Dr. Bridget Ford is an Assistant Professor in the Department of Biology at UIW. She obtained her bachelor’s degree at St. Mary’s University in Biological Sciences with a minor in Chemistry. She then went on to earn her Ph.D. in Molecular Medicine at UT Health San Antonio in 2012. She completed her postdoctoral fellowship training at the United States Army Institute of Surgical Research in the Extremity Trauma and Regenerative Medicine task area and at UT Health at San Antonio between the Magnetic Resonance Imaging Division and the Department of Medicine. During this time, Dr. Ford was an Adjunct Professor at St. Mary’s University and taught in the Biological Sciences, Chemistry, and Exercise and Sports Science Departments.
Dr. Ford teaches Anatomy and Physiology I and II, General Biology I and Lab for Majors, Cell Biology, and a Special Topics course in Endocrinology at UIW. She loves mentoring undergraduates in the research laboratory where her research focuses on understanding the molecular mechanisms involved in renal cell injury in diabetic kidney disease, with a particular emphasis on oxidative stress pathways.
Diabetic kidney disease, or diabetic nephropathy, is a serious and life-threatening complication of type 1 and type 2 diabetes. Our current understanding of the mechanisms that regulate the initiation and progression of diabetic nephropathy is not sufficient to design effective therapies to prevent or reverse kidney damage. The Ford research laboratory explores mechanisms involved in kidney cell injury in diabetic nephropathy with a specific emphasis on oxidative stress, or cell injury due to the production of damaging compounds called oxygen radicals. One specific area that may be of great importance in designing new therapies for diabetic nephropathy is to identify factors that are implicated in the death of glomerular cells, podocytes and mesangial cells, leading to subsequent loss of kidney function.
Recent undergraduate trainees have mastered mammalian tissue culture and used various molecular methods such as real time PCR, western blotting, immunocytochemistry, ELISAs, and enzyme activity assays to identify factors involved in podocyte and mesangial cell injury using an in vitro model system mimicking the diabetic environment. The overall goal Dr. Ford has for all of her trainees is to apply what they learn in the classroom to ask scientific questions in the quest to become independent and creative thinkers
Eid AA, Gorin Y, Fagg BM, Maalouf R, Barnes JL, Block K, Abboud HE. Mechanisms of podocyte injury in diabetes: role of cytochrome P450 and NADPH oxidases. Diabetes. 58(5):1201-1211, 2009. PMCID: PMC2671039
Eid AA, Ford BM, Block K, Kasinath BS, Gorin Y, Choudhury GG, Barnes JL, Abboud HE. AMP-activated protein kinase (AMPK) negatively regulates Nox4-dependent activation of p53 and epithelial cell apoptosis in diabetes. J Biol Chem. 85(48):37503-12, 2010. PMCID: PMC2988355
Eid AA, Ford BM, Bhandary B, Cavagliery R, Block K, Barnes JL, Gorin Y, Choudhury GG, Abboud HE. Mammalian target of rapamycin regulates Nox4-mediated podocyte depletion in diabetic renal injury. Diabetes. 62(8):2935-47, 2013. PMCID: PMC3717863
Ford BM, Eid AA, Gooz M, Barnes JL, Gorin YC, Abboud HE. ADAM17 mediates Nox4 expression and NADPH oxidase activity in the kidney cortex of OVE26 mice. Am J Physiol Renal Physiol. 305(3):F323-32, 2013. PMCID: PMC3742865
Chandra SB, Mohan S, Ford BM, Huang L, Janardhanan P, Deo KS, Muir ER, Duong TQ. Targeted Overexpression of endothelial nitric oxide synthase in endothelial cells improves cerebrovascular reactivity in Ins2Akita-Type 1 diabetic mice. J Cereb Blood Flow Metab. Accepted October 2015. [Epub ahead of print] PMID: 26661212
Chowdhury K, Kumar S, Sharma A, Bhagat M, Kamai A, Ford BM*, Asthana S, Mandal CC. Presence of a consensus DNA motif at nearby DNA sequence of the mutation susceptible CG nucleotides. Gene. 639:85-95, 2018. PMID: 289863
Do C, Ford BM*, Lee DY, Tan C, Escobar P, Wagner B. Gadolinium-based contrast agents: Stimulators of myeloid-induced renal fibrosis and major metabolic disruptors. Toxicol Appl Pharmacol, (2019). DOI: 10.1016/j.taap.2019.05.009 PMID: 31082427.
Bandyopadhayaya S, Ford BM*, and Mandal CC. Cold-hearted: a case for cold stress in cancer risk. Journal of Clinical Pathology. Submitted March 2019
2018 Penn R**, Ford BM, Smith HA. “Investigation of P-Glycoprotein (PGP) Induction by PGP Substrates to Induce Paclitaxel Resistance in Ovarian Cancer Cells.” 11th Annual UIW Research Week
2018 Ford BM, Wauquier F, Feliers, D, Ma R, Choudhury GG, Barnes JL, Dupuy C, Bae YS, Lee DY, Gorin YC. “Calcium-dependent dual oxidase 2 is a novel mediator of oxidative stress and mesangial cell fibrotic injury in response to angiotensin II: Role of Nox4.” 21st Annual Medicine Research Day; UT Health at San Antonio, May 22, 2018
2018 Aguilar E**, Navarro M**, Ford BM, Wauquier F, Lee, DY, Gorin, YC. “Novel role of dual oxidase 2 as a mediator of podocyte injury in the diabetic environment.” 2018 SACNAS National Diversity in STEM Conference
2018 Ramirez-Pedroza A**, Martinez A**, Ford BM, Wauquier F, Lee, DY, Gorin YC. “Calcium-dependent dual oxidase 2 is a novel source of reactive oxygen species implicated in glomerular mesangial cell fibrotic response to angiotensin II.” 2018 SACNAS National Diversity in STEM Conference
2019 Abraham SM**, Navarro MM**, Wauquier FM, Lee DY, Gorin YC, Ford BM. “Novel role of dual oxidase 2 as a mediator of podocyte injury in the diabetic environment,” 2019. The FASEB Journal 33 (1_supplement), 567.11-567.11 Experimental Biology Conference, Orlando, FL.
2019 Ramirez-Pedroza A**, Martinez A**, Ford BM, Wauquier F, Lee, DY, Gorin YC. “Calcium-dependent dual oxidase 2 is a novel source of reactive oxygen species implicated in glomerular mesangial cell fibrotic response to angiotensin II,” 2019. The FASEB Journal 33 (1_supplement), 567.13-567.13 Experimental Biology Conference, Orlando, FL.
2017 “Novel role of dual oxidase 2 as a mediator of glomerular cell injury in diabetes.” Pathology Research Conference, UT Health San Antonio, Texas
2019 “Role of dual oxidase 2 and NADPH oxidases in diabetic kidney disease." Department of Medicine Research Discussions, UT Health San Antonio, Texas