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Loss of endothelial YAP/TAZ reduces the size of chronic stroke lesions and alters the endothelial environment

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Title: Loss of endothelial YAP/TAZ reduces the size of chronic stroke lesions and alters the endothelial environment
Authors: Göttert, Ria, Kikhia, Majed, Herzog, Marie-Louise, Pan, Wen, Klaus-Bergmann, Alexandra, Weiner, January, Beule, Dieter, Knauss, Samuel, Kronenberg, Golo, Bader, Michael, Gerhardt, Holger, Endres, Matthias, Gertz, Karen
Publisher Information: American Heart Association
Publication Year: 2026
Collection: Max-Delbrueck-Center for Molecular Medicine, Berlin: MDC Repository
Subject Terms: Cardiovascular and Metabolic Diseases, Topic 3: Integrative Biomedicine
Description: BACKGROUND: Ischemic stroke remains a leading cause of morbidity and mortality worldwide, with limited treatment options available. Vascular dysfunction is a key pathomechanism, and brain endothelial cells (bECs) play a critical role in determining stroke outcomes. This study investigates the specific roles of YAP (yes-associated protein 1) and TAZ (WW domain containing transcription regulator 1) in regulating bEC functions during stroke. METHODS: Mice underwent 30-minute middle cerebral artery occlusion (MCAo) followed by reperfusion to model ischemic stroke. TAZ reporter mice were used to track stroke-induced subcellular changes in TAZ expression. Tamoxifen-inducible endothelial-specific Yap/Taz knockout and control mice were used to study YAP/TAZ's role in bEC function post-stroke. Stroke outcomes were measured by magnetic resonance imaging and NeuN (neuronal nuclei)-associated lesion analysis. Properties of bECs were assessed via immunohistochemistry and RNA sequencing. Inflammatory parameters were analyzed by flow cytometry of brain immune cells and quantitative polymerase chain reaction. RESULTS: Middle cerebral artery occlusion/reperfusion regulated Yap, Taz, and YAP/TAZ target gene expression in the brain. TAZ reporter mice confirmed stroke-induced endothelial YAP/TAZ activation. Endothelial-specific loss of YAP/TAZ reduced infarct volumes at 4 weeks after MCAo without impairing stroke-induced angiogenesis, revealing an unexpected neuroprotective role for endothelial YAP/TAZ depletion. YAP/TAZ deficiency modulated cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) and Wnt (wingless-related integration site) signaling genes in bECs and promoted myeloid cell recruitment and an anti-inflammatory vascular environment during the subacute phase of stroke. CONCLUSIONS: Our data suggest that endothelial YAP/TAZ affects the inflammatory milieu subacutely after ischemia and thereby influences the chronic course of stroke. Modulation of YAP/TAZ activity in ECs may be a promising therapeutic target ...
Document Type: article in journal/newspaper
File Description: application/pdf; other
Language: English
Relation: https://edoc.mdc-berlin.de/id/eprint/25942/1/25942oa.pdf; https://edoc.mdc-berlin.de/id/eprint/25942/2/25942suppl.zip; Loss of endothelial YAP/TAZ reduces the size of chronic stroke lesions and alters the endothelial environment. Göttert, Ria, Kikhia, Majed, Herzog, Marie-Louise, Pan, Wen, Klaus-Bergmann, Alexandra, Weiner, January, Beule, Dieter, Knauss, Samuel, Kronenberg, Golo, Bader, Michael, Gerhardt, Holger, Endres, Matthias and Gertz, Karen Journal of the American Heart Association 15 (6): e040079. 17 March 2026; PMID:41294142; https://doi.org/10.1161/jaha.124.040079
DOI: 10.1161/jaha.124.040079
Availability: https://edoc.mdc-berlin.de/id/eprint/25942/
https://edoc.mdc-berlin.de/25942/
https://doi.org/10.1161/jaha.124.040079
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Accession Number: edsbas.AC8C8C93
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  Data: Loss of endothelial YAP/TAZ reduces the size of chronic stroke lesions and alters the endothelial environment
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  Data: <searchLink fieldCode="AR" term="%22Göttert%2C+Ria%22">Göttert, Ria</searchLink><br /><searchLink fieldCode="AR" term="%22Kikhia%2C+Majed%22">Kikhia, Majed</searchLink><br /><searchLink fieldCode="AR" term="%22Herzog%2C+Marie-Louise%22">Herzog, Marie-Louise</searchLink><br /><searchLink fieldCode="AR" term="%22Pan%2C+Wen%22">Pan, Wen</searchLink><br /><searchLink fieldCode="AR" term="%22Klaus-Bergmann%2C+Alexandra%22">Klaus-Bergmann, Alexandra</searchLink><br /><searchLink fieldCode="AR" term="%22Weiner%2C+January%22">Weiner, January</searchLink><br /><searchLink fieldCode="AR" term="%22Beule%2C+Dieter%22">Beule, Dieter</searchLink><br /><searchLink fieldCode="AR" term="%22Knauss%2C+Samuel%22">Knauss, Samuel</searchLink><br /><searchLink fieldCode="AR" term="%22Kronenberg%2C+Golo%22">Kronenberg, Golo</searchLink><br /><searchLink fieldCode="AR" term="%22Bader%2C+Michael%22">Bader, Michael</searchLink><br /><searchLink fieldCode="AR" term="%22Gerhardt%2C+Holger%22">Gerhardt, Holger</searchLink><br /><searchLink fieldCode="AR" term="%22Endres%2C+Matthias%22">Endres, Matthias</searchLink><br /><searchLink fieldCode="AR" term="%22Gertz%2C+Karen%22">Gertz, Karen</searchLink>
– Name: Publisher
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  Data: American Heart Association
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  Label: Publication Year
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  Data: 2026
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  Data: Max-Delbrueck-Center for Molecular Medicine, Berlin: MDC Repository
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  Data: <searchLink fieldCode="DE" term="%22Cardiovascular+and+Metabolic+Diseases%22">Cardiovascular and Metabolic Diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Topic+3%3A+Integrative+Biomedicine%22">Topic 3: Integrative Biomedicine</searchLink>
– Name: Abstract
  Label: Description
  Group: Ab
  Data: BACKGROUND: Ischemic stroke remains a leading cause of morbidity and mortality worldwide, with limited treatment options available. Vascular dysfunction is a key pathomechanism, and brain endothelial cells (bECs) play a critical role in determining stroke outcomes. This study investigates the specific roles of YAP (yes-associated protein 1) and TAZ (WW domain containing transcription regulator 1) in regulating bEC functions during stroke. METHODS: Mice underwent 30-minute middle cerebral artery occlusion (MCAo) followed by reperfusion to model ischemic stroke. TAZ reporter mice were used to track stroke-induced subcellular changes in TAZ expression. Tamoxifen-inducible endothelial-specific Yap/Taz knockout and control mice were used to study YAP/TAZ's role in bEC function post-stroke. Stroke outcomes were measured by magnetic resonance imaging and NeuN (neuronal nuclei)-associated lesion analysis. Properties of bECs were assessed via immunohistochemistry and RNA sequencing. Inflammatory parameters were analyzed by flow cytometry of brain immune cells and quantitative polymerase chain reaction. RESULTS: Middle cerebral artery occlusion/reperfusion regulated Yap, Taz, and YAP/TAZ target gene expression in the brain. TAZ reporter mice confirmed stroke-induced endothelial YAP/TAZ activation. Endothelial-specific loss of YAP/TAZ reduced infarct volumes at 4 weeks after MCAo without impairing stroke-induced angiogenesis, revealing an unexpected neuroprotective role for endothelial YAP/TAZ depletion. YAP/TAZ deficiency modulated cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) and Wnt (wingless-related integration site) signaling genes in bECs and promoted myeloid cell recruitment and an anti-inflammatory vascular environment during the subacute phase of stroke. CONCLUSIONS: Our data suggest that endothelial YAP/TAZ affects the inflammatory milieu subacutely after ischemia and thereby influences the chronic course of stroke. Modulation of YAP/TAZ activity in ECs may be a promising therapeutic target ...
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  Data: https://edoc.mdc-berlin.de/id/eprint/25942/1/25942oa.pdf; https://edoc.mdc-berlin.de/id/eprint/25942/2/25942suppl.zip; Loss of endothelial YAP/TAZ reduces the size of chronic stroke lesions and alters the endothelial environment. Göttert, Ria, Kikhia, Majed, Herzog, Marie-Louise, Pan, Wen, Klaus-Bergmann, Alexandra, Weiner, January, Beule, Dieter, Knauss, Samuel, Kronenberg, Golo, Bader, Michael, Gerhardt, Holger, Endres, Matthias and Gertz, Karen Journal of the American Heart Association 15 (6): e040079. 17 March 2026; PMID:41294142; https://doi.org/10.1161/jaha.124.040079
– Name: DOI
  Label: DOI
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  Data: 10.1161/jaha.124.040079
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  Data: https://edoc.mdc-berlin.de/id/eprint/25942/<br />https://edoc.mdc-berlin.de/25942/<br />https://doi.org/10.1161/jaha.124.040079
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