PTP1B Modulates Carotid Plaque Vulnerability in Atherosclerosis Through Rab5‐PDGFRβ ‐Mediated Endocytosis Disruption and Apoptosis
Article Swipe
Xiaohong Zhang
,
Ran Xu
,
Tao Wang
,
Jiayao Li
,
Yixin Sun
,
Shengyan Cui
,
Zixuan Xing
,
X. R. Lyu
,
Ge Yang
,
Liqun Jiao
,
Wenjing Li
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1111/cns.70071
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1111/cns.70071
Background Protein tyrosine phosphatase 1B (PTP1B) is a protein tyrosine phosphatase and modulates platelet‐derived growth factor (PDGF)/platelet‐derived growth factor receptor (PDGFR) signaling in vascular smooth muscle cells (VSMCs) via endocytosis. However, the related molecular pathways that participated in the interaction of endo‐lysosome and the trafficking of PDGFR are largely unknown. This study aims to determine the subcellular regulating mechanism of PTP1B to the endo‐lysosome degradation of PDGFR in atherosclerotic carotid plaques, thereby offering a potential therapeutic target for the stabilization of carotid plaques. Methods The immunohistochemical staining technique was employed to assess the expression levels of both PDGFR‐β and Caspase 3 in stable and vulnerable carotid plaques. Tunnel staining was utilized to quantify the apoptosis of carotid plaques. Live‐cell imaging was employed to observe endocytic motility, while cell apoptosis was evaluated through Propidium Iodide staining. In an in vivo experiment, ApoE −/− mice were administered a PTP1B inhibitor to investigate the impact of PTP1B on atherosclerosis. Results The heightened expression of PDGFR‐β correlates with apoptosis in patients with vulnerable carotid plaques. At the subcellular level of VSMCs, PDGFR‐β plays a pivotal role in sustaining a balanced endocytosis system motility, regulated by the expression of Rab5, a key regulator of endocytic motility. And PTP1B modulates PDGFR‐β signaling via Rab5‐mediated endocytosis. Additionally, disrupted endocytic motility influences the interplay between endosomes and lysosomes, which is crucial for controlling PDGFR‐β trafficking. Elevated PTP1B expression induces cellular apoptosis and impedes migration and proliferation of carotid VSMCs. Ultimately, mice with PTP1B deficiency exhibit a reduction in atherosclerosis. Conclusion Our results illustrate that PTP1B induces disruption in endocytosis and apoptosis of VSMCs through the Rab5‐PDGFRβ pathway, suggesting a potential association with the heightened vulnerability of carotid plaques.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1111/cns.70071
- OA Status
- gold
- Cited By
- 2
- References
- 32
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4404197188
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4404197188Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1111/cns.70071Digital Object Identifier
- Title
-
PTP1B Modulates Carotid Plaque Vulnerability in Atherosclerosis Through Rab5‐PDGFRβ ‐Mediated Endocytosis Disruption and ApoptosisWork title - Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-11-01Full publication date if available
- Authors
-
Xiaohong Zhang, Ran Xu, Tao Wang, Jiayao Li, Yixin Sun, Shengyan Cui, Zixuan Xing, X. R. Lyu, Ge Yang, Liqun Jiao, Wenjing LiList of authors in order
- Landing page
-
https://doi.org/10.1111/cns.70071Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.1111/cns.70071Direct OA link when available
- Concepts
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Endocytosis, Apoptosis, Vulnerability (computing), Cell biology, Cancer research, Chemistry, Medicine, Biology, Receptor, Biochemistry, Computer science, Computer securityTop concepts (fields/topics) attached by OpenAlex
- Cited by
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2Total citation count in OpenAlex
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2025: 2Per-year citation counts (last 5 years)
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32Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| publication_date | 2024-11-01 |
| publication_year | 2024 |
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