Excess centrosomes disrupt vascular lumenization and endothelial cell adherens junctions

Buglak, Danielle B; Kushner, Erich J.; Marvin, Allison; Davis, Katy L; Bautch, Victoria L.

doi:10.1007/s10456-020-09737-7

Cited by 21 publications

(15 citation statements)

References 48 publications

(79 reference statements)

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“…Cell culture supernatants were collected by centrifugation at 1,000 rpm for 10 min [ 26 ]. After centrifugation, 100 μ L/well supernatant was added to 96-well plates to determine the activities of CK-MB and LDH in each group according to the kit's instructions [ 27 ].…”

Section: Methodsmentioning

confidence: 99%

[Retracted] LATS2 Deletion Attenuates Myocardial Ischemia‐Reperfusion Injury by Promoting Mitochondrial Biogenesis

Chen

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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Reperfusion therapy is the most effective treatment for acute myocardial infarction, but it can damage cardiomyocytes through a mechanism known as myocardial ischemia/reperfusion injury (MIRI). In this study, we investigated whether the large tumor suppressor kinase 2 (LATS2) contributes to the development of myocardial MIRI by disrupting mitochondrial biogenesis. Our in vitro data demonstrate that cardiomyocyte viability was reduced and apoptosis was increased in response to hypoxia/reoxygenation (H/R) injury. However, suppression of LATS2 by shRNA sustained cardiomyocyte viability by maintaining mitochondrial function. Compared to H/R-treated control cardiomyocytes, cardiomyocytes transfected with LATS2 shRNA exhibited increased mitochondrial respiration, improved mitochondrial ATP generation, and more stable mitochondrial membrane potential. LATS2 suppression increased cardiomyocyte viability and mitochondrial biogenesis in a manner dependent on PGC1α, a key regulator of mitochondrial metabolism. These results identify LATS2 as a new inducer of mitochondrial damage and myocardial MIRI and suggest that approaches targeting LATS2 or mitochondrial biogenesis may be beneficial in the clinical management of cardiac MIRI.

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Section: Methodsmentioning

confidence: 99%

[Retracted] LATS2 Deletion Attenuates Myocardial Ischemia‐Reperfusion Injury by Promoting Mitochondrial Biogenesis

Chen

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…MTT (Sigma) was added to the wells, and cells were incubated for 4 h in 5% CO 2 at 37°C [ 25 ]. Next, 150 μ L of dimethyl sulfoxide (DMSO) was added to each well for 10 min, and the absorbance of formazan was measured at 490 nm from 0 to 72 h [ 26 ].…”

Section: Methodsmentioning

confidence: 99%

Mst2 Overexpression Inhibits Thyroid Carcinoma Growth and Metastasis by Disrupting Mitochondrial Fitness and Endoplasmic Reticulum Homeostasis

Zhang

Han

et al. 2021

Journal of Oncology

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Although the incidence of thyroid carcinoma has increased over the past several decades, it has an excellent prognosis and overall 5-year survival, with a stable mortality rate, except in cases with advanced stages or rare malignant tumor types. Biomarkers have emerged as effective targets of molecular therapy against thyroid carcinoma due to their rapid and convenient detection; however, there has been little clinical application. Macrophage stimulating 2 (Mst2) is a proapoptotic protein with implications in carcinogenesis and metastasis. We found that Mst2 overexpression-induced endoplasmic reticulum (ER) stress in MDA-T32 thyroid carcinoma cells, accompanied by elevated caspase-12 activity, increased apoptotic rate, and reduced cell viability. In addition, Mst2 overexpression contributed to mitochondrial damage, as evidenced by increased mitochondrial oxidative stress and activated the mitochondrial apoptotic pathway. Inhibition of the JNK pathway abolished these effects. These results show Mst2 to be a novel tumor suppressor that induces mitochondrial dysfunction and ER stress via the JNK pathway. Thus, Mst2 could potentially serve as a biomarker for developing targeted therapy against thyroid carcinoma.

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“…An enhanced chemiluminescence (ECL) reagent detection kit (Thermo Fisher Scientific) was used, and an imaging machine (2200 Pro, Kodak) was employed to detect the protein bands. For ELISA, the supernatants of RAW264.7 macrophages were collected to detect the concentration of TNF- α and IL-6 (Neobioscience, China) [ 36 , 37 ].…”

Section: Methodsmentioning

confidence: 99%

BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages

Qiu

Chen

et al. 2021

Oxidative Medicine and Cellular Longevity

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Atherosclerosis (AS) is a chronic metabolic disease in arterial walls, characterized by lipid deposition and persistent aseptic inflammation. AS is regarded as the basis of a variety of cardiovascular and cerebrovascular diseases. It is widely acknowledged that macrophages would become foam cells after internalizing lipoprotein particles, which is an initial factor in atherogenesis. Here, we showed the influences of Bruton’s tyrosine kinase (BTK) in macrophage-mediated AS and how BTK regulates the inflammatory responses of macrophages in AS. Our bioinformatic results suggested that BTK was a potential hub gene, which is closely related to oxidative stress, ER stress, and inflammation in macrophage-induced AS. Moreover, we found that BTK knockdown could restrain ox-LDL-induced NK-κB signaling activation in macrophages and repressed M1 polarization. The mechanistic studies revealed that oxidative stress, mitochondrial injury, and ER stress in macrophages were also suppressed by BTK knockdown. Furthermore, we found that sh-BTK adenovirus injection could alleviate the severity of AS in ApoE-/- mice induced by a high-fat diet in vivo. Our study suggested that BTK promoted ox-LDL-induced ER stress, oxidative stress, and inflammatory responses in macrophages, and it may be a potential therapeutic target in AS.

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Excess centrosomes disrupt vascular lumenization and endothelial cell adherens junctions

Cited by 21 publications

References 48 publications

[Retracted] LATS2 Deletion Attenuates Myocardial Ischemia‐Reperfusion Injury by Promoting Mitochondrial Biogenesis

[Retracted] LATS2 Deletion Attenuates Myocardial Ischemia‐Reperfusion Injury by Promoting Mitochondrial Biogenesis

Mst2 Overexpression Inhibits Thyroid Carcinoma Growth and Metastasis by Disrupting Mitochondrial Fitness and Endoplasmic Reticulum Homeostasis

BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages

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