Dergiler / Turkish Journal of Medical Sciences / 2015 / Cilt: 45 - Sayı: 3

The expression profile of aquaporin 1 in rat myocardium after severe burns

Sayfa
481–488
Yayın Tarihi
2015-08-13
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Targeting AQP1 may provide opportunities for therapeutic intervention in myocardial edema following severe burns.

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:Background/aim: To investigate the myocardial expression profile of aquaporin 1 (AQP1) in rats after severe burns.
📊
Temel Bulgular & Veri:Materials and methods: Ninety healthy male adult Wistar rats were randomly assigned to the following treatments: sham operation (control group, n = 6), immediate fluid resuscitation treatment post scalding (IF group, n = 42), and delayed fluid resuscitation treatment after scalding (DF group, n = 42).
💡
Sonuç & Katkı:Targeting AQP1 may provide opportunities for therapeutic intervention in myocardial edema following severe burns.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Aquaporin 1 · burn · myocardial edema

Özet

Background/aim: To investigate the myocardial expression profile of aquaporin 1 (AQP1) in rats after severe burns. Materials and methods: Ninety healthy male adult Wistar rats were randomly assigned to the following treatments: sham operation (control group, n = 6), immediate fluid resuscitation treatment post scalding (IF group, n = 42), and delayed fluid resuscitation treatment after scalding (DF group, n = 42). At 3, 6, 12, 24, 48, 72, and 120 h after scalding, myocardial water contents were assayed and AQP1 expressions were detected by real-time polymerase chain reaction and western blot. The AQP levels in the myocardium at 12 h after scalding were assayed by gene microarrays. Results: Scald injuries resulted in significantly synchronized increases in the myocardial water contents and the myocardial mRNA and protein expression of AQP1, with a peak at 12 h after scalding. Rats receiving delayed fluid resuscitation treatment had more severe myocardial edema and significantly higher myocardial AQP1 expressions than the rats receiving immediate fluid resuscitation treatment. The mRNAs of 6 other AQPs (AQP2, 3, 4, 6, 7, and 12b) were found to be changed in the myocardium among rats with different treatments. Conclusion: AQP1 may play a functional role in the development of myocardial edema after scalding. Targeting AQP1 may provide opportunities for therapeutic intervention in myocardial edema following severe burns.

Abstract

Background/aim: To investigate the myocardial expression profile of aquaporin 1 (AQP1) in rats after severe burns. Materials and methods: Ninety healthy male adult Wistar rats were randomly assigned to the following treatments: sham operation (control group, n = 6), immediate fluid resuscitation treatment post scalding (IF group, n = 42), and delayed fluid resuscitation treatment after scalding (DF group, n = 42). At 3, 6, 12, 24, 48, 72, and 120 h after scalding, myocardial water contents were assayed and AQP1 expressions were detected by real-time polymerase chain reaction and western blot. The AQP levels in the myocardium at 12 h after scalding were assayed by gene microarrays. Results: Scald injuries resulted in significantly synchronized increases in the myocardial water contents and the myocardial mRNA and protein expression of AQP1, with a peak at 12 h after scalding. Rats receiving delayed fluid resuscitation treatment had more severe myocardial edema and significantly higher myocardial AQP1 expressions than the rats receiving immediate fluid resuscitation treatment. The mRNAs of 6 other AQPs (AQP2, 3, 4, 6, 7, and 12b) were found to be changed in the myocardium among rats with different treatments. Conclusion: AQP1 may play a functional role in the development of myocardial edema after scalding. Targeting AQP1 may provide opportunities for therapeutic intervention in myocardial edema following severe burns.

🔖

Bu Makaleye Atıf Yap

LI, W., ZHA, L., LI, Z., HUANG, Y., ZHOU, Y. (2015). The expression profile of aquaporin 1 in rat myocardium after severe burns. Turkish Journal of Medical Sciences, Cilt: 45 - Sayı: 3, 481–488. https://ajindex.com/articles/113945

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (12)

  1. Zhang BQ, Wang G, Zhang JP, Hu JY, Xiao R, Lei ZY, Ruan J, Dang YM, Zhang DX, Bian XW et al. Protective effects of enalapril, an angiotensin-converting enzyme inhibitor, on multiple organ damage following scald injury in rats. Biotechnol Appl Biochem 2012; 59: 307–313.
  2. Wang Q, Ishikawa T, Michiue T, Zhu BL, Guan DW, Maeda H. Molecular pathology of brain edema after severe burns in forensic autopsy cases with special regard to the importance of reference gene selection. Int J Legal Med 2013; 127: 881–889.
  3. Maass DL, White DJ, Sanders B, Horton JW. Cardiac myocyte accumulation of calcium in burn injury: cause or effect of myocardial contractile dysfunction. J Burn Care Rehabil 2005; 26: 252–259.
  4. Egan JR, Butler TL, Au CG, Tan YM, North KN, Winlaw DS. Myocardial water handling and the role of aquaporins. Biochim Biophys Acta 2006; 1758: 1043–1052.
  5. Ogura T, Imanishi S, Shibamoto T. Osmometric and water- transporting properties of guinea pig cardiac myocytes. Jpn J Physiol 2002; 52: 333–342.
  6. Ogura T, Matsuda H, Imanishi S, Shibamoto T. Sarcolemmal hydraulic conductivity of guinea-pig and rat ventricular myocytes. Cardiovasc Res 2002; 54: 590–600.
  7. Suleymanian MA, Baumgarten CM. Osmotic gradient-induced water permeation across the sarcolemma of rabbit ventricular myocytes. J Gen Physiol 1996; 107: 503–514.
  8. Connolly DL, Shanahan CM, Weissberg PL. The aquaporins: a family of water channel proteins. Int J Biochem Cell Biol 1998; 30: 169–172.
  9. Bulter TL, Au CG, Yang B, Egan JR, Tan YM, Hardeman EC, North KN, Verkman AS, Winlaw DS. Cardiac aquaporin expression in humans, rats and mice. Am J Physiol Heart Circ Physiol 2006; 291: H705–H713. Agre P, Preston GM, Smith BL, Jung JS, Raina S, Moon C, Guggino WB, Nielsen S. Aquaporin CHIP: the archetypal molecular water channel. Am J Physiol 1993; 265: F463–F476. Rutkovskiy A, Bliksoen M, Hillestad V, Amin M, Czibik G, Valen G, Vaage J, Amiry-Moghaddam M, Stenslİkken KO. Aquaporin-1 in cardiac endothelial cells is downregulated in ischemia, hypoxia and cardioplegia. J Mol Cell Cardiol 2013; 56: 22–33.
  10. King LS, Kozono D, Agre P. From structure to disease: the evolving tale of aquaporin biology. Nat Rev Mol Cell Biol 2004; 5: 687–698.
  11. Au CG, Cooper ST, Lo HP, Compton AG, Yang N, Wintour EM, North KN, Winlaw DS. Expression of aquaporin 1 in human cardiac and skeletal muscle. J Mol Cell Cardiol 2004; 36: 655–662.
  12. Kellen MR, Bassingthwaighte JB. Transient transcapillary exchange of water driven by osmotic forces in the heart. Am J P