Monoclonal Antibodies to Mechano-Growth Factor

Kravchenko, Irina V.; Furalyov, Vladimir A.; Khotchenkov, V. P.; Popov, Vladimir O.

doi:10.1089/hyb.2006.25.300

Cited by 16 publications

(9 citation statements)

References 24 publications

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“…A synthetic peptide corresponding to the 24 C-terminal amino acids of the Eb E peptide stimulated proliferation and inhibited differentiation of C2C12 cells (Yang and Goldspink, 2002). Because antibodies raised against this sequence have detected proteins larger than the intact Eb peptide or the 24-aa C-terminal fragment (Dluzniewska et al, 2005; Kravchenko et al, 2006; Philippou et al, 2008) and no published reports exist where this IGF-I Eb mRNA product has been identified in, or isolated from, injured tissues in vivo , the identity of the precise form or physiological role of MGF remains elusive.…”

Section: Discussionmentioning

confidence: 99%

Impairment of IGF-I expression and anabolic signaling following ischemia/reperfusion in skeletal muscle of old mice

Hammers

Matheny

Sell

et al. 2011

Experimental Gerontology

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With the advancement of age, skeletal muscle undergoes a progressive decline in mass, function, and regenerative capacity. Previously, our laboratory has reported an age-reduction in recovery and local induction of IGF-I gene expression with age following tourniquet (TK)-induced skeletal muscle ischemia/reperfusion (I/R). In this study, young (6 mo) and old (24-28 mo) mice were subjected to 2 hours of TK-induced ischemia of the hindlimb followed by 1, 3, 5, or 7 days of reperfusion. Real time-PCR analysis revealed clear age-related reductions and temporal alterations in the expression of IGF-I and individual IGF-I Ea and Eb splice variants. ELISA verified a reduction of IGF-I peptide with age following 7 days recovery from TK. Western blotting showed that the phosphorylation of Akt, mTOR, and FoxO3, all indicators of anabolic activity, were reduced in the muscles of old mice. These data indicate an age-related impairment of IGF-I expression and intracellular signaling does exist following injury, and potentially has a role in the impaired recovery of skeletal muscle with age.

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Section: Discussionmentioning

confidence: 99%

Impairment of IGF-I expression and anabolic signaling following ischemia/reperfusion in skeletal muscle of old mice

Hammers

Matheny

Sell

et al. 2011

Experimental Gerontology

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“…In general, the complexity introduced by the transcriptional and splicing variants, posttranscriptional regulation and posttranslational modifications of the IGF1 gene (77), giving rise to various IGF-I isoforms, probably indicate their different biological roles under various conditions or pathologies and following different stimuli (78). The development of epitope-specific antibodies for distinguishing the different IGF-I E-peptides (20,38,(79)(80)(81)(82) can contribute to a more definitive analysis of IGF-I isoforms expression in various tissues and physiological or pathophysiological conditions.…”

Section: Human Igf1 Gene Structure and Alternative Splicingmentioning

confidence: 99%

The Complexity of the IGF1 Gene Splicing, Posttranslational Modification and Bioactivity

Philippou

Maridaki

Pneumaticos

et al. 2014

Mol Med

100

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The insulinlike growth factor-I (IGF-I) is an important factor which regulates a variety of cellular responses in multiple biological systems. The IGF1 gene comprises a highly conserved sequence and contains six exons, which give rise to heterogeneous mRNA transcripts by a combination of multiple transcription initiation sites and alternative splicing. These multiple transcripts code for different precursor IGF-I polypeptides, namely the IGF-IEa, IGF-IEb and IGF-IEc isoforms in humans, which also undergo posttranslational modifications, such as proteolytic processing and glycosylation. IGF-I actions are mediated through its binding to several cell-membrane receptors and the IGF-I domain responsible for the receptor binding is the bioactive mature IGF-I peptide, which is derived after the posttranslational cleavage of the pro-IGF-I isoforms and the removal of their carboxy-terminal E-peptides (that is, the Ea, Eb and Ec). Interestingly, differential biological activities have been reported for the different IGF-I isoforms, or for their E-peptides, implying that IGF-I peptides other than the IGF-I ligand also possess bioactivity and, thus, both common and unique or complementary pathways exist for the IGF-I isoforms to promote biological effects. The multiple peptides derived from IGF-I and the differential expression of its various transcripts in different conditions and pathologies appear to be compatible with the distinct cellular responses observed to the different IGF-I peptides and with the concept of a complex and possibly isoform-specific IGF-I bioactivity. This concept is discussed in the present review, in the context of the broad range of modifications that this growth factor undergoes which might regulate its mechanism(s) of action.

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“…The cells on a 60 mm Petri dish were lysed by pipetting in 0.2 ml PBS containing 0.05% Tween 20 (PBS-T) and a mixture of protease inhibitors (Sigma-Aldrich, USA). The MGF concentration was measured with a sandwich ELISA assay based on monoclonal antibodies as described earlier [21] using an amplification system. Microtiter plates (Corning-Costar, USA) were coated with 8B9 monoclonal antibody solution (10 μg/ml) overnight at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

Potassium chloride released from contracting skeletal muscle may stimulate development of its hypertrophy

Kravchenko

Furalyov

Popov

2019

Biochemistry and Biophysics Reports

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The effects of potassium chloride on the expression of IGF-1 splice forms and myoblast proliferation were investigated. KCl at the concentrations of 7–12 mM stimulated the synthesis of IGF-1 and mechano growth factor (MGF) in murine myoblasts as well as in myotubes both at the mRNA and protein levels. Pan-calcium channel blocker CdCl2 completely abolished stimulation of growth factor expression, whereas blocker of HCN and Nav1.4 channels ZD7288 drastically reduced it. In addition, potassium chloride stimulated myoblast proliferation, while IGF-1 autocrine signaling inhibition partially suppressed these mitogenic effects.

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Monoclonal Antibodies to Mechano-Growth Factor

Cited by 16 publications

References 24 publications

Impairment of IGF-I expression and anabolic signaling following ischemia/reperfusion in skeletal muscle of old mice

Impairment of IGF-I expression and anabolic signaling following ischemia/reperfusion in skeletal muscle of old mice

The Complexity of the IGF1 Gene Splicing, Posttranslational Modification and Bioactivity

Potassium chloride released from contracting skeletal muscle may stimulate development of its hypertrophy

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