Dr. Gonzalez Bosc holds a PhD (2001) from the University of Buenos Aires (Argentina). She joined the faculty of the Cell Biology and Physiology Department in 2004. She is currently the Vice Chair of Diversity, Equity and Inclusion of the Department of Cell Biology and Physiology. She served as director of the UNM School of Medicine Biomedical Sciences Graduate Program (BSGP) from 2020 to 2023, directed the UNM HSC Cardiovascular and Metabolic Disease Signature Program (CMVD) from 2018 to 2021, and chaired the UNM HSC Institutional Animal Care and Use Committee (IACUC) from 2014 to 2021.

Personal Statement

I value and embrace diversity in the workplace. I have always felt welcomed, respected, and supported by members of my Department. I’m committed to contributing to a work environment that promotes anti-racism and social justice. I accomplish this by recognizing my implicit biases and attending workshops on upstander training, conflict resolution, emotional intelligence, and advancing inclusive teaching and learning, among others, to help make UNM a better place to work and learn.

Areas of Specialty

Vascular Biology,Pulmonary Hypertension,Hypoxia, Inflammation

Achievements & Awards

Respiration Section New Investigator Award. American Physiological Society.2010.
Dalsemer Award. Biomedical Research Grant. American Lung Association.2007.
Minority Travel Award to Experimental Biology. American Physiological Society/National Institute of Diabetes and Digestive and Kidney Diseases.2007.
Scientist Development Award. American Heart Association. Research Position. 2005. Programa Ramón y Cajal. Ministerio de Educación y Ciencia. Spain. 2004.
Affiliate Postdoctoral Fellowship. American Heart Association. 2002 and 2004.
Award of the XXVII Argentinean Congress of Cardiology. Argentinean Society of Cardiology, Argentina. 2000.
Young investigator travel award. International Society of Hypertension. 2000.
Graduate Fellowship level II. University of Buenos Aires. 1998.
Young Investigator Award. Merck Sharp & Dohme. 1999.
Graduate Fellowship level I. University of Buenos Aires. 1995.
Research fellowship (For short-term research at Laboratory of Physiology, School of Sciences. University of Balearic Islands, Spain). Ibero-American Cooperation Institute, Embassy of Spain. 1996.

Key Publications

Journal Article
Morales-Loredo, H, Jones, D, Barrera, A, Mendiola, P, J Garcia, J, Pace, C, Murphy, M, Kanagy, Nancy, Gonzalez Bosc, Laura, 2019 A dual blocker of endothelin A/B receptors mitigates hypertension but not renal dysfunction in a rat model of chronic kidney disease and sleep apnea. American journal of physiology. Renal physiology, vol. 316, Issue 5, F1041-F1052
Journal Article
Maston, L, D Jones, D, T Giermakowska, W, Howard, T, A Cannon, Judy, Wang, W, Wei, Y, Xuan, W, Resta, Tom, Gonzalez Bosc, Laura, 2017 Central role of T helper 17 cells in chronic hypoxia-induced pulmonary hypertension. American journal of physiology. Lung cellular and molecular physiology, vol. 312, Issue 5, L609-L624
Journal Article
Gonzalez Bosc, Laura, Plomaritas, D, R Herbert, L, M Giermakowska, W, Browning, C, Jernigan, Nikki, 2016 ASIC1-mediated calcium entry stimulates NFATc3 nuclear translocation via PICK1 coupling in pulmonary arterial smooth muscle cells. American journal of physiology. Lung cellular and molecular physiology, vol. 311, Issue 1, L48-58




  • Spanish
  • English


 pulmonary hypertension caused by chronic hypoxia

For the past 12 years, our research has focused on understanding the mechanisms that underlie the development of pulmonary hypertension caused by chronic hypoxia (CH).  We have made significant contributions to this field. My group was the first one to demonstrate that the calcium-regulated transcription factor, nuclear factor of activated T-cells isoform c3 (NFATc3) is required for CH-induced pulmonary arterial remodeling and hypertension. During the last 6 years, we have been studying the role of inflammation in CH-induced pulmonary hypertension. We have established that Th17 cells are localized in the perivascular region of pulmonary arteries after CH exposure and that these cells significantly contribute to the development of pulmonary hypertension. We recently identified that CH exposes collagen V in the perivascular region of pulmonary arteries, serving as a self-antigen that triggers a Th17-mediated inflammatory response contributing to pulmonary hypertension. Our research is funded by American Heart Association, NIH and Department of Defense.

Courses Taught

Medical School
Phase I. Clinical Reasoning. Group Facilitator. Spring semester. 2024 - present
Phase I. Pharmacology COPD and Asthma. Peer Instruction. Cardiovascular/Pulmonary/Renal Block. Spring 2020-2021
Phase I. Clinical Reasoning. Group Facilitator. Spring semester. 2016 - 2019
Phase I. Gastrointestinal/Nutrition Block. Tutor. 2015.
Phase I. Cardiovascular/Pulmonary/Renal Block. Tutor. 2014.
Phase I. Cardiovascular/Pulmonary/Renal Block. Tutor. 2014.
Cardiovascular/Pulmonary/Renal Block co-Chair 2017-2020

Graduate School
Course Director & Instructor, Biomed 501. University of New Mexico Health Science Center. Spring 2020 - 2023.
Course Director, Graduate Physiology (Biomed. Sci. 510). University of New Mexico Health Science Center. Spring 2010, 2015 and 2016.
Graduate Physiology (Biomed. Sci. 510). University of New Mexico Health Science Center. Lecturer (8 lecture hours/year). 2005 - Present.
Advanced Topics in Cellular and Systems Physiology (Biomed. Sci. 657). University of New Mexico Health Science Center. Lecturer (15 contact hours/year). 2005, 2007, 2011, 2013, 2017, 2020.

Research and Scholarship

Chronic inflammation in hypoxic pulmonary hypertension: My laboratory has explored the role of chronic inflammation in hypoxic pulmonary hypertension pathogenesis. We have recently established that TH17 cells infiltrate the perivascular region of pulmonary arteries after exposure to CH and that these cells significantly contribute to the pathogenesis of pulmonary hypertension. We demonstrated that IL-6 trans-signaling contributes to this process. A collaboration with Dr. William Burlingham's research group from the University of Wisconsin at Madison set my group on the course to study the role of collagen V in CH-induced lung inflammation and pulmonary hypertension. As a result, we recently reported the novel finding that smooth muscle NFATc3 is important for CH-induced pulmonary hypertension in adult mice, in part by regulating the expression of the lung self-antigen COL5A1 contributing to col V-reactive nTH17-mediated inflammation and hypertension. We have also demonstrated that CH causes a reduction in active T regulatory cells (Tregs) and promotes T regs with less suppressive capacity, called exTregs that express markers of TH17 cells. These exTregs-TH17 are pathogenic and we are currently studying whether they recognize collagen V.
- Benjamin J. Lantz, Mika Moriwaki, Olufunmilola M. Oyebamiji, Yan Guo, Laura Gonzalez Bosc. Chronic hypoxia disrupts T regulatory cell phenotype contributing to the emergence of exTreg-TH17 cells. Front. Physiol., 29 January 2024.Sec. Cell Physiology Volume 14 - 2023, PMCI10859758.
- Joshua R. Sheak, David T. Jones, Benjamin J Lantz, Levi D. Maston, Danielle Vigil, Thomas C. Resta, Micaela M. Resta, Tamara A. Howard, Nancy L. Kanagy, Yan Guo, Ewa Jankowska-Gan, Jeremy A. Sullivan, Rudolf K. Braun, William J. Burlingham, and Laura V. Gonzalez Bosc. NFATc3 Regulation of Collagen V Expression Contributes to Cellular Immunity to Collagen Type V and Hypoxic Pulmonary Hypertension. Am J Physiol Lung Cell Mol Physiol. 2020. 319(6):L968-L980. PMC7792682
- Maston LD, Jones DT, Giermakowska W, Resta TC, Ramiro-Diaz J, Howard TA, Jernigan NL, Herbert L, Maurice AA, Gonzalez Bosc LV. Interleukin-6 trans-signaling contributes to chronic hypoxia-induced pulmonary hypertension. Pulm Circ. 2018 Jul-Sep;8(3):2045894018780734. PMC6055240
- Levi D. Maston, David T. Jones, Wieslawa Giermakowska, Tamara A. Howard, Judy L. Cannon, Wei Wang, Yongyi Wei, Weimin Xuan, Thomas C. Resta, Laura V. Gonzalez Bosc. Central Role of T Helper 17 Cells in Chronic Hypoxia-Induced Pulmonary Hypertension. Am J Physiol Lung Cell Mol Physiol. 2017. 312(5):L609-L624. PMC5451600