Anibal Garza

• Dr
• PostDoc Position at University of Texas Medical School

Insights into mechanisms governing resolution of inflammatory pain are of great importance for many chronic pain–associated diseases. Here we investigate the role of macrophages/monocytes and the anti-inflammatory cytokine interleukin-10 (IL-10) in the resolution of transient inflammatory pain. Depletion of mice from peripheral monocytes/macrophage...

Chronic pain is a major clinical problem, and understanding mechanisms underlying the transition from acute to chronic pain is needed. We investigated the contribution of peripheral monocytes/macrophages to the transition from acute to persistent IL-1beta induced hyperalgesia. As a model, we used LysM-GRK2+/− mice that develop prolonged hyperalgesi...

The molecular mechanisms determining magnitude and duration of inflammatory pain are still unclear. We assessed the contribution of G protein-coupled receptor kinase (GRK)-6 to inflammatory hyperalgesia in mice. We showed that GRK6 is a critical regulator of severity and duration of cytokine-induced hyperalgesia. In GRK6⁻/⁻ mice, a significantly lo...

Scientists and clinicians have long used the level of hormones or the level of inflammatory mediators as an important parameter of functional activity of the neuro-endocrine or immune system. However, not much focus has been given to the role of the sensitivity of the target tissue, such as receptors or components of the intracellular signalosome....

Epinephrine (EPI) contributes to hyperalgesia in inflammatory and stress conditions. EPI signals via adrenoceptors, which are regulated by G protein-coupled receptor kinase 2 (GRK2). We previously reported that GRK2 is decreased in nociceptors during chronic inflammation. Herein, we investigated whether GRK2 modulates EPI-induced mechanical and the...

Pain is a hallmark of tissue damage and inflammation promoting tissue protection and thereby contributing to repair. Therefore, transient acute pain is an important feature of the adaptive response to damage. However, in a significant number of cases, pain persists for months to years after the problem that originally caused the pain has resolved....

Hyperexcitability of peripheral nociceptive pathways is often associated with inflammation and is an important mechanism underlying inflammatory pain. Here we describe a completely novel mechanism via which nociceptor G-protein-coupled receptor kinase 2 (GRK2) contributes to regulation of inflammatory hyperalgesia. We show that nociceptor GRK2 is d...

Acid sensing ion channels (ASIC) are ionic channels activated by transient pH reductions in the ext raceilularenvi ronment. Although the activation mechanism is not fully elucidated, it is clear that the channel is activated by proton binding to its extraceilular domain, a process that is modulated by calcium and zinc. The fact that divalent cation...

SUMMARY Background. Acid sensing ion channels (ASIC) are ionic channels activated by transient pH reductions in the extracellular environment. Although the activation mechanism is not fully elucidated, it is clear that the channel is activated by proton binding to its extracellular domain, a process that is modulated by calcium and zinc. Objective....