IGF-1 Protects Neurons in the Cortex and Subventricular Zone in a Periventricular Leucomalacia Model

Kim, Dong Joon; Cho, Suyeon; Kim, Seung-Un; Jo, Dong-Won; Hwang, Hyo-In; Shin, Hye-Kyoung; Jun, Yonghyun

doi:10.21873/invivo.12260

Cited by 4 publications

(4 citation statements)

References 33 publications

(33 reference statements)

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“…The several studies of chronic cerebral hypoperfusion on experimental models have shown the beneficial role of IGF-1 in neuroprotective effects. In rats with right carotid artery ligation and hypoxic exposure, administration of exogenous IGF-1 reduced the manifestations of periventricular leukomalacia, increased the number of surviving mature neurons in the cerebral cortex (Kim et al, 2021). When reproducing bilateral carotid artery stenosis in mice, white matter injury, an increase in IGF-1 expression, and the involvement of the LMP7 immunoproteasome in the regulation of TGFβ/Smad-mediated neuroinflammation, oligodendrocyte remyelination and cognitive impairment were demonstrated (Chen et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

“…IGF-1 has been shown to be involved in neuroprotection in brain ischemic stroke, cerebral trauma, Alzheimer's disease, amyotrophic lateral sclerosis, epilepsy, neurological dysfunctions, and, in vessels, can prevent atherosclerotic lesions (Bianchi et al, 2017;Lu et al, 2020;Bhalla et al, 2022;Ge et al, 2022;Wang et al, 2022;Sukhanov et al, 2023). However, the role of IGF-1 and its receptors in chronic cerebral hypoperfusion has been investigated only in a few works (Youssef et al, 2020;Chen et al, 2021;Kim et al, 2021) and needs clarification.…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of SIRT1, SIRT3, and IGF-1 in ApoE-deficient mice exacerbates neuronal damage induced by chronic cerebral hypoperfusion

Harmatina,

Rozova,

Voznesenska

et al. 2023

Regul. Mech. Biosyst.

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Chronic cerebral hypoperfusion is a widespread pathological condition caused by chronically reduced cerebral blood flow leading to brain damage, but the specific molecular mechanisms that regulate these phenomena remain poorly understood. In this study, we investigated brain damage and neuronal DNA injury in a vulnerable region of the brain, the hippocampus, as well as the involvement of apolipoprotein E (ApoE), sirtuins of 1 (SIRT1) and 3 (SIRT3) types and insulin-like growth factor 1 (IGF-1) in pathogenetic mechanisms in mice with chronic cerebral hypoperfusion caused by the permanent occlusion of the left unilateral common carotid artery. Male C57/6j (C57, wild type) and ApoE(-/-) mice were divided into four experimental groups (10 mice per group): sham-operated С57, С57 with chronic cerebral hypoperfusion, sham-operated ApoE(-/-) mice, ApoE(-/-) mice with chronic cerebral hypoperfusion. Our results showed that the number of damaged neurons in the hippocampus at 8 weeks after surgical manipulation increased in both groups of mice with chronic cerebral hypoperfusion, with more pronounced rates in ApoE(-/-) mice than in C57 mice. However, ApoE deficiency in moderate chronic cerebral hypoperfusion was accompanied by a higher level of undamaged DNA (class 0) and a low level of maximally damaged DNA (class 4) in brain cell nuclei in contrast to group C57. In ApoE-deficient mice, reduced expression of SIRT1, SIRT3, and IGF-1 was found. In chronic cerebral hypoperfusion, expression of sirtuins was preserved, but IGF-1 expression was significantly reduced in ApoE(-/-) mice in comparison to C57. The obtained results indicate that ApoE deficiency leads to downregulation of SIRT1, SIRT3 and IGF-1 in the brain; this lack of cytoprotection is enhanced in chronic cerebral hypoperfusion and may participate in the mechanisms of neuronal damage.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Downregulation of SIRT1, SIRT3, and IGF-1 in ApoE-deficient mice exacerbates neuronal damage induced by chronic cerebral hypoperfusion

Harmatina,

Rozova,

Voznesenska

et al. 2023

Regul. Mech. Biosyst.

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“…Therefore, newborns with low serum IGF-1 levels after birth may be predisposed to ROP and may require treatment. It has also been reported that low serum IGF-1 levels were strongly associated with various neonatal complications in animal models (periventricular leukomalacia model rat; cerebral hypoxic ischemia model rat; primary IGF-1-deficient mice; and a necrotizing enterocolitis model) [ 31 , 32 , 33 , 34 ] and humans (poor weight gain and brain weight, and the development of ROP and bronchopulmonary dysplasia) [ 7 , 9 , 10 , 11 ]. Early IGF-1 supplementation, such as the intravenous supplementation of human recombinant IGF-1 to attain normal serum levels, may reduce these complications and promote growth and development in extremely preterm newborns with/without SGA.…”

Section: Discussionmentioning

confidence: 99%

Percentile-Based Reference Values of Umbilical Cord Blood Insulin-like Growth Factor 1 in Japanese Newborns

Nagano

Katayama

Hara

et al. 2022

JCM

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We aimed to create percentile-based reference values of the umbilical cord blood insulin-like growth factor-1 (IGF-1) levels in Japanese newborns, as these values have not yet been established. A total of 259 newborns were classified into four gestational-age-at-birth (GA) groups: extremely preterm (<28 weeks); early preterm (28–33 weeks); late preterm (34–36 weeks); and term (≥37 weeks). They were further subclassified as small-for-gestational-age (SGA) or non-SGA. The 10th, 25th, 50th, 75th, and 90th percentiles of the umbilical cord blood IGF-1 levels were calculated and compared between the groups by using reference values of 9, 18, 33, 52, and 71 ng/mL, respectively. In the extremely preterm group, the IGF-1 levels were significantly lower than those in the early preterm, late preterm, and term groups (13.5, 24.0, 44.5, and 47.5 ng/mL, respectively; p < 0.001). The umbilical cord blood IGF-1 levels in the SGA newborns were significantly lower than those in the non-SGA newborns in all subgroups. In multivariate analyses, the GA and birth weight standard deviation scores were independent determinant factors for the umbilical cord blood IGF-1 levels. Thus, we established percentile-based reference values of umbilical cord blood IGF-1 in Japanese newborns; these reference values can be applied on the basis of the extent of prematurity and the SGA status.

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“…The location of the injection was 1.0 mm lateral and 1.0 mm posterior to the bregma and at a 3.0 mm depth from the skull surface. The injection duration was 5 min, as in the previous study (19). The rats that did not undergo surgery were included in the control group (n=22).…”

mentioning

confidence: 99%

Dexmedetomidine Stereotaxic Injection Alleviates Neuronal Loss Following Bilateral Common Carotid Artery OcclusionviaUp-Regulation of BDNF Expression

KIM,

SHIN,

CHO

et al. 2023

In Vivo

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Background/Aim: Neurogenesis is an important process in the recovery from neurological damage caused by ischemic lesions. Endogenous neurogenesis is insufficient to restore neuronal damage following cerebral ischemia. Dexmedetomidine (DEX) exerts neuroprotective effects against cerebral ischemia and ischemia/reperfusion injury. DEX promotes neurogenesis, including neuronal proliferation and maturation in the hippocampus. In a previous study, we showed that early neurogenesis increased 3 days after bilateral common carotid artery occlusion (BCCAO). In this study, we investigated the effect of DEX on neurogenesis 3 days after BCCAO. Materials and Methods: Male Sprague-Dawley (SD) rats (7-8 weeks old) were used as a BCCAO model. Right and left common carotid arteries of the rats were occluded using 4-0 silk sutures. Two hours after surgery, an intracranial DEX injection was administered to rats that underwent surgery using a stereotaxic injector. Brains were obtained from control and BCCAO rats 3 days after surgery. Immunohistochemistry was performed on the cortex and dentate gyrus of the hippocampus using a NeuN antibody. Western blot was performed with HIF1α and brain-derived neurotrophic factor (BDNF) antibodies. Results: The number of mature neurons decreased 3 days after BCCAO, but DEX treatment alleviated neural loss in the parietal cortex and hippocampus. Up-regulation of BDNF was also observed after dexmedetomidine treatment. Conclusion: Stereotaxic injection of dexmedetomidine alleviates neural loss following BCCAO by up-regulating BDNF expression. Materials and MethodsAnimal surgery. Male Sprague-Dawley (SD) rats (7-8 weeks old) were supplied by a certified breeder (Damul Laboratory Animals, Daejeon, Republic of Korea). All animal experiments were 184

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IGF-1 Protects Neurons in the Cortex and Subventricular Zone in a Periventricular Leucomalacia Model

Cited by 4 publications

References 33 publications

Downregulation of SIRT1, SIRT3, and IGF-1 in ApoE-deficient mice exacerbates neuronal damage induced by chronic cerebral hypoperfusion

Downregulation of SIRT1, SIRT3, and IGF-1 in ApoE-deficient mice exacerbates neuronal damage induced by chronic cerebral hypoperfusion

Percentile-Based Reference Values of Umbilical Cord Blood Insulin-like Growth Factor 1 in Japanese Newborns

Dexmedetomidine Stereotaxic Injection Alleviates Neuronal Loss Following Bilateral Common Carotid Artery OcclusionviaUp-Regulation of BDNF Expression

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