The Expression of Insulin-like Growth Factor-I, II and Their Cognate Receptor 1 and 2 during Mouse Tongue Embryonic and Neonatal Development

Yamane, Akira; Mayo, Mark L.; Shuler, C. F.

doi:10.2108/zsj.17.935

Cited by 18 publications

(19 citation statements)

References 47 publications

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“…Insulin-like growth factor is well known to play essential roles in the embryonic development of skeletal muscle, including roles in proliferation, differentiation and synaptogenesis. [21][22][23][24]37 Because, in the hypertrophy of various kinds of skeletal muscles such as the soleus, plantaris and masseter, the expression level of IGF was up-regulated, IGF is thought to function as a potent positive regulator. [6][7][8][9] In the present study, we measured the phosphorylation levels of IGFR and akt-1, a signaling component of IGF, and did not measure the expression of IGF because the action of IGFs in skeletal muscles is regulated and altered with IGF binding proteins (IGFBPs) outside the myofibers.…”

Section: Discussionmentioning

confidence: 99%

“…Insulin-like growth factors (IGF) are well known to play essential roles in the development, regeneration and adaptation of skeletal muscles. [19][20][21][22][23][24][25][26][27] The signal of IGF in skeletal muscles is mediated via IGF receptor 1 (IGFR1) and signaling components such as akt1 and FoxO3. 28 The signal is regulated and altered with IGF binding proteins (IGFBPs) outside of the myofibers.…”

Section: Introductionmentioning

confidence: 99%

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IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β₂‐adrenergic agonist

Abo

Iida

Kaneko

et al. 2012

Cell Biochemistry & Function

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Clenbuterol, a β₂-adrenergic agonist, increases the hypertrophy of skeletal muscle. Insulin-like growth factor (IGF) is reported to work as a potent positive regulator in the clenbuterol-induced hypertrophy of skeletal muscles. However, the precise regulatory mechanism for the hypertrophy of skeletal muscle induced by clenbuterol is unknown. Myostatin, a member of the TGFβ super family, is a negative regulator of muscle growth. The aim of the present study is to elucidate the function of myostatin and IGF in the hypertrophy of rat masseter muscle induced by clenbuterol. To investigate the function of myostatin and IGF in regulatory mechanism for the clenbuterol-induced hypertrophy of skeletal muscles, we analysed the expression of myostatin and phosphorylation levels of myostatin and IGF signaling components in the masseter muscle of rat to which clenbuterol was orally administered for 21 days. Hypertrophy of the rat masseter muscle was induced between 3 and 14 days of oral administration of clenbuterol and was terminated at 21 days. The expression of myostatin and the phosphorylation of smad2/3 were elevated at 21 days. The phosphorylation of IGF receptor 1 (IGFR1) and akt1 was elevated at 3 and 7 days. These results suggest that myostatin functions as a negative regulator in the later stages in the hypertrophy of rat masseter muscle induced by clenbuterol, whereas IGF works as a positive regulator in the earlier stages.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β₂‐adrenergic agonist

Abo

Iida

Kaneko

et al. 2012

Cell Biochemistry & Function

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“…The logarithmic value of the fluorescence intensity ratio was used to calculate the amount of endogenous target mRNA on the basis of the line formula derived from a standard curve for each target gene. The standard curve was generated as described previously (18,35). Figure 1B shows the standard curve for m-cadherin calculated using the image analysis data of electrophoretic bands shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

Satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice

Yamane¹,

Akutsu²,

Diekwisch³

et al. 2005

American Journal of Physiology-Cell Physiology

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Yamane, Akira, Satonari Akutsu, Thomas G. H. Diekwisch, and Ryoichi Matsuda. Satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice. Am J Physiol Cell Physiol 289: C42-C48, 2005. First published February 9, 2005 doi:10.1152/ajpcell.00577.2004.-To determine whether muscle satellite cells and utrophin are correlated with the degree of damage in mdx skeletal muscles, we measured the area of the degenerative region as an indicator of myofiber degeneration in the masseter, gastrocnemius, soleus, and diaphragm muscles of mdx mice. Furthermore, we analyzed the expression levels of the paired box homeotic gene 7 (pax7), m-cadherin (the makers of muscle satellite cells), and utrophin mRNA. We also investigated the immunolocalization of m-cadherin and utrophin proteins in the muscles of normal C57BL/10J (B10) and mdx mice. The expression level of pax7 mRNA and the percentage of m-cadherin-positive cells among the total number of cell nuclei in the muscle tissues in all four muscles studied were greater in the mdx mice than in the B10 mice. However, there was no significant correlation between muscle damage and expression level for pax7 mRNA (R ϭ Ϫ0.140), nor was there a correlation between muscle damage and the percentage of satellite cells among the total number of cell nuclei (R ϭ Ϫ0.411) in the mdx mice. The expression level of utrophin mRNA and the intensity of immunostaining for utrophin in all four muscles studied were greater in the mdx mice than in the B10 mice. However, there also was not a significant correlation between muscle damage and expression level of utrophin mRNA (R ϭ 0.231) in the mdx mice, although upregulated utrophin was incorporated into the sarcolemma. These results suggest that satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice. dystrophy; pax7; m-cadherin; dystrophin-related proteins THE X CHROMOSOME-LINKED MUSCULAR dystrophic mdx mouse lacks the sarcolemmal protein dystrophin and represents a genetic homolog of human Duchenne muscular dystrophy. Dystrophin is a 427-kDa cytoskeletal protein that is expressed in the sarcolemma (the membrane structure of the myofiber) and contributes to the stability of the sarcolemma. Lack of dystrophin causes myofiber degeneration caused by membrane damage, Ca 2ϩ overuptake by muscle cells, muscle overcontraction, and activation of intracellular proteinase (2, 8). The damage to myofibers varies among the muscles of the mdx mouse; the mdx diaphragm muscle is damaged more severely by dystrophy than are the other muscles (10, 27), whereas craniofacial muscles such as the masseter and extraocular muscles are less damaged (16,20). However, the mechanism underlying differences in the degree of myofiber damage among mdx skeletal muscles is unclear.Muscle satellite cells are mononucleated, quiescent stem cells that reside between the sarcolemma and the basal lamina of adult myofibers (4, 13). In response to stimuli such as mechanical loading, unloading, d...

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“…Total RNA extraction, reverse transcription, and competitive-PCR amplification were performed as previously described (Yamane et al ., 2000b, c). Briefly, total RNA extraction was performed according to the manufacturer's specifications (Rapid total RNA isolation kit, 5 Prime → 3 Prime Inc., Boulder, CO, USA).…”

Section: Rna Extraction Reverse Transcription and Competitive-polymmentioning

confidence: 99%

Changes in mRNA Expression of Nicotinic Acetylcholine Receptor Subunits during Embryonic Development of Mouse Masseter Muscle

Yamane¹,

Saito

Nakagawa

et al. 2002

Zoological Science

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The Expression of Insulin-like Growth Factor-I, II and Their Cognate Receptor 1 and 2 during Mouse Tongue Embryonic and Neonatal Development

Cited by 18 publications

References 47 publications

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β₂‐adrenergic agonist

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β₂‐adrenergic agonist

Satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice

Changes in mRNA Expression of Nicotinic Acetylcholine Receptor Subunits during Embryonic Development of Mouse Masseter Muscle

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The Expression of Insulin-like Growth Factor-I, II and Their Cognate Receptor 1 and 2 during Mouse Tongue Embryonic and Neonatal Development

Cited by 18 publications

References 47 publications

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β2‐adrenergic agonist

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β2‐adrenergic agonist

Satellite cells and utrophin are not directly correlated with the degree of skeletal muscle damage in mdx mice

Changes in mRNA Expression of Nicotinic Acetylcholine Receptor Subunits during Embryonic Development of Mouse Masseter Muscle

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IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β₂‐adrenergic agonist

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a β₂‐adrenergic agonist