Dr. Beth L Roman, PhD

Dr. Roman is a developmental biologist and molecular geneticist. She received her postdoctoral training at the National Institutes of Health and was an Assistant Professor at Georgetown University (2002-2006) and the University of Pittsburgh Department of Biological Sciences (2006-2014). She is currently Research Director for the UPMC/University of Pittsburgh HHT Center of Excellence.

 

The Roman lab studies the autosomal dominant genetic disorder, hereditary hemorrhagic telangiectasia (HHT), which is caused by decreased endothelial bone morphogenetic protein (BMP) signaling and is characterized by a predisposition to development of arteriovenous malformations (AVMs). AVMs are direct connections between arteries and veins that can lead to hemorrhage or stroke if severe shunting or rupture occurs. The Roman lab uses zebrafish models of HHT and molecular, genetic, advanced imaging, and biochemistry approaches to uncover the molecular and cellular errors that lead to AVM development. Out ultimate goal is to develop therapeutics that specifically target HHT.

 

Research Interests: Vascular development, hereditary hemorrhagic telangiectasia, zebrafish, BMP signaling, mechanotransduction.

1989 | The Pennsylvania State University, University Park, PA  |  BS Biochemistry

1997  |  The University of Wisconsin-Madison |  PhD Environmental Toxicology
2002  |  NIH/NICHD, Bethesda, MD  |  Postdoc Developmental Biology

Arulselvi Anbalagan, lab manager

Xinyan Lu, postdoctoral fellow

Teresa Capasso, PhD student

Erika Dreikorn, PhD student

Full list of publications: https://www.ncbi.nlm.nih.gov/sites/myncbi/beth.roman.2/bibliography/40386158/public/?sort=date&direction=descending

 

Laux DW, Young S, Donovan JP, Mansfield CJ, Upton PD, Roman BL. Circulating Bmp10 acts through endothelial Alk1 to mediate flow-dependent arterial quiescence. Development. 2013 Aug;140(16):3403-12. doi: 10.1242/dev.095307. Epub 2013 Jul 17. PubMed PMID: 23863480; PubMed Central PMCID: PMC3737721.

 

Wooderchak-Donahue WL, McDonald J, O'Fallon B, Upton PD, Li W, Roman BL, Young S, Plant P, Fülöp GT, Langa C, Morrell NW, Botella LM, Bernabeu C, Stevenson DA, Runo JR, Bayrak-Toydemir P. BMP9 mutations cause a vascular-anomaly syndrome with phenotypic overlap with hereditary hemorrhagic telangiectasia. Am J Hum Genet. 2013 Sep 5;93(3):530-7. doi: 10.1016/j.ajhg.2013.07.004. Epub 2013 Aug 22. PubMed PMID: 23972370; PubMed Central PMCID: PMC3769931.

 

Rochon ER, Wright DS, Schubert MM, Roman BL. Context-specific interactions between Notch and ALK1 cannot explain ALK1-associated arteriovenous malformations. Cardiovasc Res. 2015 Jul 1;107(1):143-52. doi: 10.1093/cvr/cvv148. Epub 2015 May 12. PubMed PMID: 25969392; PubMed Central PMCID: PMC4498135.

 

Rochon ER, Menon PG, Roman BL. Alk1 controls arterial endothelial cell migration in lumenized vessels. Development. 2016 Jul 15;143(14):2593-602. doi: 10.1242/dev.135392. Epub 2016 Jun 10. PubMed PMID: 27287800; PubMed Central PMCID: PMC4958337.

 

Roman BL, Hinck AP. ALK1 signaling in development and disease: new paradigms. Cell Mol Life Sci. 2017 Dec;74(24):4539-4560. doi: 10.1007/s00018-017-2636-4. Epub 2017 Sep 4. Review. PubMed PMID: 28871312; PubMed Central PMCID: PMC5687069.

 

Choi H, Conrad MB, Oh SP, Roman BL, White AJ. Highlights of the 13th International Hereditary Hemorrhagic Telangiectasia Scientific conference. Angiogenesis. 2019 Nov;22(4):583-584. doi: 10.1007/s10456-019-09685-x. PubMed PMID: 31606769.

 

Capasso TL, Li B, Volek HJ, Khalid W, Rochon ER, Anbalagan A, Herdman C, Yost HJ, Villanueva FS, Kim K, Roman BL. BMP10-mediated ALK1 signaling is continuously required for vascular development and maintenance. Angiogenesis. 2019 Dec 11;. doi: 10.1007/s10456-019-09701-0. [Epub ahead of print] PubMed PMID: 31828546; NIHMSID:NIHMS1546326.

 

Rochon ER, Krowka MJ, Bartolome S, Heresi GA, Bull T, Roberts K, Hemnes A, Forde KA, Krok KL, Patel M, Lin G, McNeil M, Al-Naamani N, Roman BL, Yu PB, Fallon MB, Gladwin MT, Kawut SM for the PVCLD2 Study Group. BMP 9/10 in pulmonary vascular complications of liver disease. Am J Resp Crit Care Med (In press).