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Article ; Online: Cyclic stretch promotes vascular homing of endothelial progenitor cells via Acsl1 regulation of mitochondrial fatty acid oxidation.

Han, Yue / Yan, Jing / Li, Zhi-Yin / Fan, Yang-Jing / Jiang, Zong-Lai / Shyy, John Y-J / Chien, Shu

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 6, Page(s) e2219630120

Abstract: Endothelial progenitor cells (EPCs) play an important role in vascular repair and re-endothelialization after vessel injury. EPCs in blood vessels are subjected to cyclic stretch (CS) due to the pulsatile pressure, but the role of CS in metabolic ... ...

Abstract	Endothelial progenitor cells (EPCs) play an important role in vascular repair and re-endothelialization after vessel injury. EPCs in blood vessels are subjected to cyclic stretch (CS) due to the pulsatile pressure, but the role of CS in metabolic reprogramming of EPC, particularly its vascular homing and repair, is largely unknown. In the current study, physiological CS applied to EPCs at a magnitude of 10% and a frequency of 1 Hz significantly promoted their vascular adhesion and endothelial differentiation. CS enhanced mitochondrial elongation and oxidative phosphorylation (OXPHOS), as well as adenosine triphosphate production. Metabolomic study and Ultra-high performance liquid chromatography-mass spectrometry assay revealed that CS significantly decreased the content of long-chain fatty acids (LCFAs) and markedly induced long-chain fatty acyl-CoA synthetase 1 (Acsl1), which in turn facilitated the catabolism of LCFAs in mitochondria via fatty acid β-oxidation and OXPHOS. In a rat carotid artery injury model, transplantation of EPCs overexpressing Acsl1 enhanced the adhesion and re-endothelialization of EPCs in vivo. MRI and vascular morphology staining showed that Acsl1 overexpression in EPCs improved vascular repair and inhibited vascular stenosis. This study reveals a mechanotransduction mechanism by which physiological CS enhances endothelial repair via EPC patency.
MeSH term(s)	Rats ; Animals ; Endothelial Progenitor Cells ; Mechanotransduction, Cellular ; Cell Differentiation ; Mitochondria/metabolism ; Fatty Acids/metabolism
Chemical Substances	Fatty Acids
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2219630120
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Article: Mechanobiology and Vascular Remodeling: From Membrane to Nucleus.

Qi, Ying-Xin / Han, Yue / Jiang, Zong-Lai

Advances in experimental medicine and biology

2018 Volume 1097, Page(s) 69–82

Abstract: Vascular endothelial cells (ECs) and smooth muscle cells (VSMCs) are constantly exposed to hemodynamic forces in vivo, including flow shear stress and cyclic stretch caused by the blood flow. Numerous researches revealed that during various ... ...

Abstract	Vascular endothelial cells (ECs) and smooth muscle cells (VSMCs) are constantly exposed to hemodynamic forces in vivo, including flow shear stress and cyclic stretch caused by the blood flow. Numerous researches revealed that during various cardiovascular diseases such as atherosclerosis, hypertension, and vein graft, abnormal (pathological) mechanical forces play crucial roles in the dysfunction of ECs and VSMCs, which is the fundamental process during both vascular homeostasis and remodeling. Hemodynamic forces trigger several membrane molecules and structures, such as integrin, ion channel, primary cilia, etc., and induce the cascade reaction processes through complicated cellular signaling networks. Recent researches suggest that nuclear envelope proteins act as the functional homology of molecules on the membrane, are important mechanosensitive molecules which modulate chromatin location and gene transcription, and subsequently regulate cellular functions. However, the studies on the roles of nucleus in the mechanotransduction process are still at the beginning. Here, based on the recent researches, we focused on the nuclear envelope proteins and discussed the roles of pathological hemodynamic forces in vascular remodeling. It may provide new insight into understanding the molecular mechanism of vascular physiological homeostasis and pathophysiological remodeling and may help to develop hemodynamic-based strategies for the prevention and management of vascular diseases.
MeSH term(s)	Endothelial Cells/cytology ; Humans ; Mechanotransduction, Cellular ; Myocytes, Smooth Muscle/cytology ; Nuclear Envelope ; Nuclear Proteins ; Stress, Mechanical ; Vascular Remodeling
Chemical Substances	Nuclear Proteins
Language	English
Publishing date	2018-10-12
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-96445-4_4
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Article ; Online: MicroRNA-29a Involvement in Phenotypic Transformation of Venous Smooth Muscle Cells Via Ten-Eleven Translocation Methylcytosinedioxygenase 1 in Response to Mechanical Cyclic Stretch.

Liu, Ji-Ting / Liu, Ze / Chen, Yi / Qi, Ying-Xin / Yao, Qing-Ping / Jiang, Zong-Lai

Journal of biomechanical engineering

2020 Volume 142, Issue 5

Abstract: Mechanical stimuli play an important role in vein graft restenosis and the abnormal migration and proliferation of vascular smooth muscle cells (VSMCs) are pathological processes contributing to this disorder. Here, based on previous high-throughput ... ...

Abstract	Mechanical stimuli play an important role in vein graft restenosis and the abnormal migration and proliferation of vascular smooth muscle cells (VSMCs) are pathological processes contributing to this disorder. Here, based on previous high-throughput sequencing data from vein grafts, miR-29a-3p and its target, the role of Ten-eleven translocation methylcytosinedioxygenase 1 (TET1) in phenotypic transformation of VSMCs induced by mechanical stretch was investigated. Vein grafts were generated by using the "cuff" technique in rats. Deep transcriptome sequencing revealed that the expression of TET1 was significantly decreased, a process confirmed by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) analysis. MicroRNA-seq showed that miR-29a-3p was significantly up-regulated, targeting TET1 as predicted by Targetscan. Bioinformatics analysis indicated that the co-expressed genes with TET1 might modulate VSMC contraction. Venous VSMCs exposed to 10%-1.25 Hz cyclic stretch by using the Flexcell system were used to simulate arterial mechanical conditions in vitro. RT-qPCR revealed that mechanical stretch increased the expression of miR-29a-3p at 3 h. Western blot analysis showed that TET1 was significantly decreased, switching contractile VSMCs to cells with a synthetic phenotype. miR-29a-3p mimics (MI) and inhibitor (IN) transfection confirmed the negative impact of miR-29a-3p on TET1. Taken together, results from this investigation demonstrate that mechanical stretch modulates venous VSMC phenotypic transformation via the mediation of the miR-29a-3p/TET1 signaling pathway. miR-29a-3p may have potential clinical implications in the pathogenesis of remodeling of vein graft restenosis.
MeSH term(s)	Animals ; Cell Proliferation ; MicroRNAs ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Rats
Chemical Substances	MicroRNAs
Language	English
Publishing date	2020-12-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	243094-0
ISSN	1528-8951 ; 0148-0731
ISSN (online)	1528-8951
ISSN	0148-0731
DOI	10.1115/1.4044581
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Article ; Online: Platelet-derived microvesicles promote endothelial progenitor cell proliferation in intimal injury by delivering TGF-β1.

Yan, Jing / Bao, Han / Fan, Yang-Jing / Jiang, Zong-Lai / Qi, Ying-Xin / Han, Yue

The FEBS journal

2020 Volume 287, Issue 23, Page(s) 5196–5217

Abstract: Intimal injury is an early stage of several cardiovascular diseases. Endothelial progenitor cells (EPCs) play a significant role in endothelial repair following vascular injury. Once the intima is damaged, EPCs are mobilized from the bone marrow to the ... ...

Abstract	Intimal injury is an early stage of several cardiovascular diseases. Endothelial progenitor cells (EPCs) play a significant role in endothelial repair following vascular injury. Once the intima is damaged, EPCs are mobilized from the bone marrow to the injury site. Meanwhile, the injury to the intimal surface triggers platelet degranulation, aggregation, and adhesion to the damaged endothelium, and exposed collagen stimulates platelet to secrete platelet-derived microvesicles (PMVs). However, the role of PMVs in EPC function during this process remains unknown. In an in vivo study, EPCs and platelets were found to adhere to the injury site in Sprague-Dawley (SD) rat vascular injury model. In vitro, collagen stimulation induced the release of PMVs, and collagen-activated PMVs (ac.PMVs) significantly promoted EPC proliferation. Transforming growth factor-β1 (TGF-β1) content was increased in ac.PMVs. Activated PMVs significantly upregulated Smad3 phosphorylation in EPCs and increased Smad3 nuclear translocation from the cytoplasm. TGF-β1 knockdown ac.PMVs downregulated EPC proliferation. Recombinant TGF-β1 enhanced EPC proliferation. The TGF-β1 inhibitor SB431542 significantly repressed the intracellular signal triggered by ac.PMVs. Furthermore, the Smad3-specific phosphorylation inhibitor SIS3 effectively reversed the cell proliferation induced by ac.PMVs. Smad3 translocated to the nucleus and enhanced EPC proliferation via its downstream genes tenascin C (TNC), CDKN1A, and CDKN2A. r-TGF-β1 promoted reendothelialization and EPC proliferation in vivo. Our data demonstrate that activated PMVs deliver TGF-β1 from collagen-activated platelets to EPCs, which in turn activates Smad3 phosphorylation and regulates TNC, CDKN1A, and CDKN2A expression to promote EPC proliferation, suggesting that PMVs act as a key transporter and a potential therapeutic target for vascular injury.
MeSH term(s)	Animals ; Blood Platelets/metabolism ; Carotid Artery Injuries/metabolism ; Carotid Artery Injuries/pathology ; Carotid Artery Injuries/therapy ; Carotid Intima-Media Thickness ; Cell Differentiation ; Cell Proliferation ; Cell-Derived Microparticles/metabolism ; Cell-Derived Microparticles/transplantation ; Cells, Cultured ; Endothelial Progenitor Cells/cytology ; Male ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Transforming Growth Factor beta1/metabolism ; Tunica Intima/injuries ; Tunica Intima/metabolism
Chemical Substances	Transforming Growth Factor beta1
Language	English
Publishing date	2020-03-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15293
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Article: Mechanical behavior and wall remodeling of blood vessels under axial twist.

Han, Hai-Chao / Liu, Qin / Jiang, Zong-Lai

Yi yong sheng wu li xue

2016 Volume 31, Issue 4, Page(s) 319–326

Abstract: Blood vessels are often subjected to axial torsion (or twist) due to body movement or surgery. However, there are few studies on blood vessel under twist. This review first summarizes the clinical observation on the twist of blood vessels and then ... ...

Abstract	Blood vessels are often subjected to axial torsion (or twist) due to body movement or surgery. However, there are few studies on blood vessel under twist. This review first summarizes the clinical observation on the twist of blood vessels and then presents what we know about the mechanical behaviors of blood vessel under twist, including the constitutive models. The state of art researches on the remodeling of blood vessels under twist via
Language	English
Publishing date	2016-09-14
Publishing country	China
Document type	Journal Article
ISSN	1004-7220
ISSN	1004-7220
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Article ; Online: Arterial cyclic stretch regulates Lamtor1 and promotes neointimal hyperplasia via circSlc8a1/miR-20a-5p axis in vein grafts.

Liu, Ji-Ting / Yao, Qing-Ping / Chen, Yi / Lv, Fan / Liu, Ze / Bao, Han / Han, Yue / Zhang, Ming-Liang / Jiang, Zong-Lai / Qi, Ying-Xin

Theranostics

2022 Volume 12, Issue 11, Page(s) 4851–4865

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Animals ; Cell Proliferation/genetics ; Hyperplasia ; In Situ Hybridization, Fluorescence ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neointima ; RNA, Small Interfering
Chemical Substances	MicroRNAs ; RNA, Small Interfering ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2022-06-21
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.69551
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Article ; Online: Platelet-derived microvesicles regulate vascular smooth muscle cell energy metabolism via PRKAA after intimal injury.

Yan, Jing / Fan, Yang-Jing / Bao, Han / Li, Yong-Guang / Zhang, Shou-Min / Yao, Qing-Ping / Huo, Yun-Long / Jiang, Zong-Lai / Qi, Ying-Xin / Han, Yue

Journal of cell science

2022 Volume 135, Issue 7

Abstract: Vascular intimal injury initiates various cardiovascular disease processes. Exposure to subendothelial collagen can cause platelet activation, leading to collagen-activated platelet-derived microvesicles (aPMVs) secretion. In addition, vascular smooth ... ...

Abstract	Vascular intimal injury initiates various cardiovascular disease processes. Exposure to subendothelial collagen can cause platelet activation, leading to collagen-activated platelet-derived microvesicles (aPMVs) secretion. In addition, vascular smooth muscle cells (VSMCs) exposed to large amounts of aPMVs undergo abnormal energy metabolism; they proliferate excessively and migrate after the loss of endothelium, eventually contributing to neointimal hyperplasia. However, the roles of aPMVs in VSMC energy metabolism are still unknown. Our carotid artery intimal injury model indicated that platelets adhered to injured blood vessels. In vitro, phosphorylated Pka (cAMP-dependent protein kinase) content was increased in aPMVs. We also found that aPMVs significantly reduced VSMC glycolysis and increased oxidative phosphorylation, and promoted VSMC migration and proliferation by upregulating phosphorylated PRKAA (α catalytic subunit of AMP-activated protein kinase) and phosphorylated FoxO1. Compound C, an inhibitor of PRKAA, effectively reversed the enhancement of cellular function and energy metabolism triggered by aPMVs in vitro and neointimal formation in vivo. We show that aPMVs can affect VSMC energy metabolism through the Pka-PRKAA-FoxO1 signaling pathway and this ultimately affects VSMC function, indicating that the shift in VSMC metabolic phenotype by aPMVs can be considered a potential target for the inhibition of hyperplasia. This provides a new perspective for regulating the abnormal activity of VSMCs after injury.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Animals ; Blood Platelets/metabolism ; Carotid Artery Injuries/genetics ; Carotid Artery Injuries/metabolism ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Disease Models, Animal ; Energy Metabolism ; Humans ; Hyperplasia/complications ; Hyperplasia/metabolism ; Hyperplasia/pathology ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Neointima/complications ; Neointima/metabolism ; Neointima/pathology
Chemical Substances	Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2022-04-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.259364
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Zs.A 1200: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Endothelial microparticles induced by cyclic stretch activate Src and modulate cell apoptosis.

Zhuang, Fei / Bao, Han / Shi, Qian / Li, Jing / Jiang, Zong-Lai / Wang, Yingxiao / Qi, Ying-Xin

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2020 Volume 34, Issue 10, Page(s) 13586–13596

Abstract: Endothelial microparticles (EMPs) are involved in various cardiovascular pathologies and play remarkable roles in communication between endothelial cells (ECs), which are constantly exposed to mechanical cyclic stretch (CS) following blood pressure. ... ...

Abstract	Endothelial microparticles (EMPs) are involved in various cardiovascular pathologies and play remarkable roles in communication between endothelial cells (ECs), which are constantly exposed to mechanical cyclic stretch (CS) following blood pressure. However, the roles of EMPs induced by CS in EC homeostasis are still unclear. Both fluorescence resonance energy transfer (FRET) and western blotting revealed the activation of Src in ECs was significantly increased by 5% CS-induced EMPs. Furthermore, proteomic analysis revealed that the contents were obvious different in the EMPs between 5%- and 15%-group. Based on the bioinformatic analysis, CD151 on EMPs was predicted to activate Src, which was further confirmed by both FRET and western blotting. Moreover, the expression of CD151 on EMPs was significantly increased by 5% CS and involved in the binding of EMPs to ECs. EC apoptosis, which was significantly decreased by 5% CS-derived EMPs, showed obvious increase after pretreatment with Src inhibitor in target ECs. Our present research suggests that mechanical stretch changes the components of EMPs, which in turn modulates EC apoptosis by Src activation. CD151 expressed on CS-induced EMPs may play important roles in EC communication and homeostasis.
MeSH term(s)	Animals ; Apoptosis ; Cell-Derived Microparticles/physiology ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Rats ; Stress, Mechanical ; Tetraspanin 24/metabolism ; src-Family Kinases/metabolism
Chemical Substances	Cd151 protein, rat ; Tetraspanin 24 ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2020-08-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202000581R
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Endothelial microvesicles induced by physiological cyclic stretch inhibit ICAM1-Dependent leukocyte adhesion.

Zhuang, Fei / Shi, Qian / Wang, Wen-Bin / Bao, Han / Yan, Jing / Gao, Shuang / Liu, Ze / Jiang, Zong-Lai / Qi, Ying-Xin

Experimental cell research

2019 Volume 386, Issue 1, Page(s) 111710

Abstract: Physiological cyclic stretch (CS), caused by artery deformation following blood pressure, plays important roles in the homeostasis of endothelial cells (ECs). Here, we detected the effect of physiological CS on endothelial microvesicles (EMVs) and their ... ...

Abstract	Physiological cyclic stretch (CS), caused by artery deformation following blood pressure, plays important roles in the homeostasis of endothelial cells (ECs). Here, we detected the effect of physiological CS on endothelial microvesicles (EMVs) and their roles in leukocyte recruitment to ECs, which is a crucial event in EC inflammation. The results showed compared with the static treatment, pretreatment of 5%-CS-derived EMVs with ECs significantly decreased the adherence level of leukocytes. Comparative proteomic analysis revealed 373 proteins differentially expressed between static-derived and 5%-CS-derived EMVs, in which 314 proteins were uniquely identified in static-derived EMVs, 34 proteins uniquely in 5%-CS-derived EMVs, and 25 proteins showed obvious differences. Based on the proteomic data, Ingenuity Pathways Analysis predicted intercellular adhesion molecule 1 (ICAM1) in EMVs might be the potential molecule involved in EC-leukocyte adhesion. Western blot and flow cytometry analyses confirmed the significant decrease of ICAM1 in 5%-CS-derived EMVs, which subsequently inhibited the phosphorylation of VE-cadherin at Tyr731 in target ECs. Moreover, leukocyte adhesion was obviously decreased after pretreatment with ICAM1 neutralizing antibody. Our present research suggested that physiological stretch changes the components of EMVs, which in turn inhibits leukocyte adhesion. ICAM1 expressed on CS-induced EMVs may play an important role in maintaining EC homeostasis.
MeSH term(s)	Animals ; Cadherins/metabolism ; Cell Adhesion ; Cell-Derived Microparticles/metabolism ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelial Cells/physiology ; Endothelium, Vascular/cytology ; Intercellular Adhesion Molecule-1/metabolism ; Leukocytes/metabolism ; Leukocytes/physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Stress, Mechanical
Chemical Substances	Cadherins ; Intercellular Adhesion Molecule-1 (126547-89-5)
Language	English
Publishing date	2019-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2019.111710
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Article: Platelet-Derived Microvesicles Promote VSMC Dedifferentiation After Intimal Injury via Src/Lamtor1/mTORC1 Signaling.

Liu, Ji-Ting / Bao, Han / Fan, Yang-Jing / Li, Zi-Tong / Yao, Qing-Ping / Han, Yue / Zhang, Ming-Liang / Jiang, Zong-Lai / Qi, Ying-Xin

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 744320

Abstract: Phenotypic switch of vascular smooth muscle cells (VSMCs) is important in vascular remodeling which causes hyperplasia and restenosis after intimal injury. Platelets are activated at injured intima and secrete platelet-derived microvesicles (PMVs). ... ...

Abstract	Phenotypic switch of vascular smooth muscle cells (VSMCs) is important in vascular remodeling which causes hyperplasia and restenosis after intimal injury. Platelets are activated at injured intima and secrete platelet-derived microvesicles (PMVs). Herein, we demonstrated the role of PMVs in VSMC phenotypic switch and the potential underlying mechanisms.
Language	English
Publishing date	2021-09-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.744320
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