Bio

Honors & Awards


  • Senior Research Fellowship, Council of Scientific and Industrial Research (CSIR), India (2014-2016)

Professional Education


  • Doctor of Philosophy, Academy of Scientific & Innovative Research (2016)
  • PhD, Academy of Scientific & Innovative Research (AcSIR), Institute of Genomics & Integrative Biology (CSIR-IGIB), New Delhi, India, Biological Sciences: "Physiological Determinants in Mesenchymal Stem Cell mediated Intercellular Mitochondrial Transfer" (2016)
  • MSc., Presidency College, University of Calcutta, India, Molecular Biology & Genetics (2009)
  • BSc., Serampore College, University of Calcutta, India, Zoology (Hons). (2007)

Stanford Advisors


Publications

All Publications


  • Transient non-integrative expression of nuclear reprogramming factors promotes multifaceted amelioration of aging in human cells. Nature communications Sarkar, T. J., Quarta, M., Mukherjee, S., Colville, A., Paine, P., Doan, L., Tran, C. M., Chu, C. R., Horvath, S., Qi, L. S., Bhutani, N., Rando, T. A., Sebastiano, V. 2020; 11 (1): 1545

    Abstract

    Aging is characterized by a gradual loss of function occurring at the molecular, cellular, tissue and organismal levels. At the chromatin level, aging associates with progressive accumulation of epigenetic errors that eventually lead to aberrant gene regulation, stem cell exhaustion, senescence, and deregulated cell/tissue homeostasis. Nuclear reprogramming to pluripotency can revert both the age and the identity of any cell to that of an embryonic cell. Recent evidence shows that transient reprogramming can ameliorate age-associated hallmarks and extend lifespan in progeroid mice. However, it is unknown how this form of rejuvenation would apply to naturally aged human cells. Here we show that transient expression of nuclear reprogramming factors, mediated by expression of mRNAs, promotes a rapid and broad amelioration of cellular aging, including resetting of epigenetic clock, reduction of the inflammatory profile in chondrocytes, and restoration of youthful regenerative response to aged, human muscle stem cells, in each case without abolishing cellular identity.

    View details for DOI 10.1038/s41467-020-15174-3

    View details for PubMedID 32210226

  • Single-cell mass cytometry reveals cross-talk between inflammation-dampening and inflammation-amplifying cells in osteoarthritic cartilage Science Advances Grandi, F. ., Baskar, R., Smeriglio, P., Murkherjee, S., Indelli, P., F. Amanatullah, D., Goodman, S., Chu, C., Bendall , S., Bhutani, N. 2020; 6 (11)

    View details for DOI 10.1126/sciadv.aay5352

  • Transient non-integrative nuclear reprogramming promotes multifaceted reversal of aging in human cells bioRxiv Sarkar, T. J., Quarta, M., Mukherjee, S., Colville, A., Paine, P., Doan, L., M. Tran, C., R. Chu, C., Horvath, S., Bhutani, N., A. Rando, T., Sebastiano, V. 2019

    View details for DOI 10.1101/573386

  • Regulation of mitochondrial transport in mesenchymal stromal cells The Biology and Therapeutic Application of Mesenchymal Cells - Set Mukherjee, S., Bhatraju, N. K., Ahmad, T., Agrawal, A. edited by Atkinson, K. Wiley-Blackwell. 2017: 104–113
  • Assessing Mitochondrial Transport via Cytoplasmic Nanotubular Bridges in Cells Bio-protocol Mukherjee, S., Ahmad, T., Agrawal, A., et al 2015; 5 (15)

    View details for DOI 10.21769/BioProtoc.1542

  • Miro1 regulates intercellular mitochondrial transport & enhances mesenchymal stem cell rescue efficacy EMBO JOURNAL Ahmad, T., Mukherjee, S., Pattnaik, B., Kumar, M., Singh, S., Kumar, M., Rehman, R., Tiwari, B. K., Jha, K. A., Barhanpurkar, A. P., Wani, M. R., Roy, S. S., Mabalirajan, U., Ghosh, B., Agrawal, A. 2014; 33 (9): 994-1010

    Abstract

    There is emerging evidence that stem cells can rejuvenate damaged cells by mitochondrial transfer. Earlier studies show that epithelial mitochondrial dysfunction is critical in asthma pathogenesis. Here we show for the first time that Miro1, a mitochondrial Rho-GTPase, regulates intercellular mitochondrial movement from mesenchymal stem cells (MSC) to epithelial cells (EC). We demonstrate that overexpression of Miro1 in MSC (MSCmiro(Hi)) leads to enhanced mitochondrial transfer and rescue of epithelial injury, while Miro1 knockdown (MSCmiro(Lo)) leads to loss of efficacy. Treatment with MSCmiro(Hi) was associated with greater therapeutic efficacy, when compared to control MSC, in mouse models of rotenone (Rot) induced airway injury and allergic airway inflammation (AAI). Notably, airway hyperresponsiveness and remodeling were reversed by MSCmiro(Hi) in three separate allergen-induced asthma models. In a human in vitro system, MSCmiro(Hi) reversed mitochondrial dysfunction in bronchial epithelial cells treated with pro-inflammatory supernatant of IL-13-induced macrophages. Anti-inflammatory MSC products like NO, TGF-β, IL-10 and PGE2, were unchanged by Miro1 overexpression, excluding non-specific paracrine effects. In summary, Miro1 overexpression leads to increased stem cell repair.

    View details for DOI 10.1002/embj.201386030

    View details for Web of Science ID 000336495500007

    View details for PubMedID 24431222

  • Computational classification of mitochondrial shapes reflects stress and redox state CELL DEATH & DISEASE Ahmad, T., Aggarwal, K., Pattnaik, B., Mukherjee, S., Sethi, T., Tiwari, B. K., Kumar, M., Micheal, A., Mabalirajan, U., GHOSH, B., Roy, S. S., Agrawal, A. 2013; 4

    Abstract

    Dynamic variations in mitochondrial shape have been related to function. However, tools to automatically classify and enumerate mitochondrial shapes are lacking, as are systematic studies exploring the relationship of such shapes to mitochondrial stress. Here we show that during increased generation of mitochondrial reactive oxygen species (mtROS), mitochondria change their shape from tubular to donut or blob forms, which can be computationally quantified. Imaging of cells treated with rotenone or antimycin, showed time and dose-dependent conversion of tubular forms to donut-shaped mitochondria followed by appearance of blob forms. Time-lapse images showed reversible transitions from tubular to donut shapes and unidirectional transitions between donut and blob shapes. Blobs were the predominant sources of mtROS and appeared to be related to mitochondrial-calcium influx. Mitochondrial shape change could be prevented by either pretreatment with antioxidants like N-acetyl cysteine or inhibition of the mitochondrial calcium uniporter. This work represents a novel approach towards relating mitochondrial shape to function, through integration of cellular markers and a novel shape classification algorithm.

    View details for DOI 10.1038/cddis.2012.213

    View details for Web of Science ID 000315767600011

    View details for PubMedID 23328668

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