Alexander Widiapradja, PhD

Research Assistant Professor

Organization:

West Virginia University School of Medicine

Department:

Physiology, Pharmacology & Toxicology

Classification:

Faculty

1. Tran T, Winardi K, Levick SP, Widiapradja A, Gemikonakli G, Howlett SE, McKay MJ, Molloy MP, Mach J, Hilmer SN. Polypharmacy in mice disrupts left ventricular function and structure and promotes proteosome reorganisation in an age- and sex-specific fashion. British Journal of Pharmacology, 2025;182(19):4625-4646.
2. Widiapradja A, Connery H, Bullock M, Kasparian AO, Clifton-Bligh R, Levick SP. The orphan nuclear receptor Nr4a1 contributes to insterstitial cardiac fibrosis via modulation of cardiac fibroblast and macrophage phenotype. Cellular and Molecular Life Sciences, 2024;81(1):484.
3. Kriska T, Natarajan J, Hernreiter AM, Park S-K, Pfister S, Thomas M, Widiapradja A, Levick SP, Campbell WB. Cellular metabolism of substance P produces neurokinin-1 receptor peptide agonists with diminished cyclic AMP signaling. American Journal of Physiology: Cell Physiology, 2024;327:C151-C167.
4. Melendez GC, Kavanagh K, Gharraee N, Lacy JL, Goslen KH, Block M, Whitfield J, Widiapradja A, Levick SP. (2023). Replacement Substance P Reduces Cardiac Fibrosis in Monkeys with Type 2 Diabetes. Biomedicine and Pharmacotherapy. 160: 114365.
5. Lim G, Widiapradja A, Levick SP, McKelvey KJ, Liao XH, Refetoff S, Bullock M, Clifton-Bligh RJ. (2022). Foxe1 Deletion in The Adult Mouse is Associated with Thyroidal Mast Cell Infiltration and Hypothyroidism. Endocrinology. 162 (12).
6. Widiapradja A, Kasparian AO, McCaffrey SL, Kolb LL, Imig JD, Lacey J, Melendez G, Levick SP. (2021). Replacement of Lost Substance P Reduces Fibrosis in the Diabetic Heart by Preventing Adverse Fibroblast and Macrophage Phenotype Changes. Cells. 10(10):2659.
7. McCaffrey SL, Lim G, Bullock M, Kasparian AO, Clifton-Bligh R, Campbell WB, Widiapradja A, Levick SP. (2020). The Histamine 3 Receptor is Expressed in the Heart and Its Activation Opposes Adverse Cardiac Remodeling in Angiotensin II Mouse Model. International Journal of Molecular Sciences. 21(24): 9757.
8. Levick SP, Widiapradja A. (2020). The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function. International Journal of Molecular Sciences. 21(3):970.
9. Widiapradja A, Manteuefel EJ, Dehlin HM, Pena J, Goldspink PH, Sharma A, Kolb LL, Imig JD, Janicki JS, Lu B, Levick SP. (2019). Regulation of Cardiac Mast Cell Maturation and Function by the Neurokinin-1 Receptor in the Fibrotic Heart. Scientific Reports. 9(1):11004.
10. Levick SP, Soto-Pantoja DR, Bi J, Hundley WG, Widiapradja A, Manteufel EJ, Bradshaw TW, Meléndez GC. (2019). Doxorubicin-Induced Myocardial Fibrosis Involves the Neurokinin-1 Receptor and Direct Effects on Cardiac Fibroblasts. Heart, Lung and Circulation. 18(10):1598-1605.
11. Levick SP, Widiapradja A. (2018). Mast cells: A key contributor to cardiac fibrosis. International Journal of Molecular Sciences 19:231. Invited Review - Special Issue: Extracellular Matrix in Development and Disease.
12. Widiapradja A, Chunduri P, Levick SP. (2017). The role of neuropeptides in adverse myocardial remodeling and heart failure. Cellular and Molecular Life Sciences. 74:2019-2038.
13. Nabizadeh JA, Manthey HD, Steyn FJ, Chen W, Widiapradja A, Md Akhir FN, Boyle GM, Taylor SM, Woodruff TM, Rolfe BE. (2016). The Complement C3a Receptor Contributes to Melanoma Tumorigenesis by Inhibiting Neutrophil and CD4+ T Cell Responses. Journal of Immunology. 196(11):4783-92.

Graduate Program Affiliations: Cellular and Integrative Physiology

My research interest is studying the molecular mechanisms in cardiac inflammation and fibrosis that lead to heart failure, particularly heart failure in diabetes. Specifically, my research focus is studying the cardio-protective role of Foxe1, a transcription factor that is pivotal for thyroid development. The loss of Foxe1 function in the mouse thyroid and heart lead to tissue fibrosis and the infiltration of pro-inflammatory macrophages and mast cells. Through molecular genetics and cardiac functional studies, my research aims to understand this newly protective role of Foxe1 in the heart and how its loss of function contributes to cardiac fibrosis and inflammation.

Techniques:

• Animal models of cardiac disease (diabetes, hypertension, myocardial infarction)
• Assessment of cardiac function and structure (echocardiography and pressure volume catheterization)
• Primary cell cultures (cardiac fibroblasts, macrophages, mast cells)
• Molecular genetics
• Histology
• Next generation sequencing (RNA-Seq, ATAC-Seq, ChIP-Seq)
• Spatial transcriptomics
• Proteomics