Young Investigator Award for UAntwerp researchers
13 October 2015
Kaat Kehoe and Jan Gielis received the 2015 Young Investigator Award for thoracic subjects at the 29th EACTS annual meeting with their manuscript 'Dysregulation of the alternative renin-angiotensin system during lung ischemia-reperfusion injury'.
To stimulate research, the EACTS has instituted prizes for the best manuscripts on topics of clinical or experimental research in the fields of Thoracic Surgery, Cardiac Surgery and Congenital Heart Disease presented by young investigators at the Annual Meeting of the European Association for Cardio-Thoracic Surgery.
Abstract manuscript 'Dysregulation of the alternative renin-angiotensin system during lung ischemia-reperfusion injury'
Activation of the renin-angiotensin system leading to increased angiotensin-(1-7) (Ang-(1-7)) and decreased angiotensin 2 (Ang 2) levels may be a new therapeutic approach to reduce acute lung injury. Prolyl carboxypeptidase (PRCP, EC.188.8.131.52) and prolyl oligopeptidase (PREP, EC 184.108.40.206) are capable of hydrolyzing Ang 2 into Ang-(1-7). However, their relation with circulating Ang 2 levels after lung ischemia-reperfusion injury (LIRI) has never been explored before. This study determines whether the activity and expression of PRCP and PREP in plasma and lung tissue is related to circulating Ang 2 levels in a murine model of LIRI.
LIRI in adult female Swiss mice (6 animals per group) was induced by temporary left lung hilar clamping (1 h) followed by 0, 1 or 24 h of reperfusion. Animals in the sham group received thoracotomy only. PRCP activity was measured via a reversed-phase high-performance liquid chromatography assay, PREP activity using a fluorogenic substrate and plasma Ang 2 levels via ELISA. Western blotting was used to determine the PRCP and PREP protein expression profiles in left lung tissue.
Plasma Ang 2 levels significantly rise after lung ischemia and remain increased after 1 h and 24 h of reperfusion compared to the sham group. While a significant decrease in plasma PREP activity was found after 24 h of reperfusion, a transient increase in plasma PRCP activity was observed after ischemia. However, no correlation with plasma Ang 2 levels could be demonstrated. The activity profiles of PRCP and PREP and the protein expression of PRCP in the lung tissues remained rather unchanged after LIRI.
LIRI causes a dysregulation of circulating Ang 2 levels and plasma PREP activity, although no direct link between both phenomena could be shown. The activity profile of pulmonary PRCP and PREP was not significantly changed after LIRI, which implies a minor role for local PRCP and PREP in the ischemic lung itself.