Senior Research Specialist
I came to RPI from Albany Medical College where I worked in the laboratory of Dr. Paul J. Higgins in the Department of Regenerative and Cancer Cell Biology. The lab’s primary focus was on the involvement of Transforming growth factor-beta (TGF-β) signaling in the development and progression of acute and chronic kidney disease, including cross-talk with epidermal growth factor receptor (EGFR) signaling and cell cycle arrest/senescence.
- M.S. in Immunology and Microbial Diseases, Albany Medical College, Albany, NY (2018)
- Research Focus: Discerning the role of resident bone marrow and spleen macrophages on the activation and effector function of donor T cells in a murine model of aplastic anemia
- B.A. in Biology, Russell Sage College, Troy, NY (2013)
- Research Focus: Evaluating the effects of Mycobacterium vaccae on learning and cognition in BALB/c mice
My current research focuses on identification of harmful cyanobacteria within algal blooms, work performed in close cooperation with the Jefferson Project at Lake George (Dr. Rick Relyea, email@example.com, https://jeffersonproject.rpi.edu/) and RPI’s Genomics Core facility (Dr. Yang Bai, firstname.lastname@example.org, https://biotech.rpi.edu/core-facilities/genomics). Cyanobacterial harmful algal blooms (CyanoHABs) pose a significant public health concern as toxins produced by some species of cyanobacteria (cyanotoxins) can cause acute and chronic illnesses in humans, as well as damage aquatic ecosystem health. Furthermore, the overabundance of cyanobacteria has downstream consequences on irrigation, recreation, and the availability of clean drinking water. The ultimate goal of this work is to identify specific toxin-producing genes and their environmental triggers (e.g. nutrients, pollutants, etc.) such that their expression can be prevented or otherwise modulated and their effects blunted.
Gifford, C.C., Lan, F., Tang, J., Costello, A., Goldschmeding, R., Samarakoon, R., & Higgins, P.J. Plasminogen Activator Inhibitor-1 (PAI-1) Induction During Kidney Injury Promotes Fibrotic Epithelial Dysfunction via Deregulation of Klotho, p53, and TGF-β1-Receptor Signaling. FASEB J. 2021; 35(7): e21725. DOI: 10.1096/fj.202002652RR.
Higgins, C.E., Tang, J., Higgins, S.P., Gifford, C.C., Mian, B.M., Jones, D.M., Zhang, W., Costello, A., Conti, D.J., Samarakoon, R., & Higgins, P.J. The Genomic Response to TGF-β1 Dictates Failed Repair and Progression of Fibrotic Disease in the Obstructed Kidney. Front Cell Dev Biol. 2021; 9:678524. DOI: 10.3389/fcell.2021.678524.
Gifford, C.C., Tang, J., Costello, A., Khakoo, N.S., Nguyen, T.Q., Goldschmeding, R., Higgins, P.J., & Samarakoon, R. Negative regulators of TGF-β1 signaling in renal fibrosis; pathological mechanisms and novel therapeutic opportunities. Clin Sci (London). 2021; 135(2): 275-303. DOI: 10.1042/CS20201213.
McCabe, A., Smith, J.N.P., Costello, A., Maloney, J., Katekani, D., & MacNamara, K.C. Hematopoietic stem cell loss and hematopoietic failure in severe aplastic anemia is driven by macrophages and aberrant podoplanin expression. Haematologica. 2018; 103(9): 1451-1461. DOI: 10.3324/haematol.2018.189449.
Zhang, K., Xu, X., Asghar Pasha, M., Siebel, C.W., Costello, A., Haczku, A., MacNamara, K.C., Liang, T., Zhu, J., Bhandoola, A., Maillard, I., & Yang, Q. Cutting Edge: Notch Signaling Promotes the Plasticity of Group-2 Innate Lymphoid Cells. J Immunol. 2017; 198(5): 1798-1803. DOI: 10.4049/jimmunol.1601421.