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Changes in the expression of insulin‐like growth factor 1 variants in the postnatal brain development and in neonatal hypoxia–ischaemia
Author(s) -
Beręsewicz Małgorzata,
Majewska Monika,
Makarewicz Dorota,
Vayro Steven,
Zabłocka Barbara,
Górecki Dariusz C.
Publication year - 2010
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2009.09.002
Subject(s) - hypoxia (environmental) , ischemia , medicine , insulin , neuroscience , endocrinology , biology , chemistry , oxygen , organic chemistry
Insulin‐like growth factor‐1 (IGF‐1) is a multifunctional peptide of which numerous isoforms exist. The predominant form, IGF‐1Ea is involved in physiological processes while IGF‐1Ec (mechano‐growth factor, MGF) is expressed in response to a different set of stimuli. We have identified specific changes in the expression patterns of these IGF‐1 variants in brain development in normal rats and following neonatal hypoxia–ischaemia (HI). Both IGF‐1Ea and IGF‐1Ec are expressed during normal postnatal brain development, albeit with highly specific temporal distributions. In contrast, HI produced increased and prolonged expression of the IGF‐1Ec isoform only. Importantly, hypoxia alone stimulated the expression of IGF‐1Ec as well. Thus, IGF‐1Ec may play a role in HI pathology. Neonatal hypoxia–ischaemia occurs in approximately 1:4000–1:10,000 newborns and causes neurological deficits in ∼75% of those affected. Unfortunately, no specific treatment is available. IGF‐1 is known to have neuroprotective activity and its IGF‐1Ec variant appears to be an endogenous protective factor in hypoxia–ischaemia. Therefore, IGF‐1Ec could potentially be developed into a therapeutic modality for the attenuation or prevention of neuronal damage in this and related disorders.