Hiranmoy Das Laboratory | Texas Tech University Health Sciences Center

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About Us

Vascular Biology and Stem Cell Research Laboratory

Stem cell therapy using autologous stem cells to treat degenerative diseases has been promising, however the limited availability and compromised quality of progenitor cells in aged and diseased patients limit its therapeutic potential. Alternatively, use of cord blood-derived stem cells is advantageous as it is easy to harvest, harmless to donor, ethical, ontogenetically primitive and can be stored in cord blood bank for years. Moreover, cord blood-derived stem cell transplantation is associated with reduced risk of developing graft versus host disease. Nevertheless, small number of stem cells provided by a single cord limits its clinical application. Our laboratory has developed a nanofiber-based ex-vivo human umbilical cord blood-derived stem cell expansion technology, which not only preserves stem cell phenotype, but also provides required number of biologically functional stem cells. Furthermore, we can genetically modify nanofiber-expanded stem cells to enhance their angiogenic and therapeutic potential for various degenerative diseases such as hind limb ischemia, myocardial ischemia, stroke-mediated ischemia, wound healing and osteoporosis. Current investigations use immunocompromised murine, rat and swine models for relevant studies. Molecular aspects of stem cell functionality are also being investigated in these animal models after cell-based therapy. We are also extending our in-depth research on human dental pulp-derived stem cells, corneal epithelial and endothelial stem cells to make them suitable for clinical use for various degenerative diseases. 

The molecular mechanisms regulating activation and functionality of monocytes remain incompletely understood in the context of inflammation. We provided evidence that a transcription factor, Krüppel-like factor 2 (KLF2), inhibits proinflammatory activation of monocytes. KLF2 expression in circulating monocytes is reduced in patients with chronic inflammatory conditions such as coronary artery disease (CAD). KLF2 inhibits the LPS-mediated induction of proinflammatory factors, cytokines, and chemokines and reduces phagocytosis in vitro. Conversely, short interfering RNA-mediated reduction in KLF2 increased inflammatory gene expression. Reconstitution of immunodeficient mice with KLF2-overexpressing monocytes significantly reduced carrageenan-induced acute paw edema formation. Mechanistically, we show that KLF2 inhibits the transcriptional activity of both NF-kB and activator protein 1, in part by means of recruitment of transcriptional coactivator p300/CBP-associated factor. These observations identify KLF2 as a novel negative regulator of monocytic activation. Current investigations focus on the role of KLF2 in the genetically altered murine model of rheumatoid arthritis.

Human gamma delta (γδ) T cells represent a small subset of T cell population that possesses distinct T cell receptor (TCR) on their surface. Majority of γδ T cells are Vγ2Vδ2 subset. This subset can increase 2- to 10-fold in peripheral blood in a variety of infectious diseases. Vγ2Vδ2 T cells may be considered part of the adaptive immune system as they have a memory phenotype, junctionally diverse TCR’s that require gene rearrangement for their cell surface expression and the ability to undergo either anergy or expansion depending on the availability of co-stimulation. On the other hand, Vγ2Vδ2 T cells are also considered a part of the innate immune response. Pattern recognition by the Vγ2Vδ2 TCR allows the expansion of memory γδ T cells into a large number in normal adults during microbial infections. These large numbers of memory T cells are capable of responding to antigens produced by microbes and thus may bridge the gap between the innate and adaptive immune responses. MHC class I chain related molecules A and B (MICA and MICB, danger signals), which are widely expressed in epithelial tumor cells, and virally or bacterially infected cells, can be recognized by γδ T cells and NK cells via NKG2D; a signaling pathway responsible for enhanced cytotoxicity against infected or tumor cells. Our current focus is to identify molecules responsible for recognition of various tumor cells (such as ovarian, breast, and cervical) by γδ T cells. The ultimate goal is to develop combined targeted immunotherapy with γδ T cells for various tumors.

Research Interest

  • KLF2
  • Stem cells
  • Myeloid cells
  • Autophagy
  • Gamma delta T cells

The Team

Derek Barthels Sariful Howlader Prathyusha Naidu  

Derek Barthels

Ph.D. Candidate/ Research Assistant

Md Sariful Islam Howlader
Graduate Student/ Research Assistant

Prathyusha Naidu

Graduate Student / Research Assistant

 

 

Das Lab

Honors & Awards

2022

  • Recipient of President’s Excellence in Research Award from the Texas Tech University Health Sciences Center, TX, USA.
  • Tenured Professor, Department of Pharmaceutical Sciences, Jerry H. Hodge School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX.
  • Received P3 Teaching team of the year award, Integrated Therapy and Practice VII; Oncology (PharmD Course), Jerry H. Hodge School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX.
  • Recipient of Chancellor’s Council Distinguished Research Award from the Texas Tech University Health Sciences Center, the highest honor granted to faculty throughout the Texas Tech University System, TX, USA. 

2021

  • Elected Fellow of American Heart Association (FAHA) conferred by the Council on Basic Cardiovascular Sciences (BCVS), USA.

2020

  • Inducted into the Arthritis, Connective Tissue and Skin (ACTS) Study Section, NIH, as a ‘Chartered Member’.

2018

  • Inducted into the National Academy of Inventors, USA.
  • Keynote Speaker, Second International Conference on Clinical Trial and Innovative Therapeutics. Organized by The South African Training Academy held at Durban, South Africa.

updated: 10/11/2022

 

Contact Us:

Hiranmoy Das

Hiranmoy Das, Ph.D.
Professor
Department of Pharmaceutical Sciences
Office: (806) 414-9623

hiranmoy.das@ttuhsc.edu

Office: ARB 2116 | Lab: ARB XXX

Amarillo Research Building
Texas Tech University Health Sciences Center
1406 S. Coulter St.
Amarillo, TX, USA, 79106

Das Lab