Is insulin-like growth factor-1 involved in Parkinson’s disease development?

Castilla‐Cortázar, Inma; Aguirre, Gabriel A.; Femat-Roldán, Giovana; Martín-Estal, Irene; Espinosa, Luís

doi:10.1186/s12967-020-02223-0

Cited by 36 publications

(31 citation statements)

References 200 publications

(221 reference statements)

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“… 26 Insulin-like growth factor 1 (IGF1) is a well-known anti-apoptotic pro-survival factor, serving a crucial role in maintaining homeostatic processes. 30 In several human disease studies, IGF1 has been identified to be the target gene of miR-18a-5p to participate in disease progression, such as muscle atrophy. 31 Notably, IGF1 has been reported to be low expressed in COPD patients.…”

Section: Discussionmentioning

confidence: 99%

LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis

Zhang

Zeng

et al. 2021

Ther Adv Respir Dis

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Aims: Chronic obstructive pulmonary disease (COPD) is a systemic disease. Several long non-coding RNAs (lncRNAs) have been identified to be aberrantly expressed in COPD patients. This study investigated the role of lncRNA cancer susceptibility candidate 2 (CASC2) in COPD, as well as its potential mechanism. Methods: Fifty smokers with COPD and another 50 smokers without COPD were recruited. Receiver operating characteristic curve was constructed to assess the diagnostic value of CASC2 in COPD patients. 16HBE cells were treated with cigarette smoke extract (CSE) to establish a cell model. qRT-PCR was used for the measurement of mRNA levels. The cell viability and apoptosis were detected by using Cell Counting Kit-8 and flow cytometry assay. Enzyme-linked immunosorbent assay was performed to detect the levels of proinflammatory cytokines. Luciferase reporter assay was performed for the target gene analysis. Results: Serum CASC2 was dramatically decreased in COPD patients compared with smokers without COPD, and was positively associated with FEV1 (forced expiratory volume in one second). Serum CASC2 was overexpressed in severe COPD patients, and had the diagnostic accuracy to distinguish COPD patients from smokers. CASC2 overexpression alleviated CSE-induced apoptosis and inflammation in 16HBE cells. CASC2 functions as a ceRNA of miR-18a-5p. Upregulation of miR-18a-5p reversed the influence of CASC2 on cell apoptosis and inflammation in 16HBE cells. IGF1 was the target gene of miR-18a-5p. Conclusion: CASC2 was downregulated in COPD patients and it might be a promising biomarker for the disease diagnosis. Overexpression of CASC2 might inhibit the bronchial epithelial cell apoptosis and inflammation via targeting miR-18a-5p/IGF1 axis. The reviews of this paper are available via the supplemental material section.

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Section: Discussionmentioning

confidence: 99%

LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis

Zhang

Zeng

et al. 2021

Ther Adv Respir Dis

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“…However, a meta-analysis based on results of nine studies comparing serum IGF-1 levels with normal subjects failed to find a significant difference between AD patients and normal subjects [228]. On the other hand, most studies on the association between PD and IGF-1 levels have reported higher IGF-1 levels in PD patients than in normal subjects [229]. More importantly, studies using rodent PD, HD, or ALS models have consistently shown that IGF-1 has beneficial effects on these diseases [230][231][232][233][234][235][236].…”

Section: Igf-1mentioning

confidence: 98%

Physical Exercise-Induced Myokines in Neurodegenerative Diseases

Lee

Shin

Park

et al. 2021

IJMS

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Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), are disorders characterized by progressive degeneration of the nervous system. Currently, there is no disease-modifying treatments for most NDs. Meanwhile, numerous studies conducted on human and animal models over the past decades have showed that exercises had beneficial effects on NDs. Inter-tissue communication by myokine, a peptide produced and secreted by skeletal muscles during exercise, is thought to be an important underlying mechanism for the advantages. Here, we reviewed studies about the effects of myokines regulated by exercise on NDs and their mechanisms. Myokines could exert beneficial effects on NDs through a variety of regulatory mechanisms, including cell survival, neurogenesis, neuroinflammation, proteostasis, oxidative stress, and protein modification. Studies on exercise-induced myokines are expected to provide a novel strategy for treating NDs, for which there are no adequate treatments nowadays. To date, only a few myokines have been investigated for their effects on NDs and studies on mechanisms involved in them are in their infancy. Therefore, future studies are needed to discover more myokines and test their effects on NDs.

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“…17β-estradiol treatment stimulates the expression of glial cell-line-derived neurotrophic factor (GDNF) and protects dopaminergic neurons from 6-hydroxydopamine toxicity [171]. Moreover, estrogen can increase circulating IGF-1 and protect postmenopausal women from PD via IGF-1 [172]. Results from a meta-analysis also showed that hormone replacement therapy in menopausal women may reduce the risk of PD [42,173].…”

Section: The Role Of Estrogen In Pdmentioning

confidence: 99%

From Menopause to Neurodegeneration—Molecular Basis and Potential Therapy

Cheng

Lin

Lane

2021

IJMS

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The impacts of menopause on neurodegenerative diseases, especially the changes in steroid hormones, have been well described in cell models, animal models, and humans. However, the therapeutic effects of hormone replacement therapy on postmenopausal women with neurodegenerative diseases remain controversial. The steroid hormones, steroid hormone receptors, and downstream signal pathways in the brain change with aging and contribute to disease progression. Estrogen and progesterone are two steroid hormones which decline in circulation and the brain during menopause. Insulin-like growth factor 1 (IGF-1), which plays an import role in neuroprotection, is rapidly decreased in serum after menopause. Here, we summarize the actions of estrogen, progesterone, and IGF-1 and their signaling pathways in the brain. Since the incidence of Alzheimer’s disease (AD) is higher in women than in men, the associations of steroid hormone changes and AD are emphasized. The signaling pathways and cellular mechanisms for how steroid hormones and IGF-1 provide neuroprotection are also addressed. Finally, the molecular mechanisms of potential estrogen modulation on N-methyl-d-aspartic acid receptors (NMDARs) are also addressed. We provide the viewpoint of why hormone therapy has inconclusive results based on signaling pathways considering their complex response to aging and hormone treatments. Nonetheless, while diagnosable AD may not be treatable by hormone therapy, its preceding stage of mild cognitive impairment may very well be treatable by hormone therapy.

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Is insulin-like growth factor-1 involved in Parkinson’s disease development?

Cited by 36 publications

References 200 publications

LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis

LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis

Physical Exercise-Induced Myokines in Neurodegenerative Diseases

From Menopause to Neurodegeneration—Molecular Basis and Potential Therapy

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