Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress
Hypertension, a multifactorial chronic inflammatory condition, is an important risk factor for neurovascular and neurodegenerative diseases, including stroke and Alzheimer’s disease. These diseases have been associated with higher concentrations of circulating interleukin (IL)-17A. However, the poss...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/4/3959 |
| _version_ | 1797620397834764288 |
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| author | Jessica Youwakim Diane Vallerand Helene Girouard |
| author_facet | Jessica Youwakim Diane Vallerand Helene Girouard |
| author_sort | Jessica Youwakim |
| collection | DOAJ |
| description | Hypertension, a multifactorial chronic inflammatory condition, is an important risk factor for neurovascular and neurodegenerative diseases, including stroke and Alzheimer’s disease. These diseases have been associated with higher concentrations of circulating interleukin (IL)-17A. However, the possible role that IL-17A plays in linking hypertension with neurodegenerative diseases remains to be established. Cerebral blood flow regulation may be the crossroads of these conditions because regulating mechanisms may be altered in hypertension, including neurovascular coupling (NVC), known to participate in the pathogenesis of stroke and Alzheimer’s disease. In the present study, the role of IL-17A on NVC impairment induced by angiotensin (Ang) II in the context of hypertension was examined. Neutralization of IL-17A or specific inhibition of its receptor prevents the NVC impairment (<i>p</i> < 0.05) and cerebral superoxide anion production (<i>p</i> < 0.05) induced by Ang II. Chronic administration of IL-17A impairs NVC (<i>p</i> < 0.05) and increases superoxide anion production. Both effects were prevented with Tempol and NADPH oxidase 2 gene deletion. These findings suggest that IL-17A, through superoxide anion production, is an important mediator of cerebrovascular dysregulation induced by Ang II. This pathway is thus a putative therapeutic target to restore cerebrovascular regulation in hypertension. |
| first_indexed | 2024-03-11T08:41:45Z |
| format | Article |
| id | doaj.art-4ebefb38549f45d9a8b15f2d021d0979 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T08:41:45Z |
| publishDate | 2023-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-4ebefb38549f45d9a8b15f2d021d09792023-11-16T21:07:30ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-02-01244395910.3390/ijms24043959Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative StressJessica Youwakim0Diane Vallerand1Helene Girouard2Département de Pharmacologie et Physiologie, Université de Montréal, Montreal, QC H3T 1J4, CanadaDépartement de Pharmacologie et Physiologie, Université de Montréal, Montreal, QC H3T 1J4, CanadaDépartement de Pharmacologie et Physiologie, Université de Montréal, Montreal, QC H3T 1J4, CanadaHypertension, a multifactorial chronic inflammatory condition, is an important risk factor for neurovascular and neurodegenerative diseases, including stroke and Alzheimer’s disease. These diseases have been associated with higher concentrations of circulating interleukin (IL)-17A. However, the possible role that IL-17A plays in linking hypertension with neurodegenerative diseases remains to be established. Cerebral blood flow regulation may be the crossroads of these conditions because regulating mechanisms may be altered in hypertension, including neurovascular coupling (NVC), known to participate in the pathogenesis of stroke and Alzheimer’s disease. In the present study, the role of IL-17A on NVC impairment induced by angiotensin (Ang) II in the context of hypertension was examined. Neutralization of IL-17A or specific inhibition of its receptor prevents the NVC impairment (<i>p</i> < 0.05) and cerebral superoxide anion production (<i>p</i> < 0.05) induced by Ang II. Chronic administration of IL-17A impairs NVC (<i>p</i> < 0.05) and increases superoxide anion production. Both effects were prevented with Tempol and NADPH oxidase 2 gene deletion. These findings suggest that IL-17A, through superoxide anion production, is an important mediator of cerebrovascular dysregulation induced by Ang II. This pathway is thus a putative therapeutic target to restore cerebrovascular regulation in hypertension.https://www.mdpi.com/1422-0067/24/4/3959neurovascular couplingangiotensin IIhypertensioninterleukin-17ANADPH oxidase 2reactive oxygen species |
| spellingShingle | Jessica Youwakim Diane Vallerand Helene Girouard Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress International Journal of Molecular Sciences neurovascular coupling angiotensin II hypertension interleukin-17A NADPH oxidase 2 reactive oxygen species |
| title | Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress |
| title_full | Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress |
| title_fullStr | Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress |
| title_full_unstemmed | Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress |
| title_short | Neurovascular Coupling in Hypertension Is Impaired by IL-17A through Oxidative Stress |
| title_sort | neurovascular coupling in hypertension is impaired by il 17a through oxidative stress |
| topic | neurovascular coupling angiotensin II hypertension interleukin-17A NADPH oxidase 2 reactive oxygen species |
| url | https://www.mdpi.com/1422-0067/24/4/3959 |
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