Dergiler / Turkish Journal of Veterinary and Animal Sciences / 2014 / Cilt: 38 - Sayı: 2

Caspase-1, -2, and -3 gene expression is enhanced in the heart and lung of chickens with pulmonary hypertension (ascites)

Sayfa
133–137
Yayın Tarihi
2014-05-18
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)

It is speculated that increased mRNA levels of caspase in the lungs and hearts of pulmonary hypertensive broilers could be evidence of upregulated apoptosis, which is involved in the pathophysiology of broiler chickens with pulmonary hypertension.

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:To investigate the involvement of apoptosis in the pathogenesis of T3-induced pulmonary hypertension in broiler chickens, caspase-1, -2, and -3 gene expressions were evaluated by semiquantitative RT-PCR in the lungs and left and right heart ventricles.
📊
Temel Bulgular & Veri:One-day-old fast-growing chickens were randomly divided into 2 equal groups with 3 replicates per group.
💡
Sonuç & Katkı:It is speculated that increased mRNA levels of caspase in the lungs and hearts of pulmonary hypertensive broilers could be evidence of upregulated apoptosis, which is involved in the pathophysiology of broiler chickens with pulmonary hypertension.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Key words: Caspase · apoptosis · broiler

Abstract

To investigate the involvement of apoptosis in the pathogenesis of T3-induced pulmonary hypertension in broiler chickens, caspase-1, -2, and -3 gene expressions were evaluated by semiquantitative RT-PCR in the lungs and left and right heart ventricles. One-day-old fast-growing chickens were randomly divided into 2 equal groups with 3 replicates per group. Chicks were reared for 7 weeks under standard conditions. T3 as a thyroid hormone was added to the ration after week 1 of rearing. Pulmonary hypertension was induced at 49 days based on RV/TV ratio index. The caspase genes were constitutively expressed in the lung and right and left ventricles of intact and pulmonary hypertensive broiler chickens. The relative amount of caspase-1, -2, and -3 mRNA in the lung and right and left ventricles of the heart was higher in pulmonary hypertensive broilers than in control broilers (P < 0.05). It is speculated that increased mRNA levels of caspase in the lungs and hearts of pulmonary hypertensive broilers could be evidence of upregulated apoptosis, which is involved in the pathophysiology of broiler chickens with pulmonary hypertension.

🔖

Bu Makaleye Atıf Yap

HASSANPOUR, H., TESHFAM, M., MOMTAZ, H., ZAREI, H., BAHADORAN, S. (2014). Caspase-1, -2, and -3 gene expression is enhanced in the heart and lung of chickens with pulmonary hypertension (ascites). Turkish Journal of Veterinary and Animal Sciences, Cilt: 38 - Sayı: 2, 133–137. https://ajindex.com/articles/121607

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (12)

  1. Baghbanzadeh A, Decuypere E. Ascites syndrome in broilers: physiological and nutritional perspectives. Avian Pathol 2008; 37: 117–126.
  2. Teshfam DM, Nikbakht Brujeni G, Hassanpour H. Evaluation of endothelial and inducible nitric oxide synthase mRNA expression in the lung of broiler chickens with developmental pulmonary hypertension due to cold stress. Br Poult Sci 2006; 47: 223–229. Olkowski AA. Pathophysiology of heart failure in broiler chickens: structural, biochemical, and molecular characteristics. Poult Sci 2007; 86: 999–1005.
  3. Wideman RF, Rhoads DD, Erf GF, Anthony NB. Pulmonary arterial hypertension (ascites syndrome) in broilers: a review. Poult Sci 2013; 92: 64–83. Balog JM. Ascites syndrome (pulmonary hypertension syndrome) in broiler chickens: are we seeing the light at the end of the tunnel? Avian Poult Biol Rev 2003; 14: 99–126.
  4. Ipek A, Sahan U. Effects of cold stress on broiler performance and ascites susceptibility. Asian Austral J Anim Sci 2006; 19: 734–738.
  5. Yuan JXJ, Rubin LJ. Pathogenesis of pulmonary arterial hypertension. Circulation 2005; 111: 534–538. Rabinovitch M. Molecular pathogenesis of pulmonary arterial hypertension. J Clin Invest 2008; 118: 2372–2379.
  6. Humbert M, Morrell NW, Archer SL, Stenmark KR, MacLean MR, Lang IM, Christman BW, Weir EK, Eickelberg O, Voelkel NF. Cellular and molecular pathobiology of pulmonary arterial hypertension. J Am Coll Cardiol 2004; 43: S13–S24. Gurbanov E, Shiliang X. The key role of apoptosis in the pathogenesis and treatment of pulmonary hypertension. Eur J Cardio-Thoracic Surg 2006; 30: 499–507.
  7. Riley DJ, Thakker-Varia S, Wilson FJ, Poiani GJ, Tozzi CA. Role of proteolysis and apoptosis in regression of pulmonary vascular remodeling. Physiol Res 2000; 49: 577–585.
  8. Zimmermann KC, Bonzon C, Green DR. The machinery of programmed cell death. Pharmacol Ther 2001; 92: 57–70.
  9. Nicholson DW, Thornberry NA. Caspases: killer proteases. Trends Biochem Sci 1997; 22: 299–306. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol 2007; 35: 495–516.
  10. Fazio S, Palmieri EA, Lombardi G, Biondi B. Effects of thyroid hormone on the cardiovascular system. Recent Prog Horm Res 2004; 59: 31–50.
  11. Igney FH, Krammer PH. Death and anti-death: tumour resistance to apoptosis. Nat Rev Cancer, 2002; 2: 277–288.
  12. Hassanpour H, Momtaz H, Shahgholian L, Bagheri R, Sarfaraz S, Heydaripoor B. Gene expression of endothelin-1 and its receptors in the heart of broiler chickens with T3-induced pulmonary hypertension. Res V