| Autor: |
de Castro Magalhães, Flávio, Fernandes, Tiago, Bassaneze, Vinícius, Coelho Mattos, Katt, Schettert, Isolmar, Navarro Marques, Fabio Luiz, Eduardo Krieger, José, Nava, Roberto, Garrone Barauna, Valério, Menezes de Oliveira, Edilamar |
| Předmět: |
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| Zdroj: |
Clinical Science; 10/15/2021, Vol. 135 Issue 20, p2377-2391, 15p |
| Abstrakt: |
One of the health benefits of endurance exercise training (ET) is the stimulation of hematopoiesis. However, the mechanisms underlying ET-induced hematopoietic adaptations are understudied. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits proliferation of early hematopoietic progenitor cells. The angiotensin I-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP. Here we demonstrate for the first time the role of ACE NH2-terminal in ET-induced hematopoietic adaptations. Wistar rats were subjected to 10 weeks of moderate-(T1) and high-(T2) volume swimming-training. Although both protocols induced classical ET-associated adaptations, only T2 increased plasma ACE NH2-domain activity (by 40%, P=0.0003) and reduced Ac-SDKP levels (by 50%, P<0.0001). T2 increased the number of hematopoietic stem cells (HSCs; ~200%, P=0.0008), early erythroid progenitor colonies (~300%, P<0.0001) and reticulocytes (~500%, P=0.0007), and reduced erythrocyte lifespan (~50%, P=0.022). Following, Wistar rats were subjected to T2 or T2 combined with ACE NH2-terminal inhibition (captopril (Cap) treatment: 10 mg.kg-1.day-1). T2 combined with ACE NH2-terminal inhibition prevented Ac-SDKP decrease and attenuated ET-induced hematopoietic adaptations. Altogether, our findings show that ET-induced hematopoiesis was at least partially associated with increased ACE NH2-terminal activity and reduction in the hematopoietic inhibitor Ac-SDKP. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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