Autophagy is required for endothelial cell alignment and atheroprotection under physiological blood flow
It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to lowSS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms hav...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 114; no. 41; pp. E8675 - E8684 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
10.10.2017
|
| Series | PNAS Plus |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 1091-6490 |
| DOI | 10.1073/pnas.1702223114 |
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| Abstract | It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to lowSS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins tomaintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α–induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. |
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| AbstractList | Atherosclerotic plaques tend to develop preferentially in areas of the vasculature exposed to low and disturbed shear stress (SS), but the mechanisms are not fully understood. In this study, we demonstrate that inefficient autophagy contributes to the development of atherosclerotic plaques in low-SS areas. Defective endothelial autophagy not only curbs endothelial alignment with the direction of blood flow, but also promotes an inflammatory, apoptotic, and senescent phenotype. Furthermore, genetic inactivation of endothelial autophagy in a murine model of atherosclerosis increases plaque burden exclusively in high-SS areas that are normally resistant to atherosclerotic plaque development. Altogether, these findings underline the role of endothelial autophagic flux activation by SS as an atheroprotective mechanism. It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins to maintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α–induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. Atherosclerotic plaques tend to develop preferentially in areas of the vasculature exposed to low and disturbed shear stress (SS), but the mechanisms are not fully understood. In this study, we demonstrate that inefficient autophagy contributes to the development of atherosclerotic plaques in low-SS areas. Defective endothelial autophagy not only curbs endothelial alignment with the direction of blood flow, but also promotes an inflammatory, apoptotic, and senescent phenotype. Furthermore, genetic inactivation of endothelial autophagy in a murine model of atherosclerosis increases plaque burden exclusively in high-SS areas that are normally resistant to atherosclerotic plaque development. Altogether, these findings underline the role of endothelial autophagic flux activation by SS as an atheroprotective mechanism. It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins to maintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α–induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins to maintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α-induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins to maintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKa inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α--induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins to maintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α-induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation.It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to low SS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins to maintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α-induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. It has been known for some time that atherosclerotic lesions preferentially develop in areas exposed to lowSS and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype. Conversely, areas exposed to high SS are protected from plaque development, but the mechanisms have remained elusive. Autophagy is a protective mechanism that allows recycling of defective organelles and proteins tomaintain cellular homeostasis. We aimed to understand the role of endothelial autophagy in the atheroprotective effect of high SS. Atheroprotective high SS stimulated endothelial autophagic flux in human and murine arteries. On the contrary, endothelial cells exposed to atheroprone low SS were characterized by inefficient autophagy as a result of mammalian target of rapamycin (mTOR) activation, AMPKα inhibition, and blockade of the autophagic flux. In hypercholesterolemic mice, deficiency in endothelial autophagy increased plaque burden only in the atheroresistant areas exposed to high SS; plaque size was unchanged in atheroprone areas, in which endothelial autophagy flux is already blocked. In cultured cells and in transgenic mice, deficiency in endothelial autophagy was characterized by defects in endothelial alignment with flow direction, a hallmark of endothelial cell health. This effect was associated with an increase in endothelial apoptosis and senescence in high-SS regions. Deficiency in endothelial autophagy also increased TNF-α–induced inflammation under high-SS conditions and decreased expression of the antiinflammatory factor KLF-2. Altogether, these results show that adequate endothelial autophagic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, senescence, and inflammation. |
| Author | Dupont, Nicolas Pic, Isabelle Lafaurie-Janvore, Julie Boulanger, Chantal M. Souyri, Michele Codogno, Patrice Hammoutene, Adel Busse, Johanna Kheloufi, Marouane Barakat, Abdul I. Julia, Pierre Viollet, Benoit Loyer, Xavier Rautou, Pierre-Emmanuel Vion, Anne-Clemence Lasselin, Juliette Poisson, Johanne Tedgui, Alain Devue, Cecile Stark, Konstantin |
| Author_xml | – sequence: 1 givenname: Anne-Clemence surname: Vion fullname: Vion, Anne-Clemence organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 2 givenname: Marouane surname: Kheloufi fullname: Kheloufi, Marouane organization: Université Paris Diderot, Sorbonne Paris Cité, 75013 Paris, France – sequence: 3 givenname: Adel surname: Hammoutene fullname: Hammoutene, Adel organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 4 givenname: Johanne surname: Poisson fullname: Poisson, Johanne organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 5 givenname: Juliette surname: Lasselin fullname: Lasselin, Juliette organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 6 givenname: Cecile surname: Devue fullname: Devue, Cecile organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 7 givenname: Isabelle surname: Pic fullname: Pic, Isabelle organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 8 givenname: Nicolas surname: Dupont fullname: Dupont, Nicolas organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 9 givenname: Johanna surname: Busse fullname: Busse, Johanna organization: Medizinische Klinik I, Klinikum der Universität München, 81377 Munich, Germany – sequence: 10 givenname: Konstantin surname: Stark fullname: Stark, Konstantin organization: Medizinische Klinik I, Klinikum der Universität München, 81377 Munich, Germany – sequence: 11 givenname: Julie surname: Lafaurie-Janvore fullname: Lafaurie-Janvore, Julie organization: Mechanics & Living Systems, Cardiovascular Cellular Engineering, Laboratoire d’Hydrodynamique, Ecole Polytechnique, UMR 7646, 91128 Palaiseau, France – sequence: 12 givenname: Abdul I. surname: Barakat fullname: Barakat, Abdul I. organization: Mechanics & Living Systems, Cardiovascular Cellular Engineering, Laboratoire d’Hydrodynamique, Ecole Polytechnique, UMR 7646, 91128 Palaiseau, France – sequence: 13 givenname: Xavier surname: Loyer fullname: Loyer, Xavier organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 14 givenname: Michele surname: Souyri fullname: Souyri, Michele organization: INSERM UMR_S1131/IHU/Université Paris Diderot, 75013 Paris, France – sequence: 15 givenname: Benoit surname: Viollet fullname: Viollet, Benoit organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 16 givenname: Pierre surname: Julia fullname: Julia, Pierre organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 17 givenname: Alain surname: Tedgui fullname: Tedgui, Alain organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 18 givenname: Patrice surname: Codogno fullname: Codogno, Patrice organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 19 givenname: Chantal M. surname: Boulanger fullname: Boulanger, Chantal M. organization: Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France – sequence: 20 givenname: Pierre-Emmanuel surname: Rautou fullname: Rautou, Pierre-Emmanuel organization: Université Paris Diderot, Sorbonne Paris Cité, 75013 Paris, France |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28973855$$D View this record in MEDLINE/PubMed https://nantes-universite.hal.science/hal-03367419$$DView record in HAL |
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| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 Author contributions: A.-C.V., M.K., C.M.B., and P.-E.R. designed research; A.-C.V., M.K., A.H., J.P., J.L., C.D., I.P., J.B., K.S., J.L.-J., X.L., and C.M.B. performed research; N.D., K.S., J.L.-J., A.I.B., M.S., B.V., P.J., and P.C. contributed new reagents/analytic tools; A.-C.V., M.K., X.L., A.T., P.C., C.M.B., and P.-E.R. analyzed data; and A.-C.V., M.K., A.T., P.C., C.M.B., and P.-E.R. wrote the paper. 1A.-C.V. and M.K. contributed equally to this work. Edited by Beth Levine, The University of Texas Southwestern Medical Center, Dallas, TX, and approved August 23, 2017 (received for review February 10, 2017) 2C.M.B. and P.-E.R. contributed equally to this work. |
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| SubjectTerms | Alignment Apoptosis Arteries Arteriosclerosis Atherosclerosis Biological Sciences Blood flow Cardiology and cardiovascular system Cellular Biology Endothelial cells Endothelium Exposure Fluctuations Flux Homeostasis Human health and pathology Inflammation Lesions Life Sciences Mice Organelles Phagocytosis PNAS Plus Proteins Rapamycin Senescence Shear stress TOR protein Transgenic mice Tumor necrosis factor-α |
| Title | Autophagy is required for endothelial cell alignment and atheroprotection under physiological blood flow |
| URI | https://www.jstor.org/stable/26488722 https://www.ncbi.nlm.nih.gov/pubmed/28973855 https://www.proquest.com/docview/1970169755 https://www.proquest.com/docview/1947096385 https://nantes-universite.hal.science/hal-03367419 https://pubmed.ncbi.nlm.nih.gov/PMC5642679 |
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