miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice

Zhang, Yang; Shi, Xiaofang; Gao, Zhen; Chu, Lan

doi:10.1155/2022/8603427

Cited by 5 publications

(3 citation statements)

References 40 publications

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“…Additionally, the expression of miRNA-155 has been previously reported and associated with resistance to antineoplastic treatment [ 36 , 119 , 120 ], tumor recurrence, and progression [ 119 , 121 , 122 ]. Likewise, the expression of miRNA-155 has been reported in EVs in diseases such as kidney cancer [ 123 ], lung injury [ 33 ], brain injury [ 124 ], and epilepsy [ 125 ], among others.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles and Their Zeta Potential as Future Markers Associated with Nutrition and Molecular Biomarkers in Breast Cancer

Mendivil-Alvarado

Limon‐Miro

Carvajal-Millán

et al. 2023

IJMS

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A nutritional intervention promotes the loss of body and visceral fat while maintaining muscle mass in breast cancer patients. Extracellular vesicles (EVs) and their characteristics can be potential biomarkers of disease. Here, we explore the changes in the Zeta potential of EVs; the content of miRNA-30, miRNA-145, and miRNA-155; and their association with body composition and biomarkers of metabolic risk in breast cancer patients, before and 6 months after a nutritional intervention. Clinicopathological data (HER2neu, estrogen receptor, and Ki67), anthropometric and body composition data, and plasma samples were available from a previous study. Plasma EVs were isolated and characterized in 16 patients. The expression of miRNA-30, miRNA-145, and miRNA-155 was analyzed. The Zeta potential was associated with HER2neu (β = 2.1; p = 0.00), Ki67 (β = −1.39; p = 0.007), estrogen positive (β = 1.57; p = 0.01), weight (β = −0.09; p = 0.00), and visceral fat (β = 0.004; p = 0.00). miRNA-30 was associated with LDL (β = −0.012; p = 0.01) and HDL (β = −0.02; p = 0.05). miRNA-155 was associated with visceral fat (β = −0.0007; p = 0.05) and Ki67 (β = −0.47; p = 0.04). Our results reveal significant associations between the expression of miRNA-30 and miRNA-155 and the Zeta potential of the EVs with biomarkers of metabolic risk and disease prognosis in women with breast cancer; particularly, the Zeta potential of EVs can be a new biomarker sensitive to changes in the nutritional status and breast cancer progression.

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Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles and Their Zeta Potential as Future Markers Associated with Nutrition and Molecular Biomarkers in Breast Cancer

Mendivil-Alvarado

Limon‐Miro

Carvajal-Millán

et al. 2023

IJMS

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“…According to the aforementioned studies, therapeutic strategies targeting autophagy modulation may be a possible approach in the management of the postischemic neurodegeneration of Alzheimer’s disease proteinopathy. To date, multiple potential therapeutic molecules have been explored [ 152 , 153 , 154 , 155 , 156 ]. These molecules influence different processes of autophagy, including inducing adaptive autophagy and inhibiting excessive autophagy after brain ischemia ( Table 2 ).…”

Section: Potential Therapeutic Strategies For Autophagy Modulation Po...mentioning

confidence: 99%

The Dual Role of Autophagy in Postischemic Brain Neurodegeneration of Alzheimer’s Disease Proteinopathy

Pluta

2023

IJMS

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Autophagy is a self-defense and self-degrading intracellular system involved in the recycling and elimination of the payload of cytoplasmic redundant components, aggregated or misfolded proteins and intracellular pathogens to maintain cell homeostasis and physiological function. Autophagy is activated in response to metabolic stress or starvation to maintain homeostasis in cells by updating organelles and dysfunctional proteins. In neurodegenerative diseases, such as cerebral ischemia, autophagy is disturbed, e.g., as a result of the pathological accumulation of proteins associated with Alzheimer’s disease and their structural changes. Postischemic brain neurodegeneration, such as Alzheimer’s disease, is characterized by the accumulation of amyloid and tau protein. After cerebral ischemia, autophagy was found to be activated in neuronal, glial and vascular cells. Some studies have shown the protective properties of autophagy in postischemic brain, while other studies have shown completely opposite properties. Thus, autophagy is now presented as a double-edged sword with possible therapeutic potential in brain ischemia. The exact role and regulatory pathways of autophagy that are involved in cerebral ischemia have not been conclusively elucidated. This review aims to provide a comprehensive look at the advances in the study of autophagy behavior in neuronal, glial and vascular cells for ischemic brain injury. In addition, the importance of autophagy in neurodegeneration after cerebral ischemia has been highlighted. The review also presents the possibility of modulating the autophagy machinery through various compounds on the development of neurodegeneration after cerebral ischemia.

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“…According to the aforementioned studies, therapeutic strategies targeting autophagy modulation may be a possible approach in the management of IS. To date, multiple potential therapeutic agents have been explored [ 150 – 154 ]. These agents modulate different processes of autophagy including (A) inducing adaptive autophagy and (B) inhibiting excessive autophagy following IS.…”

Section: Potential Therapeutic Strategies For Ischemic Stroke Targeti...mentioning

confidence: 99%

Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy

Zhang

Ding

et al. 2022

Oxidative Medicine and Cellular Longevity

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Stroke is one of the leading causes of death and disability worldwide. Autophagy is a conserved cellular catabolic pathway that maintains cellular homeostasis by removal of damaged proteins and organelles, which is critical for the maintenance of energy and function homeostasis of cells. Accumulating evidence demonstrates that autophagy plays important roles in pathophysiological mechanisms under ischemic stroke. Previous investigations show that autophagy serves as a “double-edged sword” in ischemic stroke as it can either promote the survival of neuronal cells or induce cell death in special conditions. Following ischemic stroke, autophagy is activated or inhibited in several cell types in brain, including neurons, astrocytes, and microglia, as well as microvascular endothelial cells, which involves in inflammatory activation, modulation of microglial phenotypes, and blood-brain barrier permeability. However, the exact mechanisms of underlying the role of autophagy in ischemic stroke are not fully understood. This review focuses on the recent advances regarding potential molecular mechanisms of autophagy in different cell types. The focus is also on discussing the “double-edged sword” effect of autophagy in ischemic stroke and its possible underlying mechanisms. In addition, potential therapeutic strategies for ischemic stroke targeting autophagy are also reviewed.

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miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice

Cited by 5 publications

References 40 publications

Extracellular Vesicles and Their Zeta Potential as Future Markers Associated with Nutrition and Molecular Biomarkers in Breast Cancer

Extracellular Vesicles and Their Zeta Potential as Future Markers Associated with Nutrition and Molecular Biomarkers in Breast Cancer

The Dual Role of Autophagy in Postischemic Brain Neurodegeneration of Alzheimer’s Disease Proteinopathy

Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy

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