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* Animal Growth and Development Laboratory, Department of Animal Science, University of Minnesota, St. Paul 55108; and
and
Department of Animal Sciences and Industry, Kansas State University, Manhattan 66506
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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Key Words: Estradiol • Implant • Insulin-Like Growth Factor-I • Muscle • Steer • Trenbolone Acetate
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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), and the number of actively proliferating satellite cells that can be isolated from the semimembranosus muscle (Johnson et al., 1998a). This increased population of activated satellite cells may contribute to the enhanced muscle growth observed in Revalor-S-implanted steers. Our previous studies have strongly suggested that locally produced insulin-like growth factor (IGF)-I may play a role in maintaining satellite cells in a proliferative state. This hypothesis is supported by our observations that steady-state levels of muscle IGF-I mRNA were increased by 30 d after implantation (Johnson et al., 1998b; White et al., 2003). Levels of IGF-I also are increased in the diaphragm muscle of nandrolone-treated rats (Lewis et al., 2002). It is possible that other growth factors, such as insulin-like growth factor binding protein (IGFBP)-3, hepatocyte growth factor (HGF), and myostatin, impact muscle growth in Revalor-S-implanted steers. However, unlike IGF-I mRNA levels, the levels of IGFBP-3, HGF, and myostatin mRNAs in the longissimus muscles of steers implanted with Revalor-S for 30 d were not different than those of nonimplanted steers (White et al., 2003). To better understand the potential role of IGF-I in anabolic-steroid-induced muscle growth, we need to know the timing of changes in muscle IGF-I mRNA levels relative to the time of implantation. Additionally, even though HGF, IGFBP-3, and myostatin mRNA levels were not changed 30 d after implantation, it is possible that they may be altered before this time. Consequently, we have evaluated the time course of changes in muscle levels of IGF-I, IGFBP-3, HGF, and myostatin mRNA in implanted and nonimplanted steers.
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Materials and Methods |
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Longissimus Muscle Biopsy.
Biopsies of the longissimus muscle (1.0 g) between the 10th and 13th rib were obtained from all steers on d 0, 7, 12, and 26. Samples were obtained from alternate sides for the sequential days. Briefly, steers were restrained in a hydraulic squeeze chute, hair was removed from the biopsy site and a local anesthetic (lidocaine HCl; 20 mg/mL; 8 mL per biopsy) was administered. A sterile cloth drape was placed over the biopsy site and a 1-cm incision was made with a scalpel. A sterile Bergstrom biopsy needle was used to obtain the tissue from the longissimus muscle. The incision was rinsed with 70% ethanol and closed with veterinary tissue glue. A topical antibiotic spray was applied to the incision site and then covered with a spray-on aluminum bandage. All steers were monitored for swelling during the 24-h postbiopsy period.
Sample Preparation and RNA Isolation.
Muscle biopsy samples (1.0 g) from each steer were placed in 10 mL of a 5 M guanidine thiocyanate, 50 mM Tris•HC1, 25 mM EDTA, 0.5% lauryl sarcosine, and 1% ß-mercaptoethanol solution (Solution D) in polypropylene tubes. Samples were homogenized, snap-frozen in liquid nitrogen, and stored at -80°C for subsequent RNA isolation (Chomczynski and Sacchi, 1987). Isolated RNA in diethyl pyrocarbonate (DEPC) water was mixed with one-half volume LiCl precipitation solution (7.5 M LiCl, Ambion, Austin, TX) and incubated at 20°C for 30 min. The solution was then centrifuged at high speed in a microfuge for 15 min. The resulting pellet was washed with 70% ethanol, dried, and resuspended in DEPC water. Concentration of RNA was determined by absorbance at 260 nm. Integrity of RNA was determined by electrophoresis of total RNA through a 1% agarose-formaldehyde gel followed by ethidium bromide staining to allow visualization of 28 and 18S ribosomal RNA (rRNA). After RNA integrity was assessed, samples were DNased to remove any contaminating genomic DNA, and RNA was then reverse-transcribed to produce the first-strand complementary DNA (cDNA).
Real-time RT-PCR.
Real-time RT-PCR was used to measure the quantity of IGF-I, IGFBP-3, myostatin, and hepatocyte growth factor mRNA relative to the quantity of cyclophilin (Accession No. Y00052) mRNA in total RNA isolated from longissimus muscle tissue from implanted and nonimplanted steers. Complementary DNA was produced from 0.5 µg RNA using TaqMan Reverse Transcriptase Reagents (Applied Biosystems, Foster City, CA) and the protocol recommended by the manufacturer. Random hexamers were used as primers in cDNA synthesis. Measurement of the relative quantity of the cDNA of interest was carried out using SYBR Green PCR Master Mix (Applied Biosystems, Foster City, CA), appropriate forward and reverse primers (300 nM) (Table 1), and 1 µL of the cDNA mixture. Assays were performed in the GeneAmp 5700 Sequence Detection System (Applied Biosystems) using thermal cycling parameters recommended by the manufacturer (40 cycles of 15 s at 95°C and 1 min at 60°C). Titration of cyclophilin, IGFBP-3, IGF-I, myostatin, or HGF primers (300 nM forward and reverse primers) against increasing amounts of cDNA gave linear responses with slopes between -2.8 and -3.0. In order to reduce the effect of assay-to-assay variation in the PCR assay, all values were calculated relative to a calibration standard that was run on every real-time PCR assay. The coefficient of variation for IGF, IGFBP-3, myostatin, and HGF calibration standards run on each assay were 10.2, 11.3, 9.9, and 11.5%, respectively.
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). Subsequently, IGF-I levels were measured using a heterologous RIA as previously described (Frey et al., 1994). Serum samples were diluted in RIA buffer, a rabbit anti-human IGF-I polyclonal antibody (1:18,000 dilution) (AFP4892898 provided by the National Hormone and Pituitary Program) and approximately 12,000-cpm 125I-labeled IGF-I were added, and the samples were incubated for 24 h at 4°C. Bound and free IGF-I were separated by the addition of a pre-precipitated second antibody, goat anti-rabbit gamma globulin (1:5 dilution) and normal rabbit serum (1:50 dilution), in RIA buffer. Based on the ability of the assay to detect the IGF-I standard, the effective detection range of the RIA was 10 to 640 pg IGF-I. The IGF-I RIA had an intraassay coefficient of variation of less than 3.0%, and all serum samples were analyzed within the same assay.
Statistical Analysis.
All statistical analyses were conducted with the SAS System (SAS, 2001). Data from 18 individual steers were analyzed as a completely randomized block design with the mixed model procedure for repeated measures and incorporated the spatial power law for unequally spaced data with day as the repeated effect. Overall effects of treatment and comparisons of implanted and nonimplanted values on individual days were made using d-0 values as a covariant. Comparisons of values on different days within a treatment were made on a data set that included d-0 values. When significant interactions were detected (P < 0.05), least squares means were separated using LSD tests (P < 0.05).
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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). Daily dry matter intake did not differ (P > 0.15) between nonimplanted and implanted steers (Table 2). These increases in ADG and feed efficiency are similar to those reported in other trials of similar length following implantation and establish the efficacy of the implant during this 26-d trial.
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). Additionally, circulating IGF-I concentrations in implanted steers were significantly elevated (P < 0.005) on d 7, 12, and 26 (49, 89, and 151%, respectively) as compared to d 0 (Figure 1). In contrast, circulating IGF-I concentrations in nonimplanted steers were not significantly different on d 0, 7, and 12 (P > 0.60) but were elevated 37% (P < 0.02) on d 26 relative to d 0 (Figure 1). As was the case with feedlot performance, these data are similar to those reported in other trials of similar duration and further establish the efficacy of the implant during the current trial.
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). Longissimus muscle IGF-I mRNA levels in nonimplanted steers were not significantly different on d 0, 7, 12, and 26 (P > 0.50; Figure 2), indicating that longissimus IGF-I mRNA levels did not change during the trial. In contrast, longissimus muscle IGF-I mRNA levels in implanted steers were increased (P < 0.003) relative to d-0 concentrations on d 7 and 12 (Figure 2; 101% and 128%, respectively), and by d 26, longissimus muscle mRNA levels were more than 3 times (P < 0.0001) those in the longissimus muscles of the same steers on d 0 (Figure 2). Additionally, on d 12 and 26, longissimus IGF-I mRNA levels in implanted steers were higher (40% and 94%, respectively; P < 0.02) than in nonimplanted steers (Figure 2).
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). However, IGFBP-3 mRNA levels in the longissimus muscles of nonimplanted steers were 77% higher (P < 0.01) on d 26 than on d 0 (Figure 3). Similarly, IGFBP-3 mRNA levels in the longissimus muscles of implanted steers were 141% higher (P < 0.0003) on d 26 than on d 0 (Figure 3). These data show that longissimus muscle IGFBP-3 mRNA levels increased in both nonimplanted and implanted steers during the 26-d study.
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). However, myostatin mRNA levels in the longissimus muscles of nonimplanted steers were 96% higher (P < 0.05) on d 26 than on d 0 (Figure 4). Similarly, myostatin mRNA levels in the longissimus muscles of implanted steers were 153% higher (P < 0.0005) on d 26 than on d 0 (Figure 4). As was the case for IGFBP-3, these data show that longissimus muscle myostatin mRNA levels were increased in both nonimplanted and implanted steers on d 26.
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). Hepatocyte growth factor mRNA levels in the longissimus muscles of implanted steers were 68% higher (P < 0.02) on d 26 than on d 0 (Figure 4
). Hepatocyte growth factor mRNA levels in the longissimus muscles of nonimplanted steers were 46% higher (P < 0.08) on d 26 than on d 0 (Figure 5). Although HGF mRNA levels in nonimplanted steers on d 26 are not significantly different from levels on d 0, there was a strong tendency suggesting an increased level on d 26.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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). The mechanism involved in this increase in muscle deposition is not known; however, it is well established that myofiber nuclei increase with age due to DNA accretion via satellite cell proliferation and incorporation of their nuclei into existing muscle fibers (Moss and Leblond, 1971; Swatland, 1977; Campion, 1984). Our previous studies have strongly suggested that locally produced IGF-I may play a role in maintaining satellite cells in a proliferative state, thus supporting increased rate and efficiency of muscle deposition (Johnson et al., 1998a). This hypothesis is supported by our observations that, by d 30 after implantation, steady-state levels of IGF-I mRNA in the longissimus and semimembranosus muscles are elevated and the number of actively proliferating satellite cells in the semimembranosus muscle is increased (White et al., 2003; Johnson et al., 1998b). Additionally, IGF-I levels are reportedly increased in the diaphragm muscle of nandrolone-treated rats (Lewis et al., 2002). Because virally induced overexpression of IGF-I in muscle tissue resulted in a 15% increase in muscle mass in young adult mice (Barton-Davis et al., 1998) and IGF-I extended the replicative life-span of satellite cells (Barton-Davis et al., 1999; Chakravarthy et al., 2000), increased production of IGF-I in muscle could be responsible for steroid-induced muscle growth in feedlot cattle. However, the timing of this increase relative to increases in circulating steroid levels and increased muscle deposition is crucial. Both estradiol and trenbolone acetate levels are elevated by d 2 after steroid implantation (Johnson et al., 1996). Moreover, our previous studies have shown that the steroid-induced enhancement of muscle deposition is greatest during the first 40 d of implantation (Johnson et al., 1996). Thus, in order for IGF-I to cause the enhanced muscle growth observed in implanted steers, muscle IGF-I mRNA levels must increase relatively soon after circulating steroid levels and remain elevated during the 30- to 40-d time period when steroid-induced muscle deposition is greatest. Although we have previously reported that muscle IGF-I mRNA is elevated in steers implanted for 32 to 36 d with a combined estradiol and trenbolone acetate implant (Johnson et al., 1998b), nothing is currently known about the timing of increases in muscle IGF-I mRNA levels after implantation. In the current study, we have used a muscle biopsy technique in conjunction with real-time PCR and repeated measures analysis to examine the time course of changes in muscle IGF-I mRNA in the longissimus muscles of nonimplanted and implanted steers on d 0, 7, 12, and 26 after implantation. Analyses were done on d 7 and 12 to establish when muscle IGF-I mRNA increases relative to the day of implantation, and d 26 was chosen for comparison to our previous data showing that IGF-I mRNA was elevated on d 32 to 36 after implantation. Use of the biopsy procedure to obtain multiple muscle samples from the same steers at various times after implantation greatly reduces variation and enhances our ability to detect treatment-induced changes in muscle mRNA levels as well as changes in mRNA levels due to an increase days on feed.
Longissimus muscle IGF-I mRNA levels were significantly elevated after only 7 d of implantation and continued to increase throughout the duration of the study, reaching a maximum on d 26. The data on d 26 are consistent with our previous results demonstrating increased levels of IGF mRNA in the longissimus and semimembranosus muscles of steers implanted with Revalor-S for approximately 30 d (Johnson et al., 1998b; White et al., 2003). Feed efficiency, rate of gain, and circulating IGF-I concentration were significantly increased by Revalor-S implantation. These data are consistent with those previously reported in similar studies and verify the efficacy of the implant in the current study. Even though feed efficiency and rate of gain were increased 34 and 36%, respectively, in implanted steers, DM intake was not increased significantly in steers receiving the implant as compared to nonimplanted steers (Johnson et al., 1996). Thus, consistent with previous studies (White et al., 2003), the Revalor-S-induced increase in circulating IGF-I level was not a consequence of increased intake.
The nonsignificant difference between the muscle IGF-I mRNA levels in the nonimplanted and implanted groups on d 0 reflects the animal-to-animal variation that might be expected with a biological measurement made on a relatively small number of animals. The strength of utilizing repeated measures analysis of biopsy samples taken from the same animals at different times is that each animal serves as its own control, thus, greatly reducing the effects of these unavoidable animal-to-animal variations.
The fact that IGF-I mRNA levels do not change in the nonimplanted group establishes that the biopsy procedure does not result in increased muscle IGF-I mRNA levels. Additionally, it should be noted that the d-0 and -7 biopsies were taken from separate longissimus muscles (opposite sides), and IGF-I mRNA levels are increased on d 7 as compared to d 0 in treated animals. Based on these observations, we are confident that the biopsy procedure itself does not cause the increased IGF-I mRNA levels observed in this study.
The rapid elevation of muscle IGF-I mRNA levels after implantation is very significant in view of a recent report that virally induced overexpression of IGF-I in the muscle tissue of mice resulted in a 15% increase in muscle mass in young adult mice and maintenance of muscle mass in old mice that would otherwise be losing muscle mass (Barton-Davis et al., 1998). These workers hypothesized that increased muscle growth resulted from increased activation and proliferation of satellite cells in muscles that are producing higher levels of IGF-I. This hypothesis is supported by a recent report that overexpression of IGF-I in muscle tissue increases the proliferative capacity of satellite cells (Chakravarthy et al., 2000). Additionally, it is consistent with our data showing that the number of actively proliferating satellite cells that can be isolated from the semimembranosus muscle is greater in steroid-implanted steers than in nonimplanted controls (Johnson et al., 1998a). Other workers also have suggested that IGF-I acts in an autocrine and/or paracrine manner to enhance muscle growth (Grant et al., 1991; Jennische and Matejka, 1992; Brameld et al., 1996).
The mechanism by which Revalor-S increases muscle IGF-I mRNA is not clear at present. Based on our current knowledge of how IGF-I levels are regulated, it is reasonable to speculate that Revalor-S-induced changes in growth hormone levels or growth hormone receptor levels/affinities may be responsible for the increased muscle IGF-I mRNA (Breier et al., 1998). Growth hormone has been shown to play a major role in regulating serum IGF-I levels. Additionally, growth hormone treatment of pigs raises the level of IGF-I mRNA in the liver and semimembranosus muscle but not in the longissimus muscle (Grant et al., 1991; Grant et al., 1993; Brameld et al., 1996). However, because growth hormone levels are reportedly not increased by Revalor-S treatment of steers (Hunt et al., 1991; Hongerholt et al., 1992; Hayden et al., 1992), it appears unlikely that alterations in growth hormone levels are responsible for Revalor-S-induced increases in muscle IGF-I mRNA level. This does not preclude the possibility that Revalor-S alters the number and/or affinity of growth hormone receptors in liver and muscle tissues. These alterations could enhance the responsiveness of liver and muscle to growth hormone. However, the fact that growth hormone levels are not increased by Revalor-S implantation also raises the possibility that Revalor-S may increase muscle IGF-I mRNA level via a mechanism that does not involve growth hormone. Since muscle tissue has been shown to contain both estrogen and androgen receptors, it also is possible that the estradiol and trenbolone acetate act via these specific receptors to directly affect IGF-I mRNA level.
Myostatin is a member of the transforming growth factor-ß superfamily and has been shown to suppress muscle growth in mice (McPherron et al., 1977). Additionally, mutations in the myostatin gene are responsible for the double muscling phenomenon observed in beef cattle (Grobet et al., 1997). Recent reports indicate that the level of myostatin protein and/or mRNA is altered in muscle tissue undergoing hypertrophy (Ivey et al., 2000; Sakuma et al., 2000; Zhu et al., 2000), repair (Kirk et al., 2000), or atrophy (Carlson et al., 1999). These results led us to speculate that myostatin mRNA levels might be altered (decreased) by Revalor-S implantation, thus allowing increased proliferation of muscle satellite cells. Although results of our previous studies showed that after 32 to 38 d of implantation the myostatin mRNA levels in the semimembranosus muscles of implanted steers were not significantly different than those in the semimembranosus muscles of nonimplanted steers (White et al., 2003), these studies left open the possibility that myostatin mRNA levels were elevated before 32 d after implantation. The current study shows that longissimus muscle myostatin mRNA levels were not affected on d 7, 12, or 26 after implantation. These data raise doubts as to the involvement of myostatin in Revalor-S-induced enhancement of muscle growth. However, even though we did not observe an implant-induced change in myostatin mRNA, this does not rule out a potential change in processed myostatin. In fact, a recent report showed no difference in myostatin mRNA between male and female mouse skeletal muscle but did show reduced processed myostatin levels in muscle from male mice, suggesting a potential explanation for sexual dimorphic growth (McMahon et al., 2003). Longissimus muscle myostatin mRNA levels of both nonimplanted and implanted steers were increased on d 26. These data suggest that muscle myostatin mRNA levels may increase during muscle development. Although the reason for this increase is not clear, it is possible that increasing myostatin levels could play a role in inducing satellite cells to enter the quiescent state in which they are most frequently found in mature muscle. Because the d-0 and -12 biopsies were taken from one longissimus muscle and the d-7 and -26 biopsies were taken from the contralateral longissimus, it is possible that taking multiple biopsy samples from the same longissimus muscle resulted in increased myostatin mRNA levels in the d-26 sample. However, we do not believe this is likely because no increase in myostatin mRNA is observed on d 12, and this biopsy was taken from the same longissimus muscle as the d-0 sample. Additionally, IGF-I mRNA levels did not increase on d 26 or any other day in control animals.
We have shown previously that a greater number of actively proliferating satellite cells can be isolated from the semimembranosus muscles of implanted steers than from the corresponding muscles of nonimplanted steers (Johnson et al., 1998a). The greater yield of proliferating satellite cells could result from increased activation of quiescent satellite cells or from maintaining satellite cells in an actively proliferating state. Because HGF has been reported to be a crucial element in activation of quiescent satellite cells (Allen et al., 1995; Tatsumi et al., 1998; Sheehan et al., 2000), the semimembranosus muscles of Revalor-S-implanted steers could be interpreted to mean that activation of quiescent cells does not play a significant role in the Revalor-S-induced increase in proliferating satellite cells. However, several factors need to be considered before drawing this conclusion. Our previous study measured HGF mRNA after 32 to 38 d of implantation. Consequently, it was possible that transient elevations in HGF mRNA and protein levels that were sufficient to activate quiescent satellite cells had already occurred by this time. However, the current study showing that muscle HGF mRNA was not affected on d 7, 12, or 26 after implantation strongly suggests that HGF mRNA is not affected by implantation. It is important to note that the current studies do not rule out the possibility that HGF levels are increased by releasing HGF that is stored in muscle tissue or by increasing the translation rate of HGF mRNA. Neither of these alternatives would require increases in HGF mRNA levels. Consequently, although our previous and current results raise questions as to the role of increased HGF and satellite cell activation in the Revalor-S-induced increase in actively proliferating satellite cells in the semimembranosus muscle, these results do not unequivocally eliminate activation of quiescent satellite cells as a mechanism. Our current study also shows that muscle HGF mRNA levels are slightly increased in both nonimplanted and implanted steers by d 26 of the study. The biological effect of this increase is not clear from the current data. We do not believe this increase is related to multiple biopsies from the same longissimus muscle for the reasons already discussed in detail for myostatin and IGF-I.
Longissimus muscle IGFBP-3 levels were not affected by implantation at any time point examined in the current study. This result is consistent with previous studies showing that muscle IGFBP-3 mRNA levels in implanted steers were not different from those in nonimplanted steers after 32 to 38 d of implantation (White et al., 2003). Consequently, it appears unlikely that changes in muscle IGFBP-3 levels play a role in Revalor-S-induced enhancement of muscle growth. As was the case for myostatin and HGF mRNA levels, muscle IGFBP-3 mRNA levels were increased in both nonimplanted and implanted steers by d 26 of the study. The reason for this increase and its biological significance are not clear. However, because IGFBP-3 affects the bioactivity of IGF-I and exhibits IGF-I–independent effects on myogenic cell proliferation (Pampusch et al., 2003), this apparent age-related increase in muscle IGFBP-3 mRNA should be further investigated. As with the other growth factor mRNA measured in this study, we do not believe the increase in IGFBP-3 mRNA on d 26 is related to the frequency of biopsy for the reasons described in detail previously in this discussion.
Based on the above findings, we believe that the increased IGF-I level in muscle of implanted steers acts in an autocrine and/or paracrine manner to stimulate muscle growth. Based on our previous studies and those of others, it is likely that one way in which elevated muscle IGF-I levels stimulate muscle growth is by increasing satellite cell proliferation, thus maintaining a higher number of proliferating satellite cells in the muscles of implanted steers than in the muscles of nonimplanted steers. This would prolong the period of rapid muscle growth resulting in the observed increased rate and efficiency of muscle deposition in implanted steers.
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Implications |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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Footnotes |
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2 This research was funded in part by National Research Initiative Competitive Grant No. 99-35206-7935 from the USDA Cooperative State Research, Education, and Extension Service.
3 Kansas Agric. Exp. Stn. #03-352-J.
4 Correspondence: 348 ABLMS, 1334 Eckles Ave. (phone: 612-624-2234; fax: 612-624-3677; E-mail: wdayton{at}umn.edu).
Received for publication April 16, 2003. Accepted for publication July 23, 2003.
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Literature Cited |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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-actin mRNA and insulin-like growth factor I mRNA in pigs during feeding and withdrawal of ractopamine. J. Anim. Sci. 71:3319–3326.[Abstract]
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