Insulin-Like Growth Factor-1 Levels in Term Newborns with Hypoxic–Ischemic Encephalopathy

Umran, Raid M R; Al-Tahir, Mahir; Jagdish, Desai; Chouthai, Nitin

doi:10.1055/s-0036-1571319

Cited by 12 publications

(4 citation statements)

References 26 publications

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“…The former pathway is induced early after infection where NF- κβ dissociates from its inhibitory protein (I κβ ) and translocates to the nucleus [ 28 – 30 , 106 ]. The noncanonical NF- κβ pathway involves lymphopoiesis and differentiation of immune cells [ 106 , 107 ] that seems to be in accordance with the recruits of T cells speculated precisely around the microvasculatures of the amygdala in the present work. Accordingly, chronic toxoplasmosis seems to be vitally regulated by the TNF- α /NF- κβ pathway.…”

Section: Discussionsupporting

confidence: 85%

“…Existence of the cyst-forming ME-49 T. gondii strain of the parasite was associated with IGF-1R hypoexpression in the cerebral cells especially in the amygdala. However, these low expressive patterns deprive the host cell-parasite microenvironment from (1) the modulatory and antifibrotic effects of the IGF-1 [ 105 ], (2) the protective role of IGF-1 against the inflammatory oxidative damage [ 106 ] and the hypoxic and ischemic insults [ 107 ], (3) the regeneration of the brain cells [ 60 ], (4) the normal glucose metabolism [ 58 , 59 ], (5) the protection against alterations in the hormonal axis of the hypothalamus-pituitary-adrenal gland and the circulating cortisol/dehydroepiandrosterone sulfate ratios [ 108 ], and (6) the guard against atherogenicity of the blood vessels [ 109 ]. Accordingly, this might explain the observed incidence of dementia with toxoplasmosis in prior studies [ 6 , 110 ].…”

Section: Discussionmentioning

confidence: 99%

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CanToxoplasma gondiiPave the Road for Dementia?

Saftawy

Amin

Sabry

et al. 2020

Journal of Parasitology Research

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Dementia is an ominous neurological disease. Scientists proposed a link between its occurrence and the presence of Toxoplasma gondii (T. gondii). The long-term sequels of anti-Toxoplasma premunition, chiefly dominated by TNF-α, on the neurons and their receptors as the insulin-like growth factor-1 receptor (IGF-1R), which is tangled in cognition and synaptic plasticity, are still not clear. IGF-1R mediates its action via IGF-1, and its depletion is incorporated in the pathogenesis of dementia. The activated TNF-α signaling pathway induces NF-κβ that may induce or inhibit neurogenesis. This study speculates the potential impact of anti-Toxoplasma immune response on the expression of IGF-1R in chronic cerebral toxoplasmosis. The distributive pattern of T. gondii cysts was studied in association with TNF-α serum levels, the in situ expression of NF-κβ, and IGF-1R in mice using the low virulent ME-49 T. gondii strain. There was an elevation of the TNF-α serum level (p value ≤ 0.004) and significant upsurge in NF-κβ whereas IGF-1R was of low abundance (p value < 0.05) compared to the controls. TNF-α had a strong positive correlation with the intracerebral expression of NF-κβ (r value ≈ 0.943, p value ≈ 0.005) and a strong negative correlation to IGF-1R (r value -0.584 and -0.725 for area% and O.D., respectively). This activated TNF-α/NF-κβ keeps T. gondii under control at the expense of IGF-1R expression, depriving neurons of the effect of IGF-1, the receptor’s ligand. We therefore deduce that T. gondii immunopathological reaction may be a road paver for developing dementia.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

CanToxoplasma gondiiPave the Road for Dementia?

Saftawy

Amin

Sabry

et al. 2020

Journal of Parasitology Research

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“…Since the neonatal period coincidences with the most active processes of gliogenesis, oligodendrocyte survival and differentiation, as well as myelination of the newly derived neurons, the insufficient amounts of endogenous trophic factors, including IGF-1, might unfortunately efficiently contribute to the resulting myelin deficiency, or/ and malformation of the white matter tracts [56][57][58][59]. The recent clinical studies confirmed that the IGF-1 level in serum is significantly decreased in newborns with hypoxic-ischemic encephalopathy [60]. A number of preclinical studies have been performed based on IGF-1 systemic administration in order to at least partially alleviate deleterious effects of the experienced birth asphyxia.…”

Section: Discussionmentioning

confidence: 99%

Oligodendrocyte Response to Pathophysiological Conditions Triggered by Episode of Perinatal Hypoxia-Ischemia: Role of IGF-1 Secretion by Glial Cells

et al. 2020

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Differentiation of oligodendrocyte progenitors towards myelinating cells is influenced by a plethora of exogenous instructive signals. Insulin-like growth factor 1 (IGF-1) is one of the major factors regulating cell survival, proliferation, and maturation. Recently, there is an ever growing recognition concerning the role of autocrine/paracrine IGF-1 signaling in brain development and metabolism. Since oligodendrocyte functioning is altered after the neonatal hypoxic-ischemic (HI) insult, a question arises if the injury exerts any influence on the IGF-1 secreted by neural cells and how possibly the change in IGF-1 concentration affects oligodendrocyte growth. To quantify the secretory activity of neonatal glial cells, the step-wise approach by sequentially using the in vivo, ex vivo, and in vitro models of perinatal asphyxia was applied. A comparison of the results of in vivo and ex vivo studies allowed evaluating the role of autocrine/paracrine IGF-1 signaling. Accordingly, astroglia were indicated to be the main local source of IGF-1 in the developing brain, and the factor secretion was shown to be significantly upregulated during the first 24 h after the hypoxic-ischemic insult. And conversely, the IGF-1 amounts released by oligodendrocytes and microglia significantly decreased. A morphometric examination of oligodendrocyte differentiation by means of the Sholl analysis showed that the treatment with low IGF-1 doses markedly improved the branching of oligodendroglial cell processes and, in this way, promoted their differentiation. The changes in the IGF-1 amounts in the nervous tissue after HI might contribute to the resulting white matter disorders, observed in newborn children who experienced perinatal asphyxia. Pharmacological modulation of IGF-1 secretion by neural cells could be reasonable solution in studies aimed at searching for therapies alleviating the consequences of perinatal asphyxia.

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“…A prospective clinical study of newborns found that compared with the control group, the level of IGF‐1 was measured within 6 hours after birth, or the level of IGF‐1 was measured again on the 3rd day in the hypoxic‐ischemic encephalopathy (HIE) group and the control group. The results showed that the level of serum IGF‐1 in the hypoxic ischemic encephalopathy group was significantly lower than that in the control group (Umran RM, et al, 2016). These are the changes of IGF‐1 after neonatal cerebral ischemia and the decrease of IGF‐1 after adult cerebral ischemia.…”

Section: Changes Of Igf‐1 Expression After Cerebral Ischemiamentioning

confidence: 98%

Research progress of IGF‐1 and cerebral ischemia

Zhou

et al. 2021

Ibrain

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Cerebral ischemic disease is a group of diseases that cause insufficient blood supply to the cerebrum, cerebellum or brain stem for different reasons, resulting in corresponding nervous system symptoms. Cardiovascular disease is the leading cause of death in the world. Among them, the death caused by cerebral ischemia accounts for the vast majority, and it is one of the fatal diseases in the middle‐aged and elderly at present. Epidemiologic studies have projected increasing mortality due to cardiovascular disease worldwide (about 23.3 million people by 2030) because of the aging population. However, related studies have shown that insulin‐like growth factor I (IGF‐1) is a multifunctional cell proliferation regulator. It plays an important role in cerebral ischemia. It is effective in promoting cell differentiation, proliferation and individual development. Studies have shown that IGF‐1 signaling pathway is a key pathway controlling cell growth and survival. There may be five mechanisms in cerebral ischemia: prevention of intracellular calcium overload, inhibition of the upregulation of nNOS, IGF‐1upregulations activating HIF‐1α, regulation of Bcl‐2 to resist apoptosis, and enhancement of vascular endothelial function. Three critical nodes in the IGF‐1 signaling pathway have been described in cardiomyocytes: protein kinase Akt/mammalian target of rapamycin (mTOR), Ras/Raf/extracellular signal‐regulated kinase (ERK), and phospholipase C (PLC)/inositol 1,4,5‐triphosphate (InsP3)/Ca2+. IGF‐1 plays an important role in cerebral ischemia and myocardial ischemia, mainly by activating downstream of IGF‐1, controlling cell death and differentiation or transcription work, improving the function of heart muscle cells, reducing the myocardial cell apoptosis induced by myocardial infarction, regulating endogenous protection and restoration of cerebral ischemia injury, thus protecting cerebral and myocardial injury. Related studies have shown that bcl‐2 exerts great influence on both cerebral ischemia and myocardial ischemia. Therefore, the relevant pathways and targets of cerebral ischemia and myocardial ischemia and the role of IGF‐1 in protecting the heart are reviewed in this paper.

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Insulin-Like Growth Factor-1 Levels in Term Newborns with Hypoxic–Ischemic Encephalopathy

Cited by 12 publications

References 26 publications

CanToxoplasma gondiiPave the Road for Dementia?

CanToxoplasma gondiiPave the Road for Dementia?

Oligodendrocyte Response to Pathophysiological Conditions Triggered by Episode of Perinatal Hypoxia-Ischemia: Role of IGF-1 Secretion by Glial Cells

Research progress of IGF‐1 and cerebral ischemia

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