The research lab of Matthias Clauss, PhD, is focused on vascular function and repair are involved in many diseases, in particular in those of the cardiopulmonary system. The research program in this lab is concerned with the mechanisms of vascular endothelial cell activation and aims to identify the links between aging, chronic inflammation and infection in blood vessel function and repair. A specific focus is on the regulation of proangiogenic endothelial progenitor cells (ECFC) and anti-angiogenic factors such as EMAP II.
The Clauss Lab team hopes that their research will help Americans in general and Hoosiers in particular to benefit patients with vascular-related diseases and share studies with the scientific community in highly visible journals such as the Journal of Immunology.
HIV-1 infection can cause increased risk for cardiovascular and pulmonary diseases. In HIV-1 studies researchers in the Clauss lab have identified an intracellular protein, HIV-Nef, as a likely candidate for cardiovascular and pulmonary disease development, even in the presence of anti-retroviral drugs. Noteworthy, these scientists are the first to demonstrate that HIV-Nef protein (!) levels in blood cells from un-treated patients are comparable to levels found in anti-retroviral drug treated patients (In collaboration with Homer L. Twigg III).
Research on the pro-apoptotic EMAP II culminated in the development of a humanized EMAP II neutralizing antibody as therapeutic tool for treating cigarette smoke induced emphysema and Influenza-A-induced lung injury. Currently sponsored by three awards (DoD, NIH-SBIRphaseII and NIH-STTR; PI Clauss for Allinaire), this neutralizing antibody is currently advancing towards IND approval for clinical trials (In collaboration with Irina Petrache and Natalia Bogatcheva). This antibody is currently also tested in a rat model for pulmonary hypertension (In collaboration with Tim Lahm).
The lab team has just started to analyze the role of EMAP II in cancer immune-suppression. In fact, EMAP II is a tumor produced protein that kills T cells. Neutralization of EMAP II thus may increase the ability of the immune system to keep tumors in check (In collaboration with Manal M. Saber and Catherine Ruffato Sears).
To understand the role of pro-inflammatory and infectious agents in premature aging of endothelial stem cells like progenitor cells (ECFC). The Clauss Lab team was the first to demonstrate that oxidative stress and cytokines cause premature aging (senescence) in these ECFC (Zhang et al., FASEB Journal 2009) and identified tmTNF as a protective mechanism against this senescence (Green et al., Circulation Research 2016). These scientists are currently studying ECFC stem cells in small rodents including rat and transgenic mouse models (In collaboration with Merv Yoder, David Basile, Laura Haneline and Tim Lahm).