Endocrine Involvement in Developmental Syndromes (Endocrine by Marco Cappa, Mohamad Maghnie, Sandro Loche, Gian Franco

By Marco Cappa, Mohamad Maghnie, Sandro Loche, Gian Franco Bottazzo

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According to Arima et al. [21], the assumed regulation of CDKN1C by PLAGL1/ZAC indicates a potential role of this gene in BWS but they did not detect aberrant methylation at the PLAGL1/ZAC DMR in a small number of BWS patients. Indeed they observed changes in the methylation of the ICR2 in two patients with transient neonatal diabetes mellitus (TNDM) and 6q24 disturbances. Genotype-Phenotype Correlation in SRS? With the identification of the ICR1 hypomethylation in 11p15 and UPD(7)mat the molecular confirmation of the clinical diagnosis of SRS is now possible in ~50% of patients (table 1).

The IGF-1 isoform used (cIGF-1) differed from the mIGF-1 transgene only in a variant C-terminal peptide, which was presumably responsible for the dramatic phenotypic differences of cIGF-1 mice. These animals did not display pronounced muscle hypertrophy but had increased levels of circulating IGF-1, mild cardiac hypertrophy, an increased incidence of late onset neoplasia [unpubl. ]. Thus, the choice of isoform is critical to the design of gene therapeutic strategies employing IGF-1. The increased muscle mass in mIGF-1 transgenic mice was associated with augmented force generation compared to age-matched wild-type littermates.

It is not known whether in MLC/mIGF-1 transgenic animals, the satellite cells have an increased ability for self-renewal or whether there is an increased recruitment of nonsatellite cells. Our recent experimental evidence indicates that mIGF-1 promotes the two suggested pathways, which can be considered two temporally separated events of the same biological process. IGF-1 Counteracts Muscle Wasting 33 We demonstrated that upon muscle injury, stem cells expressing c-Kit, Sca-1, and CD45 antigens increased locally and the percentage of the recruited cells were conspicuously enhanced by mIGF-1 expression [28].

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