Suppressed nuclear envelope proteins activate autophagy of vascular smooth muscle cells during cyclic stretch application

Li, Haipeng; Liu, Ji-Ting; Chen, Yuan-Xiu; Wang, Wenbin; Han, Yanyan; Yao, Qing; Qi, Ying‐Xin

doi:10.1016/j.bbamcr.2020.118855

Cited by 8 publications

(3 citation statements)

References 52 publications

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“…It is considered that excessive CMS disrupts the extracellular matrix surrounding VSMCs, leading to structural support loss and subsequent cell death [ 88 ]. Furthermore, autophagy induced by CMS triggers cell death through the degradation and recycling of cellular components [ 89 ]. In addition, abnormal CMS stimulation causes pro-inflammatory molecules to be released in the blood vessel wall, potentially contributing to VSMC death and the progression of CVDs [ 31 , 70 ].…”

Section: Exploring Cms-induced Cell Death Mechanismsmentioning

confidence: 99%

A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures

Zhao,

Yoshizumi

2024

IJMS

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Acute aortic dissection (AAD) and associated ruptures are the leading causes of death in cardiovascular diseases (CVDs). Hypertension is a prime risk factor for AAD. However, the molecular mechanisms underlying AAD remain poorly understood. We previously reported that cyclic mechanical stretch (CMS) leads to the death of rat aortic smooth muscle cells (RASMCs). This review focuses on the mechanisms of CMS-induced vascular smooth muscle cell (VSMC) death. Moreover, we have also discussed the potential therapeutics for preventing AAD and aneurysm ruptures.

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Section: Exploring Cms-induced Cell Death Mechanismsmentioning

confidence: 99%

A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures

Zhao,

Yoshizumi

2024

IJMS

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“…All Lamin types form a tight meshwork of filaments of approximately 10-30 nm thickness along the INM [191]. Above, Lamins directly interact with chromatin, transcription factors, and proteins, such as Emerin [192]. The functions of the respective Lamin isoforms are interdependent and only partially redundant, as the deletion of one isoform leads to a loosening of the whole meshwork [26,193].…”

Section: The Gist Of the Matter: Nuclear Mechanotransductionmentioning

confidence: 99%

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

et al. 2021

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Among oral tissues, the periodontium is permanently subjected to mechanical forces resulting from chewing, mastication, or orthodontic appliances. Molecularly, these movements induce a series of subsequent signaling processes, which are embedded in the biological concept of cellular mechanotransduction (MT). Cell and tissue structures, ranging from the extracellular matrix (ECM) to the plasma membrane, the cytosol and the nucleus, are involved in MT. Dysregulation of the diverse, fine-tuned interaction of molecular players responsible for transmitting biophysical environmental information into the cell’s inner milieu can lead to and promote serious diseases, such as periodontitis or oral squamous cell carcinoma (OSCC). Therefore, periodontal integrity and regeneration is highly dependent on the proper integration and regulation of mechanobiological signals in the context of cell behavior. Recent experimental findings have increased the understanding of classical cellular mechanosensing mechanisms by both integrating exogenic factors such as bacterial gingipain proteases and newly discovered cell-inherent functions of mechanoresponsive co-transcriptional regulators such as the Yes-associated protein 1 (YAP1) or the nuclear cytoskeleton. Regarding periodontal MT research, this review offers insights into the current trends and open aspects. Concerning oral regenerative medicine or weakening of periodontal tissue diseases, perspectives on future applications of mechanobiological principles are discussed.

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“…During autophagy, autophagosome initiation, elongation, and maturation, fusion of the autophagosomes to the lysosomes, and degradation within the lysosomes are tightly governed by multiple signaling mechanisms [ 6 , 7 ]. In mammals, the autophagy process correlates with a wide range of physiological events, such as embryonic development, responses to stress, and disease progress [ 8 ]. Accordingly, autophagy has become a fascination in the field of biological science, including the regulatory effects of yak follicular fluid EVs on the autophagy of cumulus cell culture in vitro.…”

Section: Introductionmentioning

confidence: 99%

Exosomes Derived from Yak Follicular Fluid Increase 2-Hydroxyestradiol Secretion by Activating Autophagy in Cumulus Cells

Wang²,

Wang³

et al. 2022

Animals

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Exosomes in the follicular fluid can carry and transfer regulatory molecules to recipient cells, thus influencing their biological functions. However, the specific effects of yak follicular fluid exosomes on 2-hydroxyestrodiol (2-OHE2) secretion remain unknown. Here, we investigated whether yak follicular fluid exosomes can increase 2-OHE2 secretion through the activation of autophagy in cumulus cells (YCCs). In vitro cultured YCCs were treated with yak follicular fluid exosomes for 6, 12, and 24 h. The effects of yak follicular fluid exosomes on autophagy and 2-OHE2 secretion were evaluated through real-time quantitative fluorescence PCR (RT-qPCR), Western blotting (WB), transfected with RFP-GFP-LC3, immunohistochemistry, and ELISA. To further investigate whether 2-OHE2 secretion was related to autophagy, YCCs were administered with yak follicular fluid exosomes, 3-methyladenine (3-MA), and rapamycin (RAPA). The results revealed that treatment with yak follicular fluid exosomes activated autophagy in YCCs and increased 2-OHE2 secretion. Conversely, the inhibition of autophagy with 3-MA blocked these effects, suggesting that autophagy has an important role in 2-OHE2 secretion in YCCs. Treatment of YCCs with rapamycin showed similar results with yak follicular fluid exosomes as there was an increase in 2-OHE2 secretion due to the activation of autophagy in the treated cumulus cells. Our results demonstrate that autophagy is enhanced by yak follicular fluid exosomes, and this is associated with an increase in 2-OHE2 secretion in YCCs.

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Suppressed nuclear envelope proteins activate autophagy of vascular smooth muscle cells during cyclic stretch application

Cited by 8 publications

References 52 publications

A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures

A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

Exosomes Derived from Yak Follicular Fluid Increase 2-Hydroxyestradiol Secretion by Activating Autophagy in Cumulus Cells

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