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Carol Artlett

Carol Artlett, PhD

Associate Professor

Department: Microbiology & Immunology


  • PhD - University of London (1996)

Carol Artlett, PhD, is an associate professor in the Department of Microbiology & Immunology at Drexel University College of Medicine.

Research Overview

My research is primarily focused on fibrosis and the signaling pathways that not only drive the expression of collagen but promote procollagen export from the endoplasmic reticulum. This interest includes several areas of expertise involving inflammasome signaling, and the role of miR-155 and IL-1 in promoting fibrosis. More recent work has focused on the endoplasmic reticulum and the role of TANGO1 in procollagen export. TANGO1 accompanied by cTAGE5 is needed for the expansion of tubules for protein export to the Golgi apparatus. Without these two proteins, collagen and indeed a milieu of other high molecular weight extracellular proteins cannot be exported and then secreted from the cell. Our research is focused on pathways that intersect with the inflammasome that induce TANGO1 and cTAGE5 expression and thereby promote fibrosis. Understanding these mechanisms is crucial to developing effective therapeutics that will control this pathology. During our research, we have identified a small molecule that is anti-fibrotic because it targets TANGO1 expression. We believe this could be an effective therapeutic for the fibrotic autoimmune disease systemic sclerosis (scleroderma). In these patients where there is uncontrolled systemic fibrosis that severely affects their quality of life leading to an early death post-diagnosis.

Our laboratory is also focused on the development of therapeutics that can advance the healing of chronic wounds. The process of normal wound repair undergoes well-defined time frames for healing, correlating with an initial inflammatory phase, a proliferative phase, and finally a remodeling phase. This process requires the recruitment of inflammatory cells into the wound but also the differentiation and proliferation of fibroblasts into myofibroblasts inducing wound closure. Myofibroblasts are the most critical cell type in wound healing mediating the expression of elevated levels of collagen and contraction of wound margins. However, chronic wounds have stalled in healing with reduced ECM expression, reduced myofibroblast numbers, and increased degradation of the ECM by metalloproteinases. We have found an FDA-approved compound promotes critical features of wound healing including increased collagen synthesis, increased expression of growth factors, and increased fibroblast proliferation and migration. The goal of this project is to develop this compound as a novel inexpensive molecule that can be added to hydrogels for release over time to enhance wound healing.

Research Interests

Inflammasome signaling; IL-1 mediated fibrosis; collagen export from the endoplasmic reticulum; miR-155; small molecule therapeutic development


We are interested in what mediates the scleroderma (SSc) phenotype by understanding what regulates fibrosis in the skin and internal tissues in these patients. SSc is a fibrotic disease of unknown origin that is predominantly found in women. What is apparent is the uncontrolled fibrosis in the dermis and internal organs that affects morbidity and leads to mortality in these patients. Understanding the mechanisms whereby myofibroblasts and fibroblasts interact with the extracellular matrix (ECM) is crucial to the understanding of fibrosis in SSc. It also has applications in wound healing as well. Fibroblasts are sensitive to signals from the ECM, and interaction of fibroblasts with the ECM is essential in many physiological and pathological processes.

In SSc, the inflammasome is integrally involved in fibrosis, and we observed a significant reduction in collagen deposition when the inflammasome was inactivated. We have also identified the crucial role for miR-155 and IL-1 in driving this fibrotic response. More recently we have become interested in the export of procollagen from the endoplasmic reticulum and the factors that regulate this during fibrosis. We have identified several crucial proteins that are required for the procollagen export that are highly upregulated. In addition, we have identified that caspase-1, and the IL-1 and TGFβ receptors are involved.

Given our expertise in fibrosis, we also work with several small biotech companies to meet their experimental needs. One project is to investigate a small novel peptide 18 amino acids in length, acALY18. The anti-fibrotic nature of acALY18 is currently under investigation.


Selected Publications

(See all Carol Artlett's publications in PubMed.)

“TANGO1 Dances to Export of Procollagen from the Endoplasmic Reticulum”
Artlett CM, Connolly LM
Fibrosis. 2023, 1(2), 10008 (December 2023)

“Caspase-1 Drives the Upregulation of TANGO1 to Promote Procollagen Export from the Endoplasmic Reticulum in Systemic Sclerosis Contributing to Fibrosis”
Connolly LM, McMahon IG, McFalls CM, Bhat AM, Artlett CM
Arthritis and Rheumatology 75:1831-1841, 2023

“The mechanism and regulation of the NLRP3 inflammasome during fibrosis”
Artlett CM
Biomolecules, 12: 634, 2022

“sRAGE Concentration İncreases Following the Treatment of Severe Diabetic Ketoacidosis”
Hoffman WH, Ishikawa T, Blum J, Tani N, Ikeda T, Artlett CM
Journal of Clinical Research in Pediatric Endocrinology, 12:160-167, 2020

“The MicroRNA miR-155 is essential in fibrosis”
Eissa MG, Artlett CM
Noncoding RNA, 12:5. pii: E23, 2019

“NADPH oxidase-mediated induction of reactive oxygen species and extracellular matrix deposition by insulin-like growth factor binding protein-5”
Yasuoka H, Garrett SM, Nguyen XX, Artlett CM, Feghali-Bostwick CA
American Journal of Physiology Lung Cell Molecular Physiology, 316: L644-L655, 2019

“Preclinical study of the long-range safety and anti-inflammatory properties of high-dose oral meglumine”
Manley K, Bravo-Nuevo A, Minton AR, Sedano S, Marcy A, Reichman M, Tobia A, Artlett CM, Gilmour SK, Laury-Kleintop LD, Prendergast GC
Journal of Cell Biochemistry, 120:12051-12062, 2019

“The IL-1 family of cytokines. Do they have a role in Scleroderma Fibrosis?”
Artlett CM
Immunology Letters, 195:30-37, 2018

“The impact of the unfolded protein response and hexosamine biosynthetic pathway on glycosylation”
Ramanathan A, Mehta A, Artlett CM
Glycobiology Insights, 6:1-12, 2017

“MiR-155 is over-expressed in systemic sclerosis fibroblasts and is required for NLRP3 inflammasome-mediated collagen synthesis during fibrosis”
Artlett CM, Sassi-Gaha S, Hope JL, Feghali-Bostwick CA, Katsikis PD
Arthritis Research Therapy, 19:144, 2017. An editorial was written about this article.

“Transforming growth factor β1 (TGFβ1)-induced CD44V6-NOX4 signaling in pathogenesis of idiopathic pulmonary fibrosis”
Ghatak S, Hascall VC, Markwald RR, Feghali-Bostwick C, Artlett CM, Gooz M, Bogatkevich GS, Atnelishvili I, Silver RM, Thannickal VJ, Misra S
Journal of Biological Chemistry. 292:10490-10519, 2017

“Markers of immune-mediated inflammation in the brains of young adults and adolescents with type 1 diabetes and fatal diabetic ketoacidosis. Is there a difference?”
Hoffman W, Artlett CM, Boodhoo D, Gilliland M, Ortiz L, Mulder D, Tjan D, Martin A, Alexandru Tatomir A, Rus H
Experimental and Molecular Pathology, 102:505-514, 2017

“Identification of Optimal Mouse Models of Systemic Sclerosis by Interspecies Comparative Genomics”
Sargent JL, Li Z, Aliprantis AO, Greenblatt M, Lemaire R, Wu M, Wei J, Harris A, Long K, Burgwin C, Artlett CM, Blankenhorn EP, Lafyatis R, Varga J, Clark SH, Whitfield ML
Arthritis and Rheumatology, 68:2003-15, 2016

"Inflammasomes in wound healing and fibrosis"
Artlett CM
Journal of Pathology; 229(2):157-67, January 2013