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The effect of acute and prolonged endurance exercise on transforming growth factor-ß1 generation in rat skeletal and heart muscle

100%

Czarkowska-Paczek B. , Zendzian-Piotrowska M. , Bartlomiejczyk I. , Przybylski J. , Gorski J.

nr 4

157-162

The serum level of the transforming growth factor-beta1 (TGF-ß1) is elevated after acute bouts of exercise and prolonged training, as well as after myocardial infarction. However, the source of this increase remains unclear. Contracting skeletal muscles are known to be the source of many cytokines. To determine whether skeletal or heart muscles produce TGF-ß1 during exercise, we investigated the effect of a single bout of acute exercise on TGF-ß1 generation in skeletal and heart muscles in untrained rats (UT, n=30) and in rats subjected to prolonged (6-week) endurance training (T, n=29). The UT and T (a day after final training) groups were subjected to an acute bout of exercise with the same work load. Rats from both groups were sacrificed and skeletal and heart muscle samples were collected before (pre), immediately after (0 h), or 3 hours (3 h) after acute exercise. TGF-ß1 mRNA was quantified by RT-PCR in these samples, and basal TGF-ß1 protein levels were determined in skeletal muscle in the UTpre and Tpre subgroups by ELISA. Acute exercise caused a non-significant increase in TGF-ß1 mRNA in skeletal muscle in UT0h rats, in compare to UTpre rats. There was a significant decrease of TGF-ß1 mRNA in the T0h group (p=0.0013) in compare to Tpre rats. Prolonged training caused a significant increase in TGF-ß1 mRNA (p=0.02); however, the TGF-ß1 protein level decreased (p=0.02). In heart muscle, there was a significant decrease of TGF-ß1 mRNA in UT0h (p=0.01) and UT3h (p=0.04) compared to UTpre rats. TGF-ß1 mRNA levels were unchanged in T0h and T3h compared to Tpre; basal TGF-ß1 mRNA expression after training was also unchanged (UTpre vs. Tpre). We conclude that physical exercise is a potent stimulus for inducing TGF-ß1 gene expression in skeletal muscle, but does not increase the protein level. Thus, skeletal and heart muscle do not contribute to increased serum levels of TGF-ß1 after physical exercise.

The effects of indomethacin on angiogenic factors mRNA expression in renal cortex of healthy rats

100%

Mucha K. , Foroncewicz B. , Koziak K. , Czarkowska-Paczek B. , Paczek L.

nr 1

Indomethacin is a nonsteroidal anti-inflammatory drug used frequently to control chronic or temporary pain. In the kidney, indomethacin decreases medullary and cortical perfusion, resulting in hypoxia. Kidney hypoxia has many effects, including changes in gene expression, and is a strong stimulus for angiogenesis. Other angiogenic factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2), transforming growth factor beta 1 (TGFß1), and platelet-derived growth factor (PDGF). Our goal was to examine the influence of indomethacin on mRNA expression of these factors and their selected receptors in the renal cortex of healthy rats. Groups of 8 healthy, male, six-week-old Wistar rats received either indomethacin (5 mg/kg/day) or placebo orally for three months. RNA from renal cortex biopsies was analyzed by real-time polymerase chain reaction to quantify the mRNA levels of each cytokine. We observed significantly higher mRNA levels for VEGF (1.73-fold), FGF-2 (5.6-fold) and TGFß receptor III (2.93-fold), PDGF receptor alpha (2.93-fold) and receptor ß (2.91-fold) in rats receiving indomethacin compared to rats given placebo (p < 0.05). Amounts of mRNA for TGFß1, PDGF, FGF receptors 1 and 2 and TGFß receptor I did not differ between analysed groups. Our data indicates that indomethacin may regulate the expression of potent angiogenic factors VEGF and FGF-2.