دورية أكاديمية
أعرض في EDS

TXNIP Suppresses the Osteochondrogenic Switch of Vascular Smooth Muscle Cells in Atherosclerosis.

التفاصيل البيبلوغرافية
العنوان: TXNIP Suppresses the Osteochondrogenic Switch of Vascular Smooth Muscle Cells in Atherosclerosis.
المؤلفون: Woo SH; Department of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Korea (S.-H.W., D.-M.G., J.-S.O., D.-Y.K.)., Kyung D; Laboratory of Developmental Biology and Genomics, Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Korea (D.K.)., Lee SH; Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences, Research Institute for Convergence of Basic Sciences, Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea (S.H.L., K.S.P., M.K., K.K., J.-H.C.)., Park KS; Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences, Research Institute for Convergence of Basic Sciences, Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea (S.H.L., K.S.P., M.K., K.K., J.-H.C.)., Kim M; Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences, Research Institute for Convergence of Basic Sciences, Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea (S.H.L., K.S.P., M.K., K.K., J.-H.C.)., Kim K; Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences, Research Institute for Convergence of Basic Sciences, Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea (S.H.L., K.S.P., M.K., K.K., J.-H.C.)., Kwon HJ; Department of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon, Korea (H.-J.K.)., Won YS; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Korea (Y.-S.W., W.K.Y.)., Choi I; Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea (I.C.)., Park YJ; Enviornmental Diseases Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea (Y.-J.P.)., Go DM; Department of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Korea (S.-H.W., D.-M.G., J.-S.O., D.-Y.K.)., Oh JS; Department of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Korea (S.-H.W., D.-M.G., J.-S.O., D.-Y.K.)., Yoon WK; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Korea (Y.-S.W., W.K.Y.)., Paik SS; Department of Pathology, Hanyang University Medical College, Seoul, Korea (S.S.P., J.H.K.)., Kim JH; Department of Pathology, Hanyang University Medical College, Seoul, Korea (S.S.P., J.H.K.)., Kim YH; Department of Biological Sciences, Research Institute of Women's Health, College of Natural Sciences, Sookmyung Women's University, Seoul, Korea (Y.-H.K.)., Choi JH; Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences, Research Institute for Convergence of Basic Sciences, Hanyang Institute of Bioscience and Biotechnology, Hanyang University, Seoul, Korea (S.H.L., K.S.P., M.K., K.K., J.-H.C.)., Kim DY; Department of Veterinary Pathology, College of Veterinary Medicine, Seoul National University, Korea (S.-H.W., D.-M.G., J.-S.O., D.-Y.K.).
المصدر: Circulation research [Circ Res] 2023 Jan 06; Vol. 132 (1), pp. 52-71. Date of Electronic Publication: 2022 Nov 30.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0047103 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1524-4571 (Electronic) Linking ISSN: 00097330 NLM ISO Abbreviation: Circ Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Baltimore, MD : Lippincott Williams & Wilkins
Original Publication: Baltimore, Md. Grune & Stratton.
مواضيع طبية MeSH: Atherosclerosis*/metabolism , Plaque, Atherosclerotic*/pathology , Calcinosis*/metabolism , Vascular Calcification*/genetics, Mice ; Humans ; Animals ; Muscle, Smooth, Vascular/metabolism ; Cells, Cultured ; Bone Morphogenetic Proteins/metabolism ; Myocytes, Smooth Muscle/metabolism ; RNA/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Thioredoxins/metabolism
مستخلص: Background: The osteochondrogenic switch of vascular smooth muscle cells (VSMCs) is a pivotal cellular process in atherosclerotic calcification. However, the exact molecular mechanism of the osteochondrogenic transition of VSMCs remains to be elucidated. Here, we explore the regulatory role of TXNIP (thioredoxin-interacting protein) in the phenotypical transitioning of VSMCs toward osteochondrogenic cells responsible for atherosclerotic calcification.
Methods: The atherosclerotic phenotypes of Txnip -/- mice were analyzed in combination with single-cell RNA-sequencing. The atherosclerotic phenotypes of Tagln -Cre; Txnip flox/flox mice (smooth muscle cell-specific Txnip ablation model), and the mice transplanted with the bone marrow of Txnip -/- mice were analyzed. Public single-cell RNA-sequencing dataset (GSE159677) was reanalyzed to define the gene expression of TXNIP in human calcified atherosclerotic plaques. The effect of TXNIP suppression on the osteochondrogenic phenotypic changes in primary aortic VSMCs was analyzed.
Results: Atherosclerotic lesions of Txnip -/- mice presented significantly increased calcification and deposition of collagen content. Subsequent single-cell RNA-sequencing analysis identified the modulated VSMC and osteochondrogenic clusters, which were VSMC-derived populations. The osteochondrogenic cluster was markedly expanded in Txnip -/- mice. The pathway analysis of the VSMC-derived cells revealed enrichment of bone- and cartilage-formation-related pathways and bone morphogenetic protein signaling in Txnip -/- mice. Reanalyzing public single-cell RNA-sequencing dataset revealed that TXNIP was downregulated in the modulated VSMC and osteochondrogenic clusters of human calcified atherosclerotic lesions. Tagln -Cre; Txnip flox/flox mice recapitulated the calcification and collagen-rich atherosclerotic phenotypes of Txnip -/- mice, whereas the hematopoietic deficiency of TXNIP did not affect the lesion phenotype. Suppression of TXNIP in cultured VSMCs accelerates osteodifferentiation and upregulates bone morphogenetic protein signaling. Treatment with the bone morphogenetic protein signaling inhibitor K02288 abrogated the effect of TXNIP suppression on osteodifferentiation.
Conclusions: Our results suggest that TXNIP is a novel regulator of atherosclerotic calcification by suppressing bone morphogenetic protein signaling to inhibit the transition of VSMCs toward an osteochondrogenic phenotype.
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فهرسة مساهمة: Keywords: TXNIP; atherosclerosis; calcification; osteochondrogenic; vascular smooth muscle cell
المشرفين على المادة: 0 (Bone Morphogenetic Proteins)
63231-63-0 (RNA)
0 (TXNIP protein, human)
0 (Carrier Proteins)
0 (Txnip protein, mouse)
52500-60-4 (Thioredoxins)
تواريخ الأحداث: Date Created: 20221130 Date Completed: 20230109 Latest Revision: 20230205
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9829043
DOI: 10.1161/CIRCRESAHA.122.321538
PMID: 36448450
قاعدة البيانات: MEDLINE
الوصف
تدمد:1524-4571
DOI:10.1161/CIRCRESAHA.122.321538