Annexin A protein family in atherosclerosis

Li, Yongzhen; Wang, Yan-Yue; Huang, Liang; Zhao, Yu-Yan; Chen, Lin-Hui; Zhang, Chi

doi:10.1016/j.cca.2022.05.009

Cited by 22 publications

(13 citation statements)

References 219 publications

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“…AnxA6 involves the coordination of various physiological and pathological extracellular matrix (ECM) mineralization processes by regulating membrane and cytoskeleton organization, membrane trafficking, and signal transduction [ 18 ]. Growing evidence indicates that the abnormal expression of AnxA6 in osteoblasts and smooth muscle cells leads to some pathological processes such as the development of osteoporosis [ 19 ] and atherosclerosis [ 20 , 21 ]. The expression and distribution of annexins in cells are highly sensitive to changes in the mechanical microenvironment, especially fluid flow [ 14 ], whereas the role of AnxA6 in FSS-mediated osteogenic mineralization is unclear.…”

Section: Introductionmentioning

confidence: 99%

Fluid Shear Stress Regulates Osteogenic Differentiation via AnnexinA6-Mediated Autophagy in MC3T3-E1 Cells

Pei

Yang

et al. 2022

IJMS

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Fluid shear stress (FSS) facilitates bone remodeling by regulating osteogenic differentiation, and extracellular matrix maturation and mineralization. However, the underlying molecular mechanisms of how mechanical stimuli from FSS are converted into osteogenesis remain largely unexplored. Here, we exposed MC3T3-E1 cells to FSS with different intensities (1 h FSS with 0, 5, 10, and 20 dyn/cm2 intensities) and treatment durations (10 dyn/cm2 FSS with 0, 0.5, 1, 2 and 4 h treatment). The results demonstrate that the 1 h of 10 dyn/cm2 FSS treatment greatly upregulated the expression of osteogenic markers (Runx2, ALP, Col I), accompanied by AnxA6 activation. The genetic ablation of AnxA6 suppressed the autophagic process, demonstrating lowered autophagy markers (Beclin1, ATG5, ATG7, LC3) and decreased autophagosome formation, and strongly reduced osteogenic differentiation induced by FSS. Furthermore, the addition of autophagic activator rapamycin to AnxA6 knockdown cells stimulated autophagy process, and coincided with more expressions of osteogenic proteins ALP and Col I under both static and FSS conditions. In conclusion, the findings in this study reveal a hitherto unidentified relationship between FSS-induced osteogenic differentiation and autophagy, and point to AnxA6 as a key mediator of autophagy in response to FSS, which may provide a new target for the treatment of osteoporosis and other diseases.

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Section: Introductionmentioning

confidence: 99%

Fluid Shear Stress Regulates Osteogenic Differentiation via AnnexinA6-Mediated Autophagy in MC3T3-E1 Cells

Pei

Yang

et al. 2022

IJMS

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“…Moreover, a previous study also showed that TRIM59 binds to AnxA2 and TRIM59 overexpression promotes the expression of AnxA2 ( 40 ). Interestingly, Li et al showed that AnxA2 was involved in the progression of AS ( 19 ). The RT-qPCR and western blot results revealed that AnxA2 expression was decreased in the ox-LDL-induced HUVECs.…”

Section: Discussionmentioning

confidence: 99%

“…A previous study showed that AnxA2 participates in a wide range of cellular functions, such as vesicle transport, cell division, and cell growth ( 18 ). Li et al conjectured that AnxA2 plays vital role in the advancement of AS ( 19 ). Interestingly, the Biogrid database ( https://thebiogrid.org/ ) predicts that TRIM59 binds to AnxA2.…”

Section: Introductionmentioning

confidence: 99%

TRIM59 attenuates ox-LDL-induced endothelial cell inflammation, apoptosis, and monocyte adhesion through AnxA2

Zeng¹,

Xie²,

Li³

2023

Ann Transl Med

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Background: Atherosclerosis (AS), a chronic inflammatory vascular disease, is a cause of heart attack and ischemic stroke. Tripartite motif-containing protein 59 (TRIM59), a member of the tripartite motif family, has been reported to be involved in inflammatory diseases. This study was to investigate the role of TRIM59 in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cells and examine the mechanism of TRIM59.Methods: To simulate a cellular model of AS in vitro, varying concentrations of ox- LDL (i.e.,20,40, 60, 80, and 100 μg/mL) were used to treat the human umbilical vein endothelial cells (HUVECs) for 24 h. The messenger ribonucleic acid (RNA) and protein levels of tripartite motif-containing protein 59 (TRIM59), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), and annexin 2 (AnxA2) were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot. The transfection efficacy of overexpression (Ov)-TRIM59 and small-interfering RNA-AnxA2 was examined by RT-qPCR and western blot. Cell counting kit-8 assays, lactate dehydrogenase (LDH) assays, enzyme-linked immunosorbent assays, and terminal-deoxynucleotidyl transferase mediated nick end labeling staining were used to examine viability, LDH expression, inflammation, and apoptosis in HUVECs. The protein levels of B-cell lymphoma 2, Bcl-2-associated X (BAX), cleaved caspase3, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 were assessed by western blot. Additionally, the adhesion of THP-1 to ox-LDL-induced HUVECs was detected using monocyte adhesion assays and the binding of TRIM59 and AnxA2 was verified by co-immunoprecipitation.Results: This study showed that TRIM59 expression was decreased in the ox-LDL-induced HUVECs while LOX-1 expression was increased. After transfection with Ov-TRIM59, TRIM59 in ox-LDL-induced HUVECs was increased, and TRIM59 overexpression alleviated the viability damage, inflammation, and apoptosis of the ox-LDL-induced HUVECs. In addition, THP-1 adhesion to the ox-LDL-induced HUVECs was also suppressed by TRIM59 overexpression. This study also showed that TRIM59 could bind to AnxA2 and promote AnxA2 expression in ox-LDL-stimulated HUVECs. Moreover, the rescue experiments revealed that TRIM59 suppressed the viability damage, inflammation, apoptosis, and monocyte adhesion of the ox-LDL-induced HUVECs via AnxA2.Conclusions: TRIM59 protected against ox-LDL-induced AS by binding to AnxA2.

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“…ANXA7 mainly functions in accordance with the Ca 2+ concentration ( 22 ). And, via binding to the cell membrane, it can change the permeability of the cell membrane, thereby facilitating the release of neurotransmitters and vesicle transport ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

Usability of serum annexin A7 as a biochemical marker of poor outcome and early neurological deterioration after acute primary intracerebral hemorrhage: A prospective cohort study

Wang

Yan

et al. 2022

Front. Neurol.

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ObjectiveAnnexin A7 (ANXA7), a calcium-dependent phospholipid-binding protein, may act to aggravate brain injury. This study aimed to assess the clinical utility of serum ANXA7 as a predictor of severity, early neurological deterioration (END), and prognosis after intracerebral hemorrhage (ICH).MethodsA total of 126 ICH patients and 126 healthy controls were enrolled. Symptomatic severity was evaluated utilizing the National Institutes of Health Stroke Scale (NIHSS) score. The lesion volume of ICH was measured according to the ABC/2 method. END was referred to as an increase of 4 or greater points in the NIHSS score or death at post-stroke 24 h. The unfavorable functional outcome was a combination of death and major disability at post-stroke 90 days.ResultsSerum ANXA7 levels were significantly higher in patients than in controls (median, 46.5 vs. 9.7 ng/ml; P < 0.001). Serum ANXA7 levels were independently correlated with NIHSS score [beta: 0.821; 95% confidence interval (CI): 0.106–1.514; variance inflation factor: 5.180; t = 2.573; P = 0.014] and hematoma volume (beta: 0.794; 95% CI: 0.418–1.173; variance inflation factor: 5.281; t = 2.781; P = 0.007). Serum ANXA7 levels were significantly elevated with increase in modified Rankin scale scores (P < 0.001). Also, serum ANXA7, which was identified as a categorical variable, independently predicted END and an unfavorable outcome with odds ratio values of 3.958 (95% CI: 1.290–12.143; P = 0.016) and 2.755 (95% CI: 1.051–7.220; P = 0.039), respectively. Moreover, serum ANXA7 levels efficiently differentiated END (area under the curve: 0.781; 95% CI: 0.698–0.849) and an unfavorable outcome (area under the curve: 0.776; 95% CI: 0.693–0.846).ConclusionSerum ANXA7 may represent a useful blood-derived biomarker for assessing the severity, END, and prognosis of ICH.

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Annexin A protein family in atherosclerosis

Cited by 22 publications

References 219 publications

Fluid Shear Stress Regulates Osteogenic Differentiation via AnnexinA6-Mediated Autophagy in MC3T3-E1 Cells

Fluid Shear Stress Regulates Osteogenic Differentiation via AnnexinA6-Mediated Autophagy in MC3T3-E1 Cells

TRIM59 attenuates ox-LDL-induced endothelial cell inflammation, apoptosis, and monocyte adhesion through AnxA2

Usability of serum annexin A7 as a biochemical marker of poor outcome and early neurological deterioration after acute primary intracerebral hemorrhage: A prospective cohort study

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