5 results on '"Sayantani Sinha"'
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2. Pbrm1 Steers Mesenchymal Stromal Cell Osteolineage Differentiation by Integrating PBAF-Dependent Chromatin Remodeling and BMP/TGF-β Signaling
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Sayantani Sinha, Mayukh Biswas, Shankha Subhra Chatterjee, Sanjay Kumar, and Amitava Sengupta
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Biology (General) ,QH301-705.5 - Abstract
Summary: Bone morphogenic protein (BMP)/transforming growth factor β (TGF-β) signaling determines mesenchymal-stromal-cell (MSC) osteolineage commitment and tissue identity. However, molecular integration of developmental signaling with MSC-intrinsic chromatin regulation remains incompletely understood. SWI/SNF-(BAF) is an ATP-dependent chromatin remodeler implicated in multi-cellular development. We show that BMPs and long-term osteogenic signals in MSCs selectively induce expression of polybromo BAF (PBAF) components Pbrm1, Arid2, and Brd7. Loss of Pbrm1/Arid2/Brd7 profoundly impairs osteolineage gene expression and osteogenesis without compromising adipogenesis. Pbrm1 loss attenuates MSC in vivo ossification. Mechanistically, Pbrm1/PBAF deficiency impairs Smad1/5/8 activation through locus-specific epi-genomic remodeling, involving Pbrm1 bromodomains, along with transcriptional downregulation of Bmpr/TgfβrII affecting BMP-early-responsive gene expression. Gain of function of BmprIβ, TgfβrII in PBAF-deficient MSCs partly restores Smad1/5/8 activation and osteogenesis. Pbrm1 loss further affects hematopoietic stem and progenitor activity through non-cell-autonomous regulation of microenvironment and niche-factor expression. Together, these findings reveal a link illustrating epi-genomic feedforward control of BMP/TGF-β signaling to transcriptional and cellular plasticity in the mesenchymal microenvironment and account for stromal-SWI/SNF in hematopoiesis. : Sinha et al. examine the role of Pbrm1/polybromo-BAF in mammalian mesenchymal stromal cell osteolineage commitment and hematopoiesis. Osteogenic signals induce Pbrm1/PBAF expression, which in turn orchestrates chromatin remodeling at BmprIβ/TgfβrII loci. These findings reveal an epi-genomic connection to feedforward control of BMP/TGF-β signaling in the mesenchymal stromal microenvironment. Keywords: BMP/TGF-β signaling, mesenchymal stromal cell, hematopoietic microenvironment, hematopoiesis, osteolineage differentiation, SWI/SNF, chromatin remodeling, bromodomain, transcriptional regulation, feedforward control
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- 2020
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3. Establishment of a Long-Term Co-culture Assay for Mesenchymal Stromal Cells and Hematopoietic Stem/Progenitors
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Amitava Sengupta, Sayan Chakraborty, and Sayantani Sinha
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Cell ,Antigens, CD34 ,Cell Separation ,Biology ,Models, Biological ,General Biochemistry, Genetics and Molecular Biology ,Qualitative analysis ,medicine ,Protocol ,Centrifugation, Density Gradient ,Humans ,Progenitor cell ,lcsh:Science (General) ,Clonogenic assay ,General Immunology and Microbiology ,Immunomagnetic Separation ,General Neuroscience ,Stem Cells ,Mesenchymal stem cell ,Mesenchymal Stem Cells ,Cell Biology ,Hematopoietic Stem Cells ,Coculture Techniques ,Cell biology ,Clone Cells ,Haematopoiesis ,medicine.anatomical_structure ,Repopulation ,Biological Assay ,Stem cell ,lcsh:Q1-390 - Abstract
Summary We describe a protocol for a long-term co-culture assay to study the contribution of mesenchymal stromal cells (MSCs) in regulating hematopoietic stem/progenitor cell (HSPC) activity. In addition, we describe the use of a clonogenic assay to determine myelo-erythroid differentiation. This long-term culture-initiating cell assay can be used for qualitative analysis of MSCs capable of supporting hematopoiesis and may also be used as a proxy readout to study HSPC repopulation. For complete details on the use and execution of this protocol, please refer to Sinha et al. (2020)., Graphical Abstract, Highlights • We report long-term co-culture of mesenchymal stroma and hematopoietic stem/progenitors • End-point colony-forming analysis helps determine myelo-erythroid differentiation • This protocol analyzes mesenchymal stromal cell potential to support hematopoiesis • Long-term culture-initiating cell assay is a surrogate for hematopoietic engraftment, We describe a protocol for a long-term co-culture assay to study the contribution of mesenchymal stromal cells (MSCs) in regulating hematopoietic stem/progenitor cell (HSPC) activity. In addition, we describe the use of a clonogenic assay to determine myelo-erythroid differentiation. This long-term culture-initiating cell assay can be used for qualitative analysis of MSCs capable of supporting hematopoiesis and may also be used as a proxy readout to study HSPC repopulation.
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- 2020
4. miRNA and Cancer
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Amitava Sengupta, Liberalis Debraj Boila, Sayantani Sinha, and Shankha Subhra Chatterjee
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0301 basic medicine ,Genome instability ,Cancer ,Biology ,medicine.disease ,Bioinformatics ,medicine.disease_cause ,Somatic evolution in cancer ,Cell fate commitment ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Cancer stem cell ,030220 oncology & carcinogenesis ,microRNA ,Cancer research ,medicine ,Gene silencing ,Carcinogenesis - Abstract
MicroRNAs (miRNAs) are 19–22 nt-long RNA molecules that mediate posttranscriptional gene silencing. Since their discovery in Caenorhabditis elegans , miRNAs gained attention after a plethora of reports suggested their contribution to cell fate commitment, cellular plasticity, and cancer. Tumorigenesis often involves tumor-cell autonomous progressive, even stochastic, accumulation of a series of genetic and epigenetic changes, somatic mutations, and genomic instability that eventually transform into an overt malignant phenotype. Hallmarks of cancer further highlight importance of tissue-resident cancer stem cells, tumor-initiating cells, and cross talk between tumor cells within the mesenchymal microenvironment, as an important prognostic index in cancer development. Fluctuation in miRNA levels causes derepression of gene expression and could lead to tumor cell dedifferentiation. In the following sections, we illustrate miRNA involvement across the crucial hallmarks of tumorigenesis. Given the current understanding of miRNA regulation in cancer, synthetic regulation with miRNA mimics and therapeutic intervention would play a key role in cancer prevention.
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- 2018
5. List of Contributors
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Santanu Adhikary, Carlos Baliñas, Shakri Banerjee, Sharmila A. Bapat, Rahul Bhome, Liberalis D. Boila, Vincenzo Bonnici, Debojit Bose, Laura Boyero, Jayprokas Chakrabarti, Damayanti Chakravarti, JiaJia Chan, Alain Chariot, Shankha S. Chatterjee, Taiping Chen, Pierre Close, Isabel F. Coira, Marta Cuadros, Juan Cui, Chandrima Das, Shaoli Das, Simone de Brot, Ng Desi, Nadya Dimitrova, Rachel L. Dittmar, Katherine Emo, Sayak Ganguli, Kshipra M. Gharpure, Suman Ghosal, Rosalba Giugno, Damjan Glavacˇ, Frank Grützner, Sohini Gupta, Agnik Halder, Nina Hauptman, Antonio Herrera, Louise House, Changzhi Huang, Shenglin Huang, Reuben Jacob, Victoria James, Daša Jevšinek Skok, Ragini Kondetimmanahalli, Eunice Lee, Sebastian A. Leidel, Yan Li, Yuan Li, Gabriel Lopez-Berestein, Jose A. Lupiáñez, Joel Martín-Padrón, Pedro P. Medina, Alex Mirnezami, Sanga Mitra, Nigel P. Mongan, Shravanti Mukherjee, Suchismita Panda, Paola Peinado, Alfredo Pulvirenti, Fernando J. Reyes-Zurita, Maria I. Rodriguez, Susanta Roychoudhury, Siddhartha Roy, Eva E. Rufino-Palomares, Catrin S. Rutland, Emre Sayan, Flavia Scoyni, Amitava Sengupta, Sharmila Sengupta, Subrata Sen, Sweta Sharma Saha, Anjali Shiras, Yuming Shi, Sayantani Sinha, Ondrej Slaby, Anil K. Sood, Kamila Souckova, Yvonne Tay, Yu Wang, Zhiguo Wang, Sherry Y. Wu, Tianqi Yang, Eda Yildirim, and Zhengzhou Ying
- Published
- 2018
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