Artem Trotsyuk is a Ph.D. student in Dr. Geoffrey Gurtner’s laboratory in the Department of Surgery at Stanford University. His research interests lie in bioengineering, gene editing, CRISPR therapy and regenerative medicine. Currently, he is using bioengineering tools coupled with artificial intelligence to improve wound healing outcomes in diabetic patients.
Education & Certifications
Bachelor of Science, University of California, Davis, Biological Sciences (2009)
TOPICAL FOCAL ADHESION KINASE INHIBITOR PROMOTES SKIN REGENERATION AND SCAR PREVENTION IN A PRECLINICAL PORCINE MODEL
WILEY. 2019: A11–A12
View details for Web of Science ID 000463117000043
ACCELERATION OF WOUND HEALING WITH PHD2-AND MIR210-TARGETING OLIGONUCLEOTIDES
WILEY. 2019: A36
View details for Web of Science ID 000463117000158
BIOMIMETIC ADIPIOSE STEM CELL DRESSING FOR SKIN REGENERATION
WILEY. 2019: A4
View details for Web of Science ID 000463117000011
Optimization of transdermal deferoxamine leads to enhanced efficacy in healing skin wounds.
Journal of controlled release : official journal of the Controlled Release Society
Chronic wounds remain a significant burden to both the healthcare system and individual patients, indicating an urgent need for new interventions. Deferoxamine (DFO), an iron-chelating agent clinically used to treat iron toxicity, has been shown to reduce oxidative stress and increase hypoxia-inducible factor-1 alpha (HIF-1α) activation, thereby promoting neovascularization and enhancing regeneration in chronic wounds. However due to its short half-life and adverse side effects associated with systemic absorption, there is a pressing need for targeted DFO delivery. We recently published a preclinical proof of concept drug delivery system (TDDS) which showed that transdermally applied DFO is effective in improving chronic wound healing. Here we present an enhanced TDDS (eTDDS) comprised exclusively of FDA-compliant constituents to optimize drug release and expedite clinical translation. We evaluate the eTDDS to the original TDDS and compare this with other commonly used delivery methods including DFO drip-on and polymer spray applications. The eTDDS displayed excellent physicochemical characteristics and markedly improved DFO delivery into human skin when compared to other topical application techniques. We demonstrate an accelerated wound healing response with the eTDDS treatment resulting in significantly increased wound vascularity, dermal thickness, collagen deposition and tensile strength. Together, these findings highlight the immediate clinical potential of DFO eTDDS to treating diabetic wounds. Further, the topical drug delivery platform has important implications for targeted pharmacologic therapy of a wide range of cutaneous diseases.
View details for DOI 10.1016/j.jconrel.2019.07.009
View details for PubMedID 31299261
Deferoxamine Can Prevent Pressure Ulcers and Accelerate Healing in Aged Mice.
Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
Chronic wounds are a significant medical and economic problem worldwide. Individuals over the age of 65 are particularly vulnerable to pressure ulcers and impaired wound healing. With this demographic growing rapidly there is a need for effective treatments. We have previously shown that defective hypoxia signaling through destabilization of the master hypoxia-inducible factor 1alpha (HIF-1alpha) underlies impairments in both aging and diabetic wound healing. To stabilize HIF-1alpha, we developed a transdermal delivery system of the FDA-approved small molecule deferoxamine (DFO) and found that transdermal DFO could both prevent and treat ulcers in diabetic mice. Here, we show that transdermal DFO can similarly prevent pressure ulcers and normalize aged wound healing. Enhanced wound healing by DFO is brought about by stabilization of HIF-1alpha and improvements in neovascularization. Transdermal DFO can be rapidly translated into the clinic and may represent a new approach to prevent and treat pressure ulcers in aged patients. This article is protected by copyright. All rights reserved.
View details for PubMedID 30152571
RNA-Based Combination Therapy for Diabetic Wound Healing
CELL PRESS. 2018: 38–39
View details for Web of Science ID 000435342200078
Controlled Delivery of a Focal Adhesion Kinase Inhibitor Results in Accelerated Wound Closure with Decreased Scar Formation.
The Journal of investigative dermatology
Formation of scars following wounding or trauma represents a significant healthcare burden costing the economy billions of dollars every year. Activation of focal adhesion kinase (FAK) has been shown to play a pivotal role in transducing mechanical signals to elicit fibrotic responses and scar formation during wound repair. We have previously shown that inhibition of FAK using local injections of a small molecule FAK inhibitor (FAKI) can attenuate scar development in a hypertrophic scar model. Clinical translation of FAKI therapy has been challenging, however, due to the lack of an effective drug delivery system for extensive burn injuries, blast injuries, and large excisional injuries. To address this issue, we have developed a pullulan collagen-based hydrogel to deliver FAKI to excisional and burn wounds in mice. Specifically, two distinct drug-laden hydrogels were developed for rapid or sustained release of FAKI for treatment of burn wounds and excisional wounds, respectively. Controlled delivery of FAKI via pullulan collagen hydrogels accelerated wound healing, reduced collagen deposition and activation of scar forming myofibroblasts in both wound healing models. Our study highlights a biomaterial-based drug delivery approach for wound and scar management that has significant translational implications.
View details for PubMedID 29775632
Acceleration of Diabetic Wound Healing with PHD2- and miR-210-targeting Oligonucleotides.
Tissue engineering. Part A
View details for PubMedID 29644938
Allogeneic Cd26/Cd55 Cell Therapy for Treating Burn Wounds
WILEY. 2018: A9
View details for Web of Science ID 000430308600032
Transdermal Deferoxamine Enhances Wound Healing in Aged Mice
WILEY. 2018: A10
View details for Web of Science ID 000430308600036
Identification of cancer stem cell subpopulations of CD34(+) PLC/PRF/5 that result in three types of human liver carcinomas.
Stem cells and development
2015; 24 (8): 1008-1021
CD34(+) stem cells play an important role during liver development and regeneration. Thus, we hypothesized that some human liver carcinomas (HLCs) might be derived from transformed CD34(+) stem cells. Here, we determined that a population of CD34(+) cells isolated from PLC/PRF/5 hepatoma cells (PLC) appears to function as liver cancer stem cells (LCSCs) by forming HLCs in immunodeficient mice with as few as 100 cells. Moreover, the CD34(+) PLC subpopulation cells had an advantage over CD34(-) PLCs at initiating tumors. Three types of HLCs were generated from CD34(+) PLC: hepatocellular carcinomas (HCCs); cholangiocarcinomas (CC); and combined hepatocellular cholangiocarcinomas (CHCs). Tumors formed in mice transplanted with 12 subpopulations and 6 progeny subpopulations of CD34(+) PLC cells. Interestingly, progenies with certain surface antigens (CD133, CD44, CD90, or EPCAM) predominantly yielded HCCs. CD34(+) PLCs that also expressed OV6 and their progeny OV6(+) cells primarily produced CHC and CC. This represents the first experiment to demonstrate that the OV6(+) antigen is associated with human CHC and CC. CD34(+) PLCs that also expressed CD31 and their progeny CD31(+) cells formed CHCs. Gene expression patterns and tumor cell populations from all xenografts exhibited diverse patterns, indicating that tumor-initiating cells (TICs) with distinct antigenic profiles contribute to cancer cell heterogeneity. Therefore, we identified CD34(+) PLC cells functioning as LCSCs generating three types of HLCs. Eighteen subpopulations from one origin had the capacity independently to initiate tumors, thus functioning as TICs. This finding has broad implications for better understanding of the multistep model of tumor initiation and progression. Our finding also indicates that CD34(+) PLCs that also express OV6 or CD31 result in types of HLCs. This is the first report that PLC/PRF/5 subpopulations expressing CD34 in combination with particular antigens defines categories of HLCs, implicating a diversity of origins for HLC.
View details for DOI 10.1089/scd.2014.0405
View details for PubMedID 25519836
View details for PubMedCentralID PMC4390116
- Human liver carcinomas originated from CD34+ hematopoietic precursors Hepatology 2012: 56():807A–808A