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ARTICLE IN PRESS J. Yu et al. / Comparative Biochemistry and Physiology, Part A xxx (2010) xxx–xxx

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Table 7 Pathway analysis result of the differentially expressed genes. KEGG

Total

P-value

Q value gene

Linoleic acid metabolism

4

7.8E-5

1.17E-4

MAPK signaling pathway

4

2.98E-4

1.63E-4

Metabolism of xenobiotics by cytochrome P450

4

6.02E-4

2.01E-4

Arachidonic acid metabolism

4

0.002249

5.39E-4

Gap junction

2

0.002606

5.39E-4

Focal adhesion

3

0.004329

7.64E-4

Antigen processing and presentation

3

0.014765

0.002272

Regulation of actin cytoskeleton

2

0.026589

0.00371

Gamma-hexachlorocyclohexane degradation Alzheimer's disease Glycerolipid metabolism mTOR signaling pathway Cell communication VEGF signaling pathway Adherens junction Cytokine–cytokine receptor interaction

1 1 1 1 1 1 1 2

0.040242 0.053302 0.066189 0.066189 0.066189 0.091454 0.103836 0.180692

0.005249 0.006663 0.007637 0.007637 0.007637 0.009799 0.010742 0.017773

Calcium signaling pathway Neuroactive ligand-receptor interaction

1 1

0.338208 0.587815

0.031707 0.053438

regulated after heat stress, consistent with previous reports. Altering gene expression is an integral part of the cellular response to heat stress as this regulates protein translation, and hence cellular function. Heat stress can affect gene transcription via three mechan-

Fig. 6. mRNA expression of HSP90, HSP70, HSP27, EGF and EGFR in the pig jejunum using real-time PCR.

CYP3A39 CYP2C49 ALOX15 EGFR Hsp27 HSP70.2 EGF CYP2B22 CYP3A39 CYP2C49 CYP2B22 CYP2C49 ALOX15 EGFR EGF EGFR VEGFA EGF HSP90 HSP70.2 EGFR EGF CYP3A39 LPL LPL VEGFA LOC396725 Hsp27 EGFR EGFR EGF EGFR MLN

Input symbol

Experiment 1

Ssc.203.1.S1_at Ssc.206.1.S1_at; Ssc.26321.1.S1_s_at Ssc.10974.1.S1_at Ssc.55.1.S1_at Ssc.11197.1.S1_at Ssc.5145.1.S1_a_at Ssc.87.1.S1_at Ssc.11267.1.S1_at Ssc.203.1.S1_at Ssc.206.1.S1_at; Ssc.26321.1.S1_s_at Ssc.11267.1.S1_at Ssc.206.1.S1_at; Ssc.26321.1.S1_s_at Ssc.10974.1.S1_at Ssc.55.1.S1_at Ssc.87.1.S1_at Ssc.55.1.S1_at Ssc.10015.1.A1_at Ssc.87.1.S1_at Ssc.12191.3.A1_at; Ssc.12191.2.A1_at Ssc.5145.1.S1_a_at Ssc.55.1.S1_at Ssc.87.1.S1_at Ssc.203.1.S1_at Ssc.16335.1.S2_at Ssc.16335.1.S2_at Ssc.10015.1.A1_at Ssc.24.1.S1_at Ssc.11197.1.S1_at Ssc.55.1.S1_at Ssc.55.1.S1_at Ssc.87.1.S1_at Ssc.55.1.S1_at Ssc.714.1.S1_at

− 2.21 − 2.23 − 2.0 − 3.01 5.22 3.26 − 3.37 −2.33 −2.21 − 2.23 − 2.33 − 2.23 − 2.0 − 3.01 − 3.37 − 3.01 − 2.27 − 3.37 5.04 3.26 −3.01 −3.37 − 2.21 2.26 2.26 −2.27 2.01 5.22 − 3.01 −3.01 −3.37 − 3.01 − 2.45

isms: 1) alter the level of transcription factors; 2) adjust the activity of transcription factors; and 3) change the cellular location of transcription factors (Sonna et al., 2002; Hahn et al., 2004). In the current study, genes relating to the regulation of translation were found to be significantly altered following heat treatment, in agreement with previous reports. We recently reported that heat stress-induced damage to the pig small intestine epithelial tissue was rapidly repaired within the following few days following heat stress (Liu et al., 2009). The regeneration of the damaged intestine epithelium encourages crypt cell proliferation and migration (Kaushik and Kaur, 2005). Consistent with rapid cellular regeneration, the current study found that the expression of genes related to the regulation of cell proliferation and migration was significantly altered after heat stress. Furthermore, the changes in gene expression following heat stress provided significant insight into the potential biological pathways activated or inhibited in response to heat stress (Table 7) in the pig small intestine. Pathway analysis of genes altered following heat treatment revealed linoleic acid metabolism, MAPK signaling, metabolism of xenobiotics by cytochrome P450 and arachidonic acid metabolism to be involved in the response to heat stress. Linoleic and arachidonic acid are essential for tissue growth and development, and play a critical role in intestinal epithelial cell differentiation and tumor development (Hui et al., 1999; Kawajiri et al., 2002). Metabolism of arachidonic and linoleic acid via prostaglandin H synthases and lipoxygenases generate an array of lipid compounds which serve as potent mediators of several physiological and pathophysiological processes (Zeldin, 2001). Our results found heat stress to stimulate genes regulating arachidonic acid metabolism, potentially in response to oxidative stress in order to alleviate the stress response.

Please cite this article as: Yu, J., et al., Effect of heat stress on the porcine small intestine: A morphological and gene expression study, Comp. Biochem. Physiol. A (2010), doi:10.1016/j.cbpa.2010.01.008

Effect of heat stress on the porcine small intestine A morphological and gene  

Keywords: Heat stress Morphology Gene expression Electron microscope Microarray Small intestine Pig Article history: Received 26 November 20...

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