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Poult Sci 2008. 87:973-978. doi:10.3382/ps.2007-00281
© 2008 Poultry Science Association
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PHYSIOLOGY, ENDOCRINOLOGY, AND REPRODUCTION

Effects of Cold Stress on the Messenger Ribonucleic Acid Levels of Corticotrophin-Releasing Hormone and Thyrotropin-Releasing Hormone in Hypothalami of Broilers

J. W. Wang*,{dagger} and S. W. Xu*,1

* College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China; {dagger} Institute of Animal Science and Veterinary Medicine, Hei Longjiang Academy of Land-Reclamation Sciences, Harbin 150038, P. R. China

1 Corresponding author: xushiwen101{at}sohu.com


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
In this study, seventy 1-d-old male broiler chicks were randomly allocated to 10 groups to investigate the effect of cold stress on the messenger RNA (mRNA) levels of corticotrophin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH) in hypothalami. The chicks were maintained at 30 ± 2°C temperature and given free access to standard chow and water. Until 15 d old, the 6 treatment groups were maintained at 12 ± 1°C. Hypothalami were collected for the assessment of the mRNA levels by semiquantitative reverse transcription-PCR after stress termination. Cold stress significantly decreased the mRNA levels of CRH in 6 and 12 h treatment groups and significantly increased the mRNA levels of TRH in 1, 6, and 12 h treatment groups during acute cold stress. There were no significant differences in the mRNA levels of CRH and TRH among different control groups during chronic cold stress. However, chronic cold stress resulted in a significant increase of the mRNA levels of CRH and a significant decrease of the mRNA levels of TRH compared with the corresponding control groups. The results indicate that the 2 genes show different response to cold stress at the mRNA levels, and on the other hand, the different degree of cold stress also produces different effects on the identical gene.

Key Words: broiler • cold stress • semi-quantitative reverse transcription polymerase chain reaction • corticotrophin-releasing hormone messenger ribonucleic acid • thyrotropin-releasing hormone messenger ribonucleic acid


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cold is one of the main barriers limiting the development of the animal husbandry in cold regions (Yang and Li, 1999; Li et al., 2006). The research has proved that the central nervous system and its central locus were the dominant sections that played the integrated and regulative role in the cold stress reaction and carried out the regulation through the sympathetic-adrenal-medullary-axis, the hypothalamic-pituitary-adrenal-axis, and the hypothalamic-pituitary-thyroid-axis (Kim et al., 1999; Cheng et al., 2004; Helmreich et al., 2005). Corticotrophin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH) synthesized and secreted by hypothalami not only adjusted the corresponding hormonal release from the pituitary, adrenal, and thyroid (Yi and Baram, 1994; Zhu and Yu, 1999; Wang and Zuo, 2001; Collin et al., 2003; Van-den-Burg et al., 2003), but also played an important role in many physiological regulations (Hendriksen et al., 1992; Hangalapura et al., 2004; Lechan and Fekete, 2006). So the changes of CRH and TRH synthesis and secretion were very important for the regulation of the stress reaction. However, most studies about this were in mammals (Jobin et al., 1975; Ceccatelli and Orazzo, 1993; Uribe et al., 1993; Yang et al., 1994; Sanchez et al., 2001; Ming et al., 2002). Little research has been conducted to investigate the effect of cold stress on the CRH and TRH genes of broilers. The goal of this study was to evaluate the effect of cold stress on the mRNA levels of CRH and TRH genes in hypothalami of broilers.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Birds and Tissue Collection

All procedures used in the present experiment were approved by the Institutional Animal Care and Use Committee of Northeast Agricultural University. Seventy 1-d-old male broiler chicks were purchased from Weiwei Co. Ltd. (Harbin, China) and were randomly allocated to 10 groups (4 groups for the acute cold stress experiment, and 6 groups for the chronic cold stress experiment). The chicks were maintained in our animal facility, kept under a 16L:8D cycle and temperature (30 ± 2°C) and given free access to standard chow and water. Until 15 d old, the 6 treatment groups were maintained at 12 ± 1°C temperature (1, 6, and 12 h treatment groups for the acute cold stress, and 5, 10, and 20 d treatment groups for the chronic cold stress). The chicks were killed by decapitation after stress termination. The killed order of the chicks was 1 h treatment group, 6 h treatment group, acute control group, 12 h treatment group, 5 d treatment group, 5 d control group, 10 d treatment group, 10 d control group, 20 d treatment group, and 20 d control group. The hypothalami were collected, immediately frozen on dry ice, and then stored at –70°C for RNA isolation.

Reagents

Escherichia coli TG1 competent cells and the restriction enzymes were presented by J. T. Wang. The Taq DNA polymerase, pMD18-T vector, T4 DNA ligase, and DNA gel recovery kit were purchased from Takara Company in Dalian, China. Trizol and M-MLV reverse transcription reagents were purchased from Invitrogen (Beijing, China). Agarose was purchased from Yito Company in Shanghai, China. Other chemical reagents were all analytical pure reagents made in China.

Primer Design

To develop primers, we used the chicken CRH and TRH mRNA GenBank sequences with accession numbers of AJ621492 [GenBank] and AJ703806 [GenBank] , respectively. Turkey β-actin (GenBank accession number NM_205518 [GenBank] ) was used as a housekeeping gene. Primers (Table 1Go) were designed using the Oligo 6.0 Software (Molecular Biology Insights, Cascade, CO).) and were synthesized by Boya Biotechnological Co. Ltd. in Shanghai, China.


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  		Table 1. Gene-special primers for β-actin, CRH, and TRH used in the semiquantitative reverse transcription-PCR
 
Total RNA Isolation and Reverse Transcription

Total RNA was isolated from tissue samples using Trizol reagent according to the manufacturer’s instructions (Invitrogen). The RNA concentrations were determined using the GeneQuant 1300, and RNA quality was verified by electrophoresis on 1% formaldehyde agarose gel.

Reverse transcription reaction (40 µL) consisted of the following: 10 µg of total RNA, 1 µL of M-MLV reverse transcription, 1 µL of RNase inhibitor, 4 µL of dNTP, 2 µL of Oligo dT, 4 µL of dithiothreitol, and 8 µL of 5x buffer. The procedure of the reverse transcription was according to the manufacturer’s instructions (Invitrogen).

Reverse Transcription PCR and Sequence Analysis

Through the optimization of the annealing temperature and reaction conditions, PCR was performed in 25-µL reactions containing the following: 2.5 µL of 10x buffer, 1 µL of Taq DNA polymerase; 0.2 mM dNTP, 10 pmol of each gene-specific primer (Table 1Go), and 1 µL of the reverse transcription product. Thermal cycling parameters were as follows: denaturation at 95°C for 4 min, followed by 30 cycles of 95°C for 1 min, 54°C for 45 s (β-actin), 72°C for 1 min, with a final extension at 72°C for 7 min. The annealing temperature of CRH and TRH were 54.5 and 50.5°C, respectively. The products from reverse transcription PCR were analyzed on a 1% agarose gel containing ethidium bromide.

To validate the reverse transcription-PCR, all amplicons were sequenced by Yingjun Biotechnological Co. Ltd. in Shanghai, China. The sequencing results were compared with the GenBank sequences.

Two microliters of CRH/TRH gene and 2 µL of β-actin gene reverse transcription PCR products were mixed and analyzed on 1.0% agarose gel with the ChampGel-3000 gel image processing system. The relative ratio of the optical density (OD) of the CRH/TRH gene and β-actin gene was used to indicate the relative amount of the CRH/TRH gene.

Statistical Analysis

Statistical analysis of all data was performed using SAS procedures (SAS Institute Inc., Cary, NC). The effect of cold stress on mRNA levels in chicks was assessed by 1-way ANOVA. All values were expressed as means ± SD. The mRNA levels were demonstrated with the relative ratio of OD of the CRH/TRH gene and β-actin gene. A P-value < 0.05 was considered a significant difference.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The Result of Total RNA Isolation

Total RNA isolated from hypothalami was verified by electrophoresis on 1% formaldehyde agarose gel (Figure 1Go).


Figure 1
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  		Figure 1. Electrophoresis on 1% formaldehyde agarose gel of total RNA isolated from the hypothalami; lane 1: DNA marker DL2000; lane 2 to 5: total RNA isolated from the hypothalami.

 
The Identified Result of Reverse Transcription PCR Products

The results are presented in Figures 2Go to 5GoGoGo.


Figure 2
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  		Figure 2. The PCR, plasmid PCR, and restriction enzymes identification of β-actin, corticotrophin-releasing hormone (CRH), and thyrotropin-releasing hormone (TRH); lane 1, 12, and 13: DNA marker DL2000; lane 6, 7, and 18: DNA marker DL15000; lane 2, 11, and 14: reverse transcription PCR products of β-actin, CRH, and TRH; lane 3, 10, and 15: plasmid PCR products of β-actin, CRH, and TRH; lane 4, 9, and 16: recombinant plasmids of β-actin, CRH, and TRH digested by XbaI and PstI; lane 5, 8, and 17: recombinant plasmids of β-actin, CRH, and TRH digested by XbaI.

 

Figure 3
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  		Figure 3. The comparative result of the sequencing result and the GenBank sequence. The upper sequence is the sequencing result. The lower sequence is the GenBank sequence. The homology of the 2 sequences was 99.6%.

 

Figure 4
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  		Figure 4. The comparative result of the sequencing result and the GenBank sequence. The upper sequence is the sequencing result. The lower sequence is the GenBank sequence. The homology of the 2 sequences was 100%.

 

Figure 5
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  		Figure 5. The comparative result of the sequencing result and the GenBank sequence. The upper sequence is the sequencing result. The lower sequence is the GenBank sequence. The homology of the 2 sequences was 99.8%.

 
Effects of Cold Stress on the mRNA Levels of CRH in Hypothalami of Broilers

Effects of acute cold stress on the mRNA levels of CRH are presented in Table 2Go and Figure 6Go. Compared with the 0 h control group, acute cold stress in 6 and 12 h treatment groups significantly decreased (P < 0.05) the mRNA levels of CRH in hypothalami by 14.5 and 32.6%, respectively. There were significant differences (P < 0.05) in the mRNA levels of CRH among different treatment groups.


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  		Table 2. Effects of acute cold stress on the mRNA levels of corticotrophin-releasing hormone (CRH) in hypothalami of broilers1
 

Figure 6
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  		Figure 6. Effects of acute and chronic cold stress on the mRNA levels of corticotrophin-releasing hormone (CRH) in hypothalami of broilers; lane 1: 0 h control group; lane 2 to 4: 1, 6, and 12 h treatment groups; lane 5: DNA marker DL2000; lane 6 to 8: 5, 10, and 20 d control groups; lane 9 to 11: 5, 10, and 20 d treatment groups.

 
Effects of chronic cold stress on the mRNA levels of CRH are presented in Table 3Go and Figure 6Go. Compared with the corresponding control groups, chronic cold stress in 5, 10, and 20 d treatment groups significantly increased (P < 0.05) the mRNA levels of CRH in hypothalami. There were significant differences (P < 0.05) in the mRNA levels of CRH between the 5 and 20 d treatment groups.


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  		Table 3. Effects of chronic cold stress on the mRNA levels of corticotrophin-releasing hormone (CRH) in hypothalami of broilers
 
Effects of Cold Stress on the mRNA Levels of TRH in Hypothalami of Broilers

Effects of acute cold stress on the mRNA levels of TRH are presented in Table 4Go and Figure 7Go. Compared with the 0 h control group, acute cold stress in 1, 6, and 12 h treatment groups significantly increased (P < 0.05) the mRNA levels of TRH in hypothalami by 7.6, 15.7, and 25.2%, respectively. There were significant differences (P < 0.05) in the mRNA levels of TRH in hypothalami among different treatment groups.


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  		Table 4. Effects of acute cold stress on the mRNA levels of thyrotropin-releasing hormone (TRH) in hypothalami of broilers1
 

Figure 7
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  		Figure 7. Effects of acute and chronic cold stress on the mRNA levels of thyrotropin-releasing hormone (TRH) in hypothalami of broilers; lane 1: 0 h control group; lane 2 to 4: 1, 6, and 12 h treatment groups; lane 5: DNA Marker DL2000; lane 6 to 8: 5, 10, and 20 d control groups; lane 9 to 11: 5, 10, and 20 d treatment groups.

 
Effects of chronic cold stress on the mRNA levels of TRH are presented in Table 5Go and Figure 7Go. Compared with the corresponding control groups, chronic cold stress in 5, 10, and 20 d treatment groups significantly decreased (P < 0.05) the mRNA levels of TRH in hypothalami. There were no significant differences in the mRNA levels of TRH in hypothalami among different treatment groups.


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  		Table 5. Effects of chronic cold stress on the mRNA levels of thyrotropin-releasing hormone (TRH) in hypothalami of broilers1
 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The current study indicated that cold stress could change the mRNA levels of CRH in hypothalami. The experiment has demonstrated that corticotrophin-releasing factor mRNA in the paraventricular nucleus increased in response to i.p. hypertonic saline, restraint, and swim stress, but that would not happen in the cold stress in the rat (Harbuz and Lightman, 1989). Yi and Baram (1994) also reported that cold-separation stress resulted in CRH mRNA increased in rats aged 9 d or older, but not in 6-d-old rats. In this experiment, acute cold stress in 6 and 12 h treatment groups significantly decreased the mRNA levels of CRH in hypothalami compared with the 0 h control group, and there were significant differences in the mRNA levels of CRH in hypothalami among different treatment groups. Compared with the corresponding control groups, chronic cold stress in 5, 10, and 20 d treatment groups significantly increased (P < 0.05) the mRNA levels of CRH in hypothalami, and there were significant differences at the mRNA levels of CRH in hypothalami between the 5 and 20 d treatment groups. Additionally, the current experiments also indicated that the regulation of the mRNA levels of CRH in hypothalami of rats also had been studied including protein kinase A and protein kinase C, alpha1-adrenergic receptors, glucocorticoids, and so on (Emanuel et al., 1990; Kiss et al., 1996; Hatalski et al., 2000; Kiss and Aguilera, 2000; Ma et al., 2001). So the regulatory mechanism of CRH gene was still very complex and needed to be further studied, especially the research in poultry.

In this experiment, acute cold stress in 1, 6, and 12 h treatment groups significantly increased the mRNA levels of TRH in hypothalami compared with the 0 h control group, and there were significant differences (P < 0.05) in the mRNA levels of TRH in hypothalami among different treatment groups. Compared with the corresponding control groups, chronic cold stress in 5, 10, and 20 d treatment groups significantly decreased the mRNA levels of TRH in hypothalami, and there were no significant differences in the mRNA levels of TRH in hypothalami among different treatment groups. The series of results show that cold stress may change the mRNA levels of TRH in hypothalami of broilers. Rage et al. found cold exposure increased the TRH mRNA abundance, but TRH content was significantly decreased in rat hypothalamus. This indicated that cold stress may regulate the TRH gene expression at translational or posttranslational levels (Rage et al., 1994). Ceccatelli and Orazzo (1993) reported that the effect of the immobilization, cold, and swimming stress on the mRNA levels of TRH in the hypothalamic paraventricular nucleus of adult male rats were all not significant. Now, about the regulation of TRH mRNA expression in hypothalami, most studies proved the negative feedback of thyroid hormones was the mainly regulatory mechanism (Dyess et al., 1988; Taylor et al., 1990; Kim et al., 1996). But some studies found that the nerve-mediated effects also existed, and it could inhibit the effect of the thyroid hormones (Zoeller et al., 1990).

In conclusion, acute and chronic stress could influence the mRNA levels of CRH and TRH in hypothalami of broilers. The 2 genes showed different response to the same cold stress at mRNA levels, but on the other hand, the different degree of cold stress also produced different effects on the identical gene. However, because of little research, the mechanism of the cold stress response in poultry is still an open question.


   ACKNOWLEDGMENTS
 
The authors thank Zhao Xiaojing at Institute of Animal Science and Veterinary Medicine, Hei Longjiang Academy of Land-Reclamation Sciences for critically reviewing the paper.

Received for publication July 12, 2007. Accepted for publication February 8, 2008.


   REFERENCES
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 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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Dyess, E. M., T. P. Segerson, Z. Liposits, W. K. Paull, M. M. Kaplan, P. Wu, I. M. Jackson, and R. M. Lechan. 1988. Triiodothyronine exerts direct cell-specific regulation of thyrotropin-releasing hormone gene expression in the hypothalamic paraventricular nucleus. Endocrinology 123:2291–2297.[Abstract/Free Full Text]

Emanuel, R. L., D. M. Girard, D. L. Thull, and J. A. Majzoub. 1990. Second messengers involved in the regulation of corticotropin-releasing hormone mRNA and peptide in cultured rat fetal hypothalamic primary cultures. Endocrinology 126:3016–3021.[Abstract/Free Full Text]

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