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Mol. Life Sci."],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                <jats:title>Background<\/jats:title>\n                <jats:p>Exposure to chronic psychological stress (CPS) is a risk factor for thrombotic cardiocerebrovascular diseases (CCVDs). The expression and activity of the cysteine cathepsin K (CTSK) are upregulated in stressed cardiovascular tissues, and we investigated whether CTSK is involved in chronic stress-related thrombosis, focusing on stress serum-induced endothelial apoptosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods and results<\/jats:title>\n                <jats:p>Eight-week-old wild-type male mice (CTSK<jats:sup>+\/+<\/jats:sup>) randomly divided to non-stress and 3-week restraint stress groups received a left carotid artery iron chloride3 (FeCl<jats:sub>3<\/jats:sub>)-induced thrombosis injury for biological and morphological evaluations at specific timepoints. On day 21 post-stress\/injury, the stress had enhanced the arterial thrombi weights and lengths, in addition to harmful alterations of plasma ADAMTS13, von Willebrand factor, and plasminogen activation inhibitor-1, plus injured-artery endothelial loss and CTSK protein\/mRNA expression. The stressed CTSK<jats:sup>+\/+<\/jats:sup> mice had increased levels of injured arterial cleaved Notch1, Hes1, cleaved caspase8, matrix metalloproteinase-9\/-2, angiotensin type 1 receptor, galactin3, p16<jats:sup>IN4A<\/jats:sup>, p22phox, gp91<jats:sup>phox<\/jats:sup>, intracellular adhesion molecule-1, TNF-\u03b1, MCP-1, and TLR-4 proteins and\/or genes. Pharmacological and genetic inhibitions of CTSK ameliorated the stress-induced thrombus formation and the observed molecular and morphological changes. In cultured HUVECs, CTSK overexpression and silencing respectively increased and mitigated stressed-serum- and H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-induced apoptosis associated with apoptosis-related protein changes. Recombinant human CTSK degraded \u03b3-secretase substrate in a dose-dependent manor and activated Notch1 and Hes1 expression upregulation.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>CTSK appeared to contribute to stress-related thrombosis in mice subjected to FeCl<jats:sub>3<\/jats:sub> stress, possibly via the modulation of vascular inflammation, oxidative production and apoptosis, suggesting that CTSK could be an effective therapeutic target for CPS-related thrombotic events in patients with CCVDs.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00018-024-05240-0","type":"journal-article","created":{"date-parts":[[2024,5,4]],"date-time":"2024-05-04T06:01:26Z","timestamp":1714802486000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Cathepsin K deficiency prevented stress-related thrombosis in a mouse FeCl3 model"],"prefix":"10.1007","volume":"81","author":[{"given":"Xueying","family":"Jin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xueling","family":"Yue","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhe","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangkun","family":"Meng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shengnan","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuna","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aiko","family":"Inoue","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megumi","family":"Narisawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lina","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo-Ping","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyuki","family":"Umegaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toyoaki","family":"Murohara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanna","family":"Lei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masafumi","family":"Kuzuya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9758-0632","authenticated-orcid":false,"given":"Xian Wu","family":"Cheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,5,4]]},"reference":[{"key":"5240_CR1","doi-asserted-by":"publisher","first-page":"105","DOI":"10.1038\/s41467-020-20302-0","volume":"12","author":"YM Khaw","year":"2021","unstructured":"Khaw YM, Majid D, Oh S, Kang E, Inoue M (2021) Early-life-trauma triggers interferon-beta resistance and neurodegeneration in a multiple sclerosis model via downregulated beta1-adrenergic signaling. 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