ArticleJournal of the American Heart Association2019
Increased Complement 3 With Suppression of miR-145 Induces the Synthetic Phenotype in Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- The new perspective on understanding the mechanisms of cardiovascular diseases development.Scientific reports · 2025Article
- Association between Resistant Arterial Hypertension, Type 2 Diabetes, and Selected microRNAs.Journal of clinical medicine · 2024Article
- Impact of the transforming growth factor-β pathway on vascular restenosis and its mechanism.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- Beneficial effects of Panax notoginseng (Burkill) F. H. Chen flower saponins in rats with metabolic hypertension by inhibiting the activation of the renin-angiotensin-aldosterone system through complement 3.BMC complementary medicine and therapies · 2023Article
- How vascular smooth muscle cell phenotype switching contributes to vascular disease.Cell communication and signaling : CCS · 2022Review
- Dysregulated miRNAs network in the critical COVID-19: An important clue for uncontrolled immunothrombosis/thromboinflammation.International immunopharmacology · 2022Review
- Role of complement 3 in the pathogenesis of hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Down-regulation of Suv39h1 attenuates neointima formation after carotid artery injury in diabetic rats.Journal of cellular and molecular medicine · 2020Article
- Increased Complement 3 With Suppression of miR-145 Induces the Synthetic Phenotype in Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats.Journal of the American Heart Association · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Background We previously reported that vascular smooth muscle cells ( VSMC s) from spontaneously hypertensive rats ( SHR s) show the increased expression of complement 3 (C3) and the synthetic phenotype. We targeted the SHR C3 gene (C3 knockout [C3 KO] SHRs ) by the zinc finger gene editing method. In the current study, we investigated the mechanisms underlying the increased expression of C3 and the role of endogenous C3 in the synthetic phenotype of SHR VSMC s in comparison to cells from Wistar-Kyoto ( WKY) rats and C3 KO SHR s. Methods and Results Nonmuscle myosin heavy chain staining of aortas from SHR s at 1 day after birth was stronger in comparison to WKY rats and C3 KO SHR s. DNA synthesis in VSMC s from SHR s was significantly higher in comparison to WKY rats and C3 KO SHR s. Immunohistochemical staining of renin and liver X receptor α in VSMC s from SHR s was stronger in comparison to WKY rats and C3 KO SHR s. The expression of renin, Krüppel-like factor 5, and liver X receptor α proteins in VSMC s from SHR s was significantly higher in comparison to WKY rats and C3 KO SHR s. The expression of synthetic phenotype markers osteopontin, matrix gla, and l-caldesmon, growth factors transforming growth factor-β1 and platelet-derived growth factor-A, transcription factors Krüppel-like factor 5 and liver X receptor α, and angiotensinogen mRNA s in VSMC s from SHR s was significantly higher in comparison to WKY rats and C3 KO SHR s. The expression of miR-145 mRNA in VSMC s from SHR s was suppressed in comparison to cells from WKY rats. miR-145 inhibitor significantly increased the expression of C3 in VSMC s from WKY rats, but not in cells from SHR s. Conclusions These findings indicate that the increased C3 with the suppression of miR-145 induces the synthetic phenotype through Krüppel-like factor 5 and the activation of the renin-angiotensin system through liver X receptor α in VSMC s from SHR s.
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