The overarching goal of my research is to understand vascular function in cardiovascular and renal diseases. Specifically, I study the mechanisms of injury-associated vascular dysfunction during hypertension, inflammation, sepsis, and chronic kidney diseases.

My first project is entitled: “Intrarenal arteries sense trauma-derived mitochondrial N-formyl peptides and lead to kidney injury in SIRS”. This project aims to understand the mechanisms associated with vascular damage and acute kidney injury following trauma.

My second project is entitled: “Formyl peptide receptor blockade ameliorates intrarenal resistance artery function and decreases blood pressure in spontaneously hypertensive rats (SHRs)”. It is well established that chronic immune system activation contributes to hypertension and chronic kidney injury. Recently, we have observed that mitochondrial fragments are elevated in the circulation of SHR, and that mitochondrial N-formyl peptides infusion in rats induces systemic inflammation and vascular dysfunction via formyl peptide receptor (FPR) activation.  However, we do not know if FPRs play a role in chronic kidney injury and hypertension. The goal of this project is to understand the cellular mechanisms that lead to the damage of intrarenal arteries via FPR activation, and subsequently, kidney injury and hypertension.

I have been trying to answer the question: Why do almost 50% of trauma patients present sepsis-like symptoms in the absence of infection? Our publications below demonstrated strong evidence that sterile trauma induces the release of mitochondrial N-formyl peptides (F-MIT) and lead to sepsis-like symptoms (SIRS) in rats. Also, we observed that the infusion of F-MIT lead to cardiovascular collapse and leukocyte depletion abolished this response.

1. Wenceslau CF, McCarthy CG, Szasz T, Goulopoulou S, Webb RC. Mitochondrial N-formyl peptides induce cardiovascular collapse and sepsis-like syndrome. American Journal of Physiology. Heart and circulatory physiology. 2015; 308(7):H768-77.

1. Wenceslau CF, McCarthy CG, Szasz T, Spitler K, Goulopoulou S, Webb RC. Mitochondrial damage-associated molecular patterns and vascular function. European Heart Journal. 2014; 35(18):1172-7.

1. Wenceslau CF, McCarthy CG, Goulopoulou S, Szasz T, NeSmith EG, Webb RC.Mitochondrial-derived N-formyl peptides: novel links between trauma, vascular collapse and sepsis. Med Hypotheses. 2013 Oct;81(4):532-5. doi: 10.1016/j.mehy.2013.06.026.

In addition to the contributions described above, our laboratory has also observed how mitochondrial DNA release by cell injury is associated with hypertension. In this publication we observed that in SHR, the kidney is the principal source of mitochondrial damage-associated molecular patterns (DAMPs).

1. McCarthy CG, Wenceslau CF, Goulopoulou S, Ogbi S, Baban B, Sullivan JC, Matsumoto T, Webb RC. Circulating mitochondrial DNA and Toll-like receptor 9 are associated with vascular dysfunction in spontaneously hypertensive rats. Cardiovasc Res. 2015, in press.

1. McCarthy CG, Goulopoulou S, Wenceslau CF, Spitler K, Matsumoto T, Webb RC. Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension. Am J Physiol Heart Circ Physiol. 2014 Jan 15;306(2):H184-96. doi: 10.1152/ajpheart.00328.2013.

I really like the paper from David Bohr. (Vascular Smooth Muscle: Dual Effect of Calcium. Science. 1963 Feb 15;139(3555):597-9). He was the first to demonstrate that calcium causes contraction of vascular smooth muscle. (PMID: 17788298)

As Clinton says, networking is the best facility you can have to do a great research.

My proudest moment in research was my very first award (best poster presentation). I received this when I was a Master’s student on my work with ouabain-induced hypertension. This award stands out because I worked so hard to collect data to take to the Experimental Biology Societies Federation meeting.

My most challenging situation was when I decided to leave Brazil and to become a postdoctoral fellow in the US. While staying in Brazil, close to my family and my research peers, was a consideration, my potential growth as an independent researcher outweighed this drawback.

I am planning to attend EB (Chicago) and Council on Hypertension (San Francisco), both in 2017.

The furthest I have traveled for a conference was to Manchester, UK.

I would like to specialize in injury-associated vascular dysfunction on cardiorenal physiology.

Clinton Webb and my previous mentor Luciana V Rossoni are my role models in Science. The funny thing is that they have completely different mentorship styles. Nonetheless, both have been extremely important for my career.

My long-term career goal is to establish a strong independent research program using integrative approaches to study the effects of injury-associated vascular dysfunction on cardiorenal physiology.

My advice for talent emerging scientists is: “Never, ever give up. If you fail, try again. You are going to get it!”