Insulin Increases Viability of Neurons in Rat Cerebral Cortex and Normalizes Bax/Bcl-2 Ratio under Conditions of Oxidative Stress

Bayunova, L. V.; Zorina, I. I.; Захарова, И. О.; Аврова, Н. Ф.

doi:10.1007/s10517-018-4088-8

Cited by 8 publications

(5 citation statements)

References 13 publications

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“…Many studies have confirmed that NGS technology can improve the diagnosis of chromosomal abnormalities. 31 , 32 CNV‐seq is a genomic copy number variation detection technology based on low‐depth whole‐genome sequencing. CNV‐seq can detect CNVs of different sizes by adjusting the sequencing depth and changing the resolution.…”

Section: Discussionmentioning

confidence: 99%

Copy number variation characterization and possible candidate genes in miscarriage and stillbirth by next‐generation sequencing analysis

Zhang

Huang

et al. 2021

The Journal of Gene Medicine

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Background: The present study aimed to explore the etiological relationship between miscarriage and stillbirth and copy number variations (CNVs), as well as provide useful genetic guidance for high-risk pregnancy.Methods: In total, 659 fetal samples were recruited and subjected to DNA extraction and CNV sequencing (CNV-seq), relevant medical records were collected.Results: There were 322 cases (48.86%) with chromosomal abnormalities, including 230 with numerical abnormalities and 92 with structural abnormalities. Chromosomal monosomy variations mainly occurred on sex chromosomes and trisomy variations mainly occurred on chromosomes 16, 22, 21, 18, 13 and 15. In total, 41 pathogenic CNVs (23 microdeletions and 18 microduplications) were detected in 27 fetal tissues.The rates of numerical chromosomal abnormalities were 29.30% (109/372), 32.39% (57/176) and 57.66% (64/111) in < 30-year-old, 30-34-year-old and ≥ 35-year-old age pregnant women, respectively, and increased with an increasing age (p < 0.001).There was statistically significant difference (χ 2 = 7.595, p = 0.022) in the rates of structural chromosomal abnormalities in these groups (13.71%, 18.75% and 7.21%, respectively). The rates of numerical chromosomal abnormalities were 45.44% (219/482), 7.80% (11/141) and 0% (0/36) in the ≤ 13 gestational weeks, 14-27 weeks and ≥ 28 weeks groups, respectively, and decreased with respect to the increasing gestational age of the fetuses (p < 0.001). Conclusions:The present study has obtained useful and accurate genetic etiology information that will provide useful genetic guidance for high-risk pregnancies.

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Section: Discussionmentioning

confidence: 99%

Copy number variation characterization and possible candidate genes in miscarriage and stillbirth by next‐generation sequencing analysis

Zhang

Huang

et al. 2021

The Journal of Gene Medicine

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“…The proteins of the BCL-2 family are the most important regulators of mitochondria-related apoptosis. The ratio of pro- and antiapoptotic proteins (BCL2 and Bax) determines whether mitochondria initiate the cell death program by releasing cytochrome C and other proapoptotic factors [ 22 ]. There was no significant difference in the number of TUNEL-positive cells or in the expression of BCL2, Bax, and cleaved-caspase-3 between the H 2 O 2 , overexpression vector, and knockdown vector groups ( P > 0.05, Figure 4 ).…”

Section: Resultsmentioning

confidence: 99%

The lncRNA-AK046375 Upregulates Metallothionein-2 by Sequestering miR-491-5p to Relieve the Brain Oxidative Stress Burden after Traumatic Brain Injury

Tang

Chai

et al. 2022

Oxidative Medicine and Cellular Longevity

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We previously discovered that traumatic brain injury (TBI) induces significant perturbations in long noncoding RNA (lncRNA) levels in the mouse cerebral cortex, and lncRNA-AK046375 is one of the most significantly changed lncRNAs after TBI. lncRNA-AK046375 overexpression and knockdown models were successfully constructed both in vitro and in vivo. In cultured primary cortical neurons and astrocytes, lncRNA-AK046375 sequestered miR-491-5p, thereby enhancing the expression of metallothionein-2 (MT2), which ameliorated oxidative-induced cell injury. In addition, upregulated lncRNA-AK046375 promoted the recovery of motor, learning, and memory functions after TBI in C57BL/6 mice, and the underlying mechanism may be related to ameliorated apoptosis, inhibited oxidative stress, reduced brain edema, and relieved loss of tight junction proteins at the blood-brain barrier in the mouse brain. Therefore, we conclude that lncRNA-AK046375 enhances MT2 expression by sequestering miR-491-5p, ultimately strengthening antioxidant activity, which ameliorates neurological deficits post-TBI.

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“…99 As part of these role, it streamlines cellular energy production and health in a variety of ways. It opposes oxidative stress by promoting GSH synthesis, 152,153 opposes with GSH the apoptosis-promoting effects of H2O2, 154 acts as an anti-inflammatory agent in the immune system, 155 promotes mitochondria health, oxidative phosphorylation, ATP production, and protein synthesis, 156,157 promotes synaptic plasticity, 158 and opposes calcium overload and toxicity. [159][160][161][162][163][164][165][166] Insulin promotes the production of N-Acetylglucosamine (GlcNAc), 167 whose use in O-GlcNAcylation decreases intracellular Ca 2+ load, 168 H2O2 production, and permeability pore opening.…”

Section: Insulin Protection In Alsmentioning

confidence: 99%

Insulin in Amyotrophic Lateral Sclerosis: Impairment, Tests and Treatment

Rappoport¹

2023

Preprint

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Background. Amyotrophic Lateral Sclerosis (ALS) is a devastating disease involving motor neuron degeneration. The few drugs approved for treatment have at most a marginal benefit, and death usually occurs 2-5 years after diagnosis. Methods. A thorough manual examination of the relevant literature, covering over 35,000 papers. Results. Two major phenomena that are generally not known to clinicians were found. First, insulin signaling is impaired in ALS even in patients not diagnosed with diabetes (DB). Almost all studies that have explicitly tested insulin function in non-DB ALS patients using glucose tolerance tests (18 out of 20, 1964-2022, different groups) have found it to be impaired. Second, there is strong evidence for excessive insulin-independent glucose uptake (IIGU) in ALS. In addition, (i) early/late diabetes are associated with increased/decreased risk, respectively; (ii) insulin-based diabetes drugs are protective in ALS in large retrospective human studies; and (iii) strong animal and human evidence shows that insulin opposes all of the major pathological processes in ALS. Conclusion. Most ALS patients have insulin impairment, yet this is commonly not diagnosed, likely because excessive IIGU normalizes glucose levels. The impairment promotes disease progression. Late diabetes is associated with decreased risk because high glucose levels indicate non-excessive IIGU, and because diabetes drugs are protective. Insulin-based treatment (e.g., GLP1 agonists, insulin) is beneficial and can be disease-modifying in ALS and in frontotemporal dementia variants comorbid with ALS. ALS patients should be routinely tested for insulin function and treated if test results are positive.

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Insulin Increases Viability of Neurons in Rat Cerebral Cortex and Normalizes Bax/Bcl-2 Ratio under Conditions of Oxidative Stress

Cited by 8 publications

References 13 publications

Copy number variation characterization and possible candidate genes in miscarriage and stillbirth by next‐generation sequencing analysis

Copy number variation characterization and possible candidate genes in miscarriage and stillbirth by next‐generation sequencing analysis

The lncRNA-AK046375 Upregulates Metallothionein-2 by Sequestering miR-491-5p to Relieve the Brain Oxidative Stress Burden after Traumatic Brain Injury

Insulin in Amyotrophic Lateral Sclerosis: Impairment, Tests and Treatment

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