Plasma PTX3 increases during exercise: An exercise-factor from the heart

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 796-817-Diabetes Genetics & Epidemiology
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-798
Anders Rinnov*1, Jakob Hansen1, Bente Klarlund Pedersen2, Claus Brandt1 and Peter Plomgaard3
1Centre of Inflammation and Metabolism, Department of Infectious Diseases and CMRC, Rigshospitalet, Faculty of Health Science, University of Copenhagen, Denmark, 2Rigshospitalet, copenhagen, Denmark, 3Rigshospitalet, Copenhagen, Denmark
Background and aim

Pentraxin 3 (PTX3) belongs to the pentraxin superfamily which also includes C-reactive protein. In humans, resting levels of plasma PTX3 are increased after resistance exercise and endurance training. Human studies show increase in plasma PTX3 during acute myocardial ischemia. However, PTX3 has a cardio-protective effect as PTX3 is able to reduce myocardial damage following cardiac ischemia. The association between PTX3 as an exercise-factor and a marker of myocardial ischemia is unexplained. The aim of this study is to examine the effect of endurance exercise on plasma PTX3 and to measure tissue expression of PTX3 in order to determine origin of exercise stimulated PTX3 production.


Ten healthy male subjects performed 3 hrs of endurance cycling exercise at 50% of VO2max and 8 subjects served as resting controls. Plasma PTX3 was measured before cycling exercise, during exercise, and into recovery.

Mice performed 1 h of swimming exercise. Groups of 8 mice were sacrificed: before swimming exercise, immediately after swimming, and 1 and 4 hrs post-swimming exercise. PTX3 mRNA was measured in: the skeletal muscle (soleus and gastrocnemius), kidney, heart, sc fat, visceral fat, liver and spleen.


Plasma PTX3 increased 2-fold (p < 0.05) during cycling exercise in human subjects and continued to increase (3-fold, p < 0.05) with peak plasma PTX3 levels later than 6 hrs post-exercise. After 24 hrs plasma PTX3 had returned to resting values. In the resting group PTX3 did not change with time.

Tissue PTX3 mRNA was increased 3-fold (p < 0.05) in heart muscle of mice immediately after swimming and increased further (5-fold, p < 0.05) 1 h post-exercise. Four hrs post-exercise PTX3 mRNA levels had almost returned to resting values. Expression of PTX3 mRNA showed a decrease in soleus post-exercise. No change was seen in PTX3 mRNA levels in gastrocnemius, kidney, sc fat or visceral fat. PTX3 mRNA was undetectable in liver and spleen.


We show that PTX3 mRNA levels are highly up-regulated in the heart of mice following swimming exercise. Furthermore we show a solid increase in plasma PTX3 in human subjects - during and after cycling exercise. Our findings emphasize PTX3 as an exercise-factor and point to the heart as a site of PTX3 production. PTX3 is expressed in human cardiomyocytes and the heart may contribute to the increase in plasma PTX3 found during exercise in humans. This finding is in line with the cardio-protective function observed in animal models. Thus, PTX3 may be a mediator of some of the beneficial effects on the heart observed with exercise.

Nothing to Disclose: AR, JH, BKP, CB, PP

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