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Ching-Yi Tsai
Associate Professor
Central cardiovascular regulation
Signal transduction
Molecular image
Pharmacology of pesticides and anesthetics
Redox signaling and oxidative stress
Research Overview
Unravel cellular and molecular mechanisms of brainstem regulation of cardiovascular functions in health and disease
Our research interests are primarily on signaling cascades and neural circuits involved in brainstem cardiovascular regulation associated with brainstem death, neurogenic hypertension and hepatic encephalopathy. Our approach is to integrate cellular and molecular biology into systemic physiology using clinically-relevant animal models. In recent years, we have expanded her research horizons on brainstem cardiovascular regulation to image changes in functional connectivity between key brainstem nuclei involved in the baroreflex circuits of mice and rats, and showed that these changes bear physiological, pathophysiological and pathological meaning.
1. Proposed cellular mechanisms at the RVLM in the mevinphos-intoxication model of brainstem death.
Activation of PI3K/Akt signaling in the RVLM via upregulation of the NF-κB/NOS II/peroxynitrite cascade that leads to impairment of the baroreflex-mediated sympathetic vasomotor tone and loss of the “life-and-death” signals that underpins experimental brainstem death. Upregulation of FLJ10540, a PI3K-association protein, which is upstream to activation of PI3K/Akt signaling cascade, elicits circulatory depression. On the other hand, augmented PTEN activity via decreasing its oxidized form sustains brain stem cardiovascular regulatory function during experimental brain stem death as a negative regulator of PI3K/Akt signaling in the RVLM.
(Biochem Pharmacol. 2018 Sep; 155:207-212.)
2. We also combined molecular imaging with our physiological evaluation of brainstem cardiovascular regulation using diffusion tensor imaging (DTI) to detect functional connectivity between key brainstem nuclei involved in the baroreflex circuit.
Under pathophysiological conditions when the disruption of the functional connectivity is reversible, the associated disease condition (e.g. neurogenic hypertension) is amenable to remedial measurements. However, fatality ensues when pathophysiological conditions evolve to pathological conditions (e.g. hepatic encephalopathy) when the functional connectivity is irreversibly severed. (J Physiol. 2019 Jan; 597(1):41-55.)
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