by CD4 T cells in the context of allergic pulmonary inflammation and the asthma surrogate, airway hyperresponsiveness, in a murine acute model of asthma. In this study, we show how knocking out HB-EGF expression in CD4 T cells in vivo attenuates IL-5 synthesis in the lung that is accompanied by diminished eosinophilic inflammation and airway hyperresponsiveness. HB-EGF coimmunoprecipitates with the transcriptional repressor B cell lymphoma 6 (Bcl-6) in CD4 T cells. Knocking out HB-EGF in CD4 T cells resulted in increased Bcl-6 binding to the IL-5 gene and decreased IL-5 mRNA expression. Thus, these findings suggest an immunoregulatory function for intrinsic HB-EGF expressed by CD4 T cells in T
MeSH term(s)	Animals ; Asthma/immunology ; CD4 Antigens/metabolism ; Disease Models, Animal ; Eosinophilia/immunology ; Gene Expression Regulation ; Heparin-binding EGF-like Growth Factor/genetics ; Heparin-binding EGF-like Growth Factor/metabolism ; Humans ; Interleukin-5/genetics ; Interleukin-5/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Proto-Oncogene Proteins c-bcl-6/genetics ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Respiratory Hypersensitivity/immunology ; Th2 Cells/immunology
Chemical Substances	CD4 Antigens ; Heparin-binding EGF-like Growth Factor ; Interleukin-5 ; Proto-Oncogene Proteins c-bcl-6
Language	English
Publishing date	2019-05-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1801686
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Regulating the transcriptomes that mediate the conversion of fibroblasts to various nervous system neural cell types.

Khazaei, Niusha / Rastegar-Pouyani, Shima / O'Toole, Nicholas / Wee, Ping / Mohammadnia, Abdulshakour / Yaqubi, Moein

Journal of cellular physiology

2017 Volume 233, Issue 4, Page(s) 3603–3614

Abstract: Our understanding of the mechanism of cell fate transition during the direct reprogramming of fibroblasts into various central nervous system (CNS) neural cell types has been limited by the lack of a comprehensive analysis on generated cells, ... ...

Abstract	Our understanding of the mechanism of cell fate transition during the direct reprogramming of fibroblasts into various central nervous system (CNS) neural cell types has been limited by the lack of a comprehensive analysis on generated cells, independently and in comparison with other CNS neural cell types. Here, we applied an integrative approach on 18 independent high throughput expression data sets to gain insight into the regulation of the transcriptome during the conversion of fibroblasts into induced neural stem cells, induced neurons (iNs), induced astrocytes, and induced oligodendrocyte progenitor cells (iOPCs). We found common down-regulated genes to be mostly related to fibroblast-specific functions, and suggest their potential as markers for screening of the silencing of the fibroblast-specific program. For example, Tagln was significantly down-regulated across all considered data sets. In addition, we identified specific profiles of up-regulated genes for each CNS neural cell types, which could be potential markers for maturation and efficiency screenings. Furthermore, we identified the main TFs involved in the regulation of the gene expression program during direct reprogramming. For example, in the generation of iNs from fibroblasts, the Rest TF was the main regulator of this reprogramming. In summary, our computational approach for meta-analyzing independent expression data sets provides significant details regarding the molecular mechanisms underlying the regulation of the gene expression program, and also suggests potentially useful candidate genes for screening down-regulation of fibroblast gene expression profile, maturation, and efficiency, as well as candidate TFs for increasing the efficiency of the reprogramming process.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Cell Differentiation/physiology ; Cellular Reprogramming/physiology ; Central Nervous System/metabolism ; Fibroblasts/metabolism ; Humans ; Mice ; Neural Stem Cells/metabolism ; Neurons/metabolism ; Transcription Factors/metabolism ; Transcriptome/physiology
Chemical Substances	Transcription Factors
Language	English
Publishing date	2017-11-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.26221
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Meta-Analysis of Transcriptome Regulation During Induction to Cardiac Myocyte Fate From Mouse and Human Fibroblasts.

Rastegar-Pouyani, Shima / Khazaei, Niusha / Wee, Ping / Yaqubi, Moein / Mohammadnia, Abdulshakour

Journal of cellular physiology

2017 Volume 232, Issue 8, Page(s) 2053–2062

Abstract: Ectopic expression of a defined set of transcription factors (TFs) can directly convert fibroblasts into a cardiac myocyte cell fate. Beside inefficiency in generating induced cardiomyocytes (iCMs), the molecular mechanisms that regulate this process ... ...

Abstract	Ectopic expression of a defined set of transcription factors (TFs) can directly convert fibroblasts into a cardiac myocyte cell fate. Beside inefficiency in generating induced cardiomyocytes (iCMs), the molecular mechanisms that regulate this process remained to be well defined. The main purpose of this study was to provide better insight on the transcriptome regulation and to introduce a new strategy for candidating TFs for the transdifferentiation process. Eight mouse and three human high quality microarray data sets were analyzed to find differentially expressed genes (DEGs), which we integrated with TF-binding sites and protein-protein interactions to construct gene regulatory and protein-protein interaction networks. Topological and biological analyses of constructed gene networks revealed the main regulators and most affected biological processes. The DEGs could be categorized into two distinct groups, first, up-regulated genes that are mainly involved in cardiac-specific processes and second, down-regulated genes that are mainly involved in fibroblast-specific functions. Gata4, Mef2a, Tbx5, Tead4 TFs were identified as main regulators of cardiac-specific gene expression program; and Trp53, E2f1, Myc, Sfpi1, Lmo2, and Meis1 were identified as TFs which mainly regulate the expression of fibroblast-specific genes. Furthermore, we compared gene expression profiles and identified TFs between mouse and human to find the similarities and differences. In summary, our strategy of meta-analyzing the data of high-throughput techniques by computational approaches, besides revealing the mechanisms involved in the regulation of the gene expression program, also suggests a new approach for increasing the efficiency of the direct reprogramming of fibroblasts into iCMs. J. Cell. Physiol. 232: 2053-2062, 2017. © 2016 Wiley Periodicals, Inc.
MeSH term(s)	Animals ; Cell Lineage ; Cell Transdifferentiation ; Cellular Reprogramming ; Computational Biology ; Databases, Genetic ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression Profiling/methods ; Gene Expression Regulation ; Gene Regulatory Networks ; Heart Diseases/genetics ; Heart Diseases/metabolism ; Heart Diseases/pathology ; Humans ; Mice ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Protein Interaction Maps ; Signal Transduction ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Transcriptome
Chemical Substances	Transcription Factors
Language	English
Publishing date	2017-08
Publishing country	United States
Document type	Journal Article ; Meta-Analysis
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.25580
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Role of Hepatic-Specific Transcription Factors and Polycomb Repressive Complex 2 during Induction of Fibroblasts to Hepatic Fate.

Rastegar-Pouyani, Shima / Khazaei, Niusha / Wee, Ping / Mohammadnia, Abdulshakour / Yaqubi, Moein

PloS one

2016 Volume 11, Issue 11, Page(s) e0167081

Abstract: Direct reprogramming using defined sets of transcription factors (TFs) is a recent strategy for generating induced hepatocytes (iHeps) from fibroblasts for use in regenerative medicine and drug development. Comprehensive studies detailing the regulatory ... ...

Abstract	Direct reprogramming using defined sets of transcription factors (TFs) is a recent strategy for generating induced hepatocytes (iHeps) from fibroblasts for use in regenerative medicine and drug development. Comprehensive studies detailing the regulatory role of TFs during this reprogramming process could help increase its efficiency. This study aimed to find the TFs with the greatest influences on the generation of iHeps from fibroblasts, and to further understand their roles in the regulation of the gene expression program. Here, we used systems biology approaches to analyze high quality expression data sets in combination with TF-binding sites data and protein-protein interactions data during the direct reprogramming of fibroblasts to iHeps. Our results revealed two main patterns for differentially expressed genes (DEGs): up-regulated genes were categorized as hepatic-specific pattern, and down-regulated genes were categorized as mesoderm- and fibroblast-specific pattern. Interestingly, hepatic-specific genes co-expressed and were regulated by hepatic-specific TFs, specifically Hnf4a and Foxa2. Conversely, the mesoderm- and fibroblast-specific pattern was mainly silenced by polycomb repressive complex 2 (PRC2) members, including Suz12, Mtf2, Ezh2, and Jarid2. Independent analysis of both the gene and core regulatory network of DE-TFs showed significant roles for Hnf4a, Foxa2, and PRC2 members in the regulation of the gene expression program and in biological processes during the direct conversion process. Altogether, using systems biology approaches, we clarified the role of Hnf4a and Foxa2 as hepatic-specific TFs, and for the first time, introduced the PRC2 complex as the main regulator that favors the direct reprogramming process in cooperation with hepatic-specific factors.
MeSH term(s)	Cellular Reprogramming ; Fibroblasts/cytology ; Gene Regulatory Networks ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Organ Specificity ; Polycomb Repressive Complex 2/metabolism ; Protein Interaction Maps ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2016-11-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0167081
Database	MEDical Literature Analysis and Retrieval System OnLINE

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