Investigation of gender differences in the incidence of ascites and profile of gene expression in kidney tissue of broiler chickens

Document Type : Research Paper

Authors

1 Ph.D Student, Department of Animal Science, Sari Agricultural Sciences and Natural Resources University, Sari, Iran

2 Associate Professor, Department of Animal Science, Sari Agricultural Sciences and Natural Resources University, Sari, Iran

3 Professor, Department of Animal Science, Sari Agricultural Sciences and Natural Resources University, Sari, Iran

4 Assistant Professor, Department of Animal Science, Faculty of Agriculture, University of Tabriz, Tabriz, Iran

Abstract

Ascites syndrome is one of the most important causes of death in the poultry industry, in which various tissues of the body, including the kidneys, are involved. This syndrome occurs with different frequencies in males and females, and different mechanisms of ascites in the two sexes have not been studied to date. In this study, the gene expression profile of kidney tissue of male and female chickens with ascites syndrome from the paternal line (B) of the Arian commercial line was compared using RNA-Seq data. Due to severe cold stress applied, the mortality rate was high and about 59%, which was higher in males (63.4%) than females (54.1%). The results of transcriptome analysis showed that 240 genes were significantly different in comparison between ascites male and female birds. The annotation analysis of these genes showed that the metabolic pathways of antibiotic biosynthesis and amino acids, carbon metabolism, cell adhesion, receptor-extracellular matrix interaction (ECM) were involved in this process. The body's response to ascites-induced damage to kidney tissue is the development of renal fibrosis (to repair the damage) and reduced activity of the glycolysis pathways and increased gluconeogenesis to reduce energy and oxygen consumption in these pathways. Furthermore, an increase of the STAT-JAK2 signaling pathway activity (due to the high expression of JAK2 and STAT3 genes) was observed. This signal stimulates cell growth, angiogenesis, differentiation, migration, and apoptosis. It is expected that the results of the present study to provide new insights into understanding the molecular mechanism of ascites incidence and also differences in its occurrence in males compared to female broiler chickens.

Keywords

Main Subjects

References

جباری عوری ر. 1398. آنالیز پروفایل ترنسکریپتومی و فاکتور­های متابولیکی سندرم آسیت القا شده در یک لاین مرغ گوشتی. رساله دکتری علوم دامی، دانشکده کشاورزی، دانشگاه تبریز.
صحرایی س.، نصیری م.، جوادمنش ع.، توحیدی ر.، و ابراهیمی ا. 1398. بررسی بیان ژن و شبکه های ژنی مرتبط با آپوپتوزیس در مرغان حساس و مقاوم به آسیت والدین جوجه گوشتی آرین با استفاده از RNA-seq. تحقیقات تولیدات دامی، 8(1): 53-66.
Caley M .P., Martins V .L. and O'Toole E .A. 2015. Metalloproteinases and wound healing.  Advances in Wound Care, 4(4): 225-234.
Canto E., Isobe N., Didonna A., Hauser S .L., Oksenberg J .R. and MS-EPIC Study Group. 2018. Aberrant STAT phosphorylation signaling in peripheral blood mononuclear cells from multiple sclerosis patients. Journal of Neuroinflammation, 15(1): 72.
Cisar C. R., Balog J. M. and Anthony N. B. 2005. Differential expression of cardiac muscle mitochondrial matrix proteins in broilers from ascites resistant and susceptible lines. Poultry Science, 84: 704-708.
Daneshyar M., Kermanshahi H. and Golian A. 2009. Changes of biochemical parameters and enzyme activities in broiler chickens with cold-induced ascites. Poultry Science, 88(1): 106-110.
Demeule M., Bertrand Y., Michaud-Levesque J., Jodoin J., Rolland Y., Gabathuler R. and Béliveau R. 2003. Regulation of plasminogen activation: a role for melanotransferrin (p97) in cell migration. Blood, 102(5): 1723-1731.
Dewil E., Buys N., Albers G .A. and Decuypere E. 1996. Different characteristics in chick embryos of two broiler lines differing in susceptibility to ascites. British Poultry Science, 37(5): 1003-1013.
Dreesen O. and A. H. Brivanlou. 2007. Signaling pathways in cancer and embryonic stem cells. Stem Cell Reviews, 3(1): 7-17.
Elbein S. C. 2002. Perspective: the search for genes for type 2 diabetes in the post-genome era. Endocrinology, 143(6): 2012-2018.
Gonçalves J., Friães A. and Moura L. 2007. Congenital adrenal hyperplasia: focus on the molecular basis of 21-hydroxylase deficiency. Expert Rewiews in Molecular Medicine, 9(11): 1-23.
Goralska M., Nagar S., Fleisher L. N. and McGahan M. C. 2005. Differential degradation of ferritin H-and L-chains: accumulation of L-chain-rich ferritin in lens epithelial cells. Investigative Ophthalmology and Visual Science, 46(10): 3521-3529.
Haigney M. C., Zareba W., Gentlesk P. J., Goldstein R. E., Illovsky M., McNitt S., Andrews M .L., Moss A. J. and MADIT II Investigators. 2004. QT interval variability and spontaneous ventricular tachycardia or fibrillation in the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II patients. Journal of the American College of Cardiology, 44(7): 1481-1487.
Haque I., Ghosh A., Acup S., Banerjee S., Dhar K., Ray A., Sarkar S., Kambhampati S. and Banerjee S .K.  2018. Leptin-induced ER-α-positive breast cancer cell viability and migration is mediated by suppressing CCN5-signaling via activating JAK/AKT/STAT-pathway. BMC Cancer,18(1): 99.
Hasanpur K., Nassiri M., Salekdeh G .H., Torshizi R .V., Pakdel A. and Kermanshahi H. 2015. Association between early growth-related traits and ascites induced in broiler sire lines by saline drinking water or cool temperatures. European Poultry Science, 79: 1-10.
Hasanpur K., Nassiri M. and Salekdeh G. H. 2019. The comparative analysis of phenotypic and whole transcriptome gene expression data of ascites susceptible versus ascites resistant chickens. Molecular Biology Reports, 46(1): 793-804.
Hassanpour H., Momtaz H., Shahgholian L., Bagheri R., Sarfaraz S. and Heydaripoor B. 2011. Gene expression of endothelin-1 and its receptors in the heart of broiler chickens with T3-induced pulmonary hypertension. Research in Veterinary Science, 91(3): 370-375.
Jabbari Ori R., Shoja J., Esmailizadeh A., Rafat S. A. and Hasanpur K. 2019. Changes in biochemical parameters of a broiler chicken line with cold-induced ascites. Journal of Livestock Science and Technologies, 7(2):47-55.
Kumar M. and P. Ratwan. 2018. Genetic variability and significance of STAT gene in dairy animals. Research & Reviews: Journal of Dairy Science and Technology, 5(3): 1-6.
Mahabeleshwar G. H., Feng W., Phillips D. R. and Byzova T .V. 2006. Integrin signaling is critical for pathological angiogenesis. The Journal of Experimental Medicine, (11): 2495-2507.
Masterson T., Klein K., Karouzakis E., Distler O., Ospelt C. and Bertoncelj M. F. 2018. OP0165 Joint-specific differences in the activation of the jak-stat pathway in rheumatoid arthritis. Annals of the Rheumatic Diseases, 77: 133.
Maxwell M. H., Spence S., Robertson G. W. and Mitchell M. A. 1990. Haematological and morphological responses of broiler chicks to hypoxia. Avian Pathology, 19(1): 23-40.
Olander H. J., Burton R. R. and Adler H. E. 1967. The pathophysiology of chronic hypoxia in chickens. Avian Diseases, 11(4): 609-620.
Petit V. and Thiery J. P. 2000. Focal adhesions: structure and dynamics. Biology of the Cell, 92(7): 477-494.
Richardson D. 2000. The role of the membrane‐bound tumour antigen, melanotransferrin (p97), in iron uptake by the human malignant melanoma cell. European Journal of Biochemistry, 267(5): 1290-1298.
Sanders E. and Diehl S. 2015. Analysis and interpretation of transcriptomic data obtained from extended Warburg effect genes in patients with clear cell renal cell carcinoma. Oncoscience, 2(2): 151.
Sekyere E. O., Dunn L. L., Rahmanto Y. S. and Richardson D. R. 2006. Role of melanotransferrin in iron metabolism: studies using targeted gene disruption in vivo. Blood, 107(7): 2599-2601.
Sheppard A. M. 1994. ligands in development. Cell Adhesion and Communication, 2(1): 27-43.
Shi S., Shen Y., Zhao Z., Hou Z., Yang Y., Zhou H., Zou J. and Guo Y. 2014. Integrative analysis of transcriptomic and metabolomic profiling of ascites syndrome in broiler chickens induced by low temperature. Molecular Biosystems, 10(11): 2984-2993.
Tan F. K., Tercero G. M., Arnett F. C., Wang N. and Chakraborty R. 2003. Examination of the possible role of biologically relevant genes around FBN1 in systemic sclerosis in the Choctaw population. Arthritis and Rheumatism, 48(11): 3295-3296.
Wang Y., Guo Y., Ning D., Peng Y., Yang Y. and Liu D. 2012. Analysis of liver transcriptome in broilers with ascites and regulation by L-carnitine. The Journal of Poultry Science, 50(2): 126-137.
Wideman  R. F. 2000. Cardio-pulmonary hemodynamics and ascites in broiler chickens. Poultry and Avian Biology Reviews, 11(1): 21-44.
Wideman R. F. and Bottje W. G. 1993. Current understanding of the ascites syndrome and future research directions. Nutrition and Technical Symposium Proceedings. Novus International, Inc., St. Louis, MO. pp. 1-20.
Wideman R. F., Rhoads D. D., Erf G. F. and Anthony N. B. 2013. Pulmonary arterial hypertension (ascites syndrome) in broilers: (a review). Poultry Science, 92(1): 64-83.
Yang F., Cao H., Xiao Q., Guo X., Zhuang Y., Zhang C., Wang T., Lin H., Song Y., Hu G. and Liu P. 2016. Transcriptome analysis and gene identification in the pulmonary artery of broilers with ascites syndrome. PloS One, 11(6): e0156045.
Animal Production Research
Volume 10, Issue 3
December 2021
Pages 33-44

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