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High-density lipoprotein regulates angiogenesis by affecting autophagy via miRNA-181a-5p

Science China(Life Sciences) 2024年第2期67卷 286-300页

作者： Bi-Ang Kang Hua-Ming Li Ya-Ting Chen Meng-Jie deng Yan Li Yue-Ming Peng Jian-Jun Gao Zhi-Wei Mo Jia-Guo Zhou Zhi-Jun Ou Jing-Song Ou Division of Cardiac Surgery Cardiovascular Diseases InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of vascular Diseases Guangzhou 510080China NHC key Laboratory of Assisted Circulation(Sun Yat-sen University) Guangzhou 510080China Guangdong Provincial Engineering and Technology Center for Diagnosis and Treatment of vascular Diseases Guangzhou 510080China Division of vascular Surgery The First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China department of Pharmacology Cardiac and Cerebral Vascular Research CenterZhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China Division of Hypertension and vascular Diseases Department of CardiologyCardiovascular Diseases InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Guangdong Provincial Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China

We previously demonstrated that normal high-density lipoprotein(nHDL)can promote angiogenesis,whereas HDL from patients with coronary artery disease(d HDL)is dysfunctional and impairs angiogenesis.Autophagy plays a critical role in angiogenesis,and HDL regulates autophagy.However,it is unclear whether n HDL and d HDL regulate angiogenesis by affecting autophagy.Endothelial cells(ECs)were treated with n HDL and d HDL with or without an autophagy inhibitor.Autophagy,endothelial nitric oxide synthase(e NOS)expression,miRNA expression,nitric oxide(NO)production,superoxide anion(O2^(·-))generation,EC migration,and tube formation were evaluated.n HDL suppressed the expression of miR-181a-5p,which promotes autophagy and the expression of e NOS,resulting in NO production and the inhibition of O2^(·-)generation,and ultimately increasing in EC migration and tube formation.d HDL showed opposite effects compared to n HDL and ultimately inhibited EC migration and tube formation.We found that autophagy-related protein 5(ATG5)was a direct target of miR-181a-5p.ATG5 silencing or miR-181a-5p mimic inhibited n HDL-induced autophagy,e NOS expression,NO production,EC migration,tube formation,and enhanced O2^(·-)generation,whereas overexpression of ATG5 or miR-181a-5p inhibitor reversed the above effects of d HDL.ATG5 expression and angiogenesis were decreased in the ischemic lower limbs of hypercholesterolemic low-density lipoprotein receptor null(LDLr^(-/-))mice when compared to C57BL/6 mice.ATG5 overexpression improved angiogenesis in ischemic hypercholesterolemic LDLr^(-/-)mice.Taken together,nHDL was able to stimulate autophagy by suppressing miR-181a-5p,subsequently increasing e NOS expression,which generated NO and promoted angiogenesis.In contrast,d HDL inhibited angiogenesis,at least partially,by increasing miR-181a-5p expression,which decreased autophagy and e NOS expression,resulting in a decrease in NO production and an increase in O2^(·-)generation.Our findings reveal a novel mechanism by which HDL affects angiogenesis b

关键词： high-density lipoprotein angiogenesis autophagy ATG5 miRNA endothelial nitric oxide synthase

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The short form of the SUR1 and its functional implications in the damaged brain

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Neural Regeneration Research 2022年第3期17卷 488-496页

作者： Iván Alquisiras-Burgos Javier Franco-Pérez Moisés Rubio-Osornio Penélope Aguilera Laboratorio de Patología Vascular Cerebral Instituto Nacional de Neurología y Neurocirugía“Manuel Velasco Suárez”CDMXMexico laboratorio de Formación Reticular Instituto Nacional de Neurología y Neurocirugía“Manuel Velasco Suárez”CDMXMexico laboratorio Experimental de Enfermedades Neurodegenerativas Instituto Nacional de Neurología y Neurocirugía“Manuel Velasco Suárez”CDMXMexico.

Sulfonylurea receptor(SUR) belongs to the adenosine 5′-triphosphate(ATP)-binding cassette(ABC) transporter family;however,SUR is associated with ion channels and acts as a regulatory subunit determining the opening or closing of the pore.Abcc8 and Abcc9 genes code for the proteins SUR1 and SUR2,respectively.The SUR1 transcript encodes a protein of 1582 amino acids with a mass around 140–177 k Da expressed in the pancreas,brain,heart,and other tissues.It is well known that SUR1 assembles with Kir6.2 and TRPM4 to establish K_(ATP) channels and non-selective cation channels,respectively.Abbc8 and 9 are alternatively spliced,and the resulting transcripts encode different isoforms of SUR1 and SUR2,which have been detected by different experimental strategies.Interestingly,the use of binding assays to sulfonylureas and Western blotting has allowed the detection of shorter forms of SUR(-65 k Da).Identity of the SUR1 variants has not been clarified,and some authors have suggested that the shorter forms are unspecific.However,immunoprecipitation assays have shown that SUR2 short forms are part of a functional channel even coexisting with the typical forms of the receptor in the heart.This evidence confirms that the structure of the short forms of the SURs is fully functional and does not lose the ability to interact with the channels.Since structural changes in short forms of SUR modify its affinity to ATP,regulation of its expression might represent an advantage in pathologies where ATP concentrations decrease and a therapeutic target to induce neuroprotection.Remarkably,the expression of SUR1 variants might be induced by conditions associated to the decrease of energetic substrates in the brain(e.***.during stroke and epilepsy).In this review,we want to contribute to the knowledge of SUR1 complexity by analyzing evidence that shows the existence of short SUR1 variants and its possible implications in brain function.

关键词： brain edema epilepsy Parkinson's disease stroke sulfonylurea receptor 1 SUR1 traumatic brain injury TRPM4

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Molecular biomarkers for vascular cognitive impairment and dementia:the current status and directions for the future

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Neural Regeneration Research 2024年第12期19卷 2579-2580页

作者： Satoshi Hosoki Perminder SSachdev Centre for Healthy Brain Ageing Discipline of Psychiatry and Mental HealthSchool of Clinical MedicineFaculty of Medicine and HealthUniversity of New South WalesSydneyAustralia department of Neurology National Cerebral and Cardiovascular CenterOsakaJapan

dementia is a syndrome with various underlying pathologies acting independently or in concert to cause cognitive dysfunction.The development of disease-specific treatments and targeted prevention strategies requires precise clinical sub-typing via etiology and pathophysiological processes.Furthermore,recent research advances in biomarkers,especially for Alzheimer's disease(AD)diagnosis,have improved diagnostic precision for dementia.

关键词： prevention diagnosis impairment

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Involvement of glucose transporter overexpression in the protection or damage after ischemic stroke

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Neural Regeneration Research 2022年第4期17卷 783-784页

作者： Iván Alquisiras-Burgos Penélope Aguilera Laboratorio de Patología Vascular Cerebral Instituto Nacional de Neurología y Neurocirugía Manuel Velasco SuárezInsurgentes Sur#3877Col.La FamaTlalpanCiudad de MéxicoMéxico

cerebral ischemia and resultant energy collapse:The ischemic stroke is a complex neurological condition that can be devastating for patients and their families.This disease is the second leading cause of death worldwide and is characterized by a sudden decrease in cerebral blood flow due to major blood vessel blockage.Ischemic stroke generates two damaged zones with distinctive metabolic characteristics.The first is the ischemic core,the region directly irrigated by the occluded artery.A reduction to less than 20%of the baseline blood flow levels defines the area;therefore,depletion of glucose and adenosine triphosphate(ATP)cause an irreversible failure in the energy metabolism that leads to loss of ionic homeostasis,acidosis,and necrosis.The second is the region surrounding the ischemic core,called the penumbra,characterized by significantly depressed tissue perfusion that is barely sufficient to support basal oxygen,glucose,and ATP levels.

关键词： metabolism damage homeostasis

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Resveratrol as an inductor of autophagy: is there a unique pathway of activation?

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Neural Regeneration Research 2021年第1期16卷 101-103页

作者： Narayana Pineda-Ramírez Penélope Aguilera Laboratorio de Patología Vascular Cerebral.Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez Ciudad de MéxicoMéxico

Autophagy is a process of cellular degradation for the removal of damaged components and eventual recycling of the resulting molecules that help to the maintenance of cellular homeostasis.Through this pathway,proteins with relatively long half-life and whole organelles(e.g.,mitochondria,peroxisomes,and ribosomes)are degraded in the cytoplasm for the continuous turnover of cellular structures to facilitate their renewal.However,the beneficial effect of autophagy goes beyond cellular“cleaning”and resides to a large extent on its ability to recycle cell components back into the cytosol.Thus,autophagy is a fundamental mechanism to regulate cellular functions,including DNA repair,proliferation,differentiation,embryonic development,and the immune response.

关键词： homeostasis activation autophagy

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Author correction to“TMEM16A inhibits angiotensin Ⅱ-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner”[Acta Pharm Sin B 11(12)(2021)3994–4007]

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Acta Pharmaceutica Sinica B 2023年第9期13卷 1340-1343页

作者： Huaqing Zheng Xiaolong Li Xin Zeng Chengcui Huang Mingming Ma Xiaofei Lv Yajuan Zhang Lu Sun Guanlei Wang Yanhua Du Yongyuan Guan department of Pharmacology Cardiac&Cerebral Vascular Research CenterZhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China

The authors regret that there were some picture errors in the Fig.1D,G,I,Fig.4L,Fig.6C,H and Supporting Information Fig.S1A owing to copy and paste mistakes when preparing the representative images.The revisions do not affect the data value,significant difference,and conclusions of the current work and the description of the whole article.The original data of this figure have been provided to the Editorial Office,and the Editorial Office or the corresponding authors can be contacted for original data access.

关键词： correction preparing paste

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Association of DNA methylation/demethylation with the functional outcome of stroke in a hyperinflammatory state

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Neural Regeneration Research 2024年第10期19卷 2229-2239页

作者： Yubo Wang Ling Zhang Tianjie Lyu Lu Cui Shunying Zhao Xuechun Wang Meng Wang Yongjun Wang Zixiao Li vascular Neurology Department of NeurologyBeijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical Research Center for Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina National Center for Healthcare Quality Management in Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Chinese Institute for Brain Research BeijingChina Research Unit of Artificial Intelligence in Cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina Beijing Engineering Research Center of Digital Healthcare for Neurological Diseases BeijingChina

Inflammation is closely related to stroke prognosis, and high inflammation status leads to poor functional outcome in stroke. DNA methylation is involved in the pathogenesis and prognosis of stroke. However, the effect of DNA methylation on stroke at high levels of inflammation is unclear. In this study, we constructed a hyperinflammatory cerebral ischemia mouse model and investigated the effect of hypomethylation and hypermethylation on the functional outcome. We constructed a mouse model of transient middle cerebral artery occlusion and treated the mice with lipopolysaccharide to induce a hyperinflammatory state. To investigate the effect of DNA methylation on stroke, we used small molecule inhibitors to restrain the function of key DNA methylation and demethylation enzymes. 2,3,5-Triphenyltetrazolium chloride staining, neurological function scores, neurobehavioral tests, enzyme-linked immunosorbent assay, quantitative reverse transcription PCR and western blot assay were used to evaluate the effects after stroke in mice. We assessed changes in the global methylation status by measuring DNA 5-mc and DNA 5-hmc levels in peripheral blood after the use of the inhibitor. In the group treated with the DNA methylation inhibitor, brain tissue 2,3,5-triphenyltetrazolium chloride staining showed an increase in infarct volume, which was accompanied by a decrease in neurological scores and worsening of neurobehavioral performance. The levels of inflammatory factors interleukin 6 and interleukin-1 beta in ischemic brain tissue and plasma were elevated, indicating increased inflammation. Related inflammatory pathway exploration showed significant overactivation of nuclear factor kappa B. These results suggested that inhibiting DNA methylation led to poor functional outcome in mice with high inflammation following stroke. Further, the effects were reversed by inhibition of DNA demethylation. Our findings suggest that DNA methylation regulates the inflammatory response in stroke and has an important role in the functional out

关键词： DNA demethylation DNA methylation DNMT3A functional outcome hyperinflammatory state interleukin neuroinflammation stroke TET2

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Efficacy of Different Types of Self-expandable Stents in Carotid Artery Stenting for Carotid Bifurcation Stenosis

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2016年第1期36卷 95-98页

作者：刘亚民秦皓张波王毓婧冯骏吴翔 department of cerebral vascular Diseases the First Affiliated Hospital of Xi'an Jiao Tong University

Both open and closed loop self-expandable stents were used in carotid artery stenting（CAS） for carotid bifurcation stenosis. We sought to compare the efficacy of two types of stents in CAS. The data of 212 patients treated with CAS（42 and 170 cases implanted with closed and open loop stents, respectively） for carotid bifurcation stenosis and distal filtration protection devices were retrospectively analyzed. Between closed and open loop stents, there were no significant differences in hospitalization duration, NIHSS score before and after the treatment, stenosis at 12 th month, and cumulative incidence of primary endpoint events within 30 days or from the 31 st day to the 12 th month; while there were significant differences in hemodynamic changes and rate of difficulty in recycling distal filtration protection devices. Use of open vs. closed loop stents for carotid bifurcation stenosis seems to be associated with similar incidence of complications, except for greater rate of hemodynamic changes and lower rate of difficulty in recycling the distal filtration protection devices.

关键词： stroke artery occlusion diseases carotid artery stent intervention self-expandable stents

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QIU Chang-lin’s Experience in the Differential Treatment of Senile dementia Based on Phlegm

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Journal of Traditional Chinese Medicine 2009年第2期29卷 131-136页

作者：林祖辉 TCM department of Cardio-cerebral-vascular Diseases Lishui Municipal People’s HospitalLishui 323000 China

Senile dementia refers to the various dementia syndromes occurring in the geratic period, including Alzheimer’s dementia (AD), vascular dementia (VD), and mixed type dementia. It is mainly manifested by disturbance o... 详细信息

关键词：老年性痴呆辨证治疗化痰老年痴呆症阿尔茨海默氏症中医临床实践痴呆综合征血管性痴呆

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deciphering the role of PGC-1α in neurological disorders: from mitochondrial dysfunction to synaptic failure

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Neural Regeneration Research 2022年第2期17卷 237-245页

作者： Jessica D.Panes Aline Wendt Oscar Ramirez-Molina Patricio A.Castro Jorge Fuentealba laboratorio de Screening de Compuestos Neuroactivos(LSCN) Departamento de FisiologiaFacultad de Ciencias BiologicasUniversidad de ConcepcionConcepcionChile Centro de Investigaciones Avanzadas en Biomedicina(CIAB-UdeC) Facultad de Ciencias BiologicasUniversidad de ConcepcionConcepcionChile departamento de Fisiologia Facultad de Ciencias BiologicasUniversidad de ConcepcionConcepcionChile

The onset and mechanisms underlying neurodegenerative diseases remain uncertain. The main features of neurodegenerative diseases have been related with cellular and molecular events like neuronal loss, mitochondrial dysfunction and aberrant accumulation of misfolded proteins or peptides in specific areas of the brain. The most prevalent neurodegenerative diseases belonging to age-related pathologies are Alzheimer's disease, Huntington's disease, Parkinson's disease and amyotrophic lateral sclerosis. Interestingly, mitochondrial dysfunction has been observed to occur during the early onset of several neuropathological events associated to neurodegenerative diseases. The master regulator of mitochondrial quality control and energetic metabolism is the transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PGC-1α). Additionally, it has been observed that PGC-1α appears to be a key factor in maintaining neuronal survival and synaptic transmission. In fact, PGC-1α downregulation in different brain areas(hippocampus, substantia nigra, cortex, striatum and spinal cord) that occurs in function of neurological damage including oxidative stress, neuronal loss, and motor disorders has been seen in several animal and cellular models of neurodegenerative diseases. Current evidence indicates that PGC-1α upregulation may serve as a potent therapeutic approach against development and progression of neuronal damage. Remarkably, increasing evidence shows that PGC-1α deficient mice have neurodegenerative diseases-like features, as well as neurological abnormalities. Finally, we discuss recent studies showing novel specific PGC-1α isoforms in the central nervous system that appear to exert a key role in the age of onset of neurodegenerative diseases and have a neuroprotective function in the central nervous system, thus opening a new molecular strategy for treatment of neurodegenerative diseases. The purpose of this review is to provide an up-to-date overview of the PGC-1α role in the physio

关键词： Alzheimer's disease amyotrophic lateral sclerosis Huntington's disease mitochondrial dysfunction Parkinson's disease PGC-1α synaptic function vascular dementia

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