Background: To characterize the cells responsible for neointima formation after porcine coronary artery wall injury, we studied the expression of smooth muscle cell (SMC) differentiation markers in 2 models: (1) self-expanding stent implantation resulting in no or little interruption of internal elastic lamina and (2) percutaneous transluminal coronary angioplasty (PTCA) resulting in complete medial rupture and exposure of adventitia to blood components.
Methods And Results: The expression of alpha-smooth muscle (SM) actin, SM myosin heavy chain isoforms 1 and 2, desmin, and smoothelin was investigated by means of immunohistochemistry and Western blots in tissues of the arterial wall collected at different time points and in cell populations cultured from these tissues. The expression of smoothelin, a marker of late SMC differentiation, was used to discriminate between SMCs and myofibroblasts. Both stent- and PTCA-induced neointimal tissues and their cultured cell populations expressed all 4 markers. The adventitial tissue underlying PTCA-induced lesions temporarily expressed alpha-SM actin, desmin, and SM myosin heavy chain isoforms, but not smoothelin. When placed in culture, adventitial cells expressed only alpha-SM actin.
Conclusions: Our results suggest that SMCs are the main components of coronary artery neointima after both self-expanding stent implantation and PTCA. The adventitial reaction observed after PTCA evolves with a chronology independent of that of neointima formation and probably corresponds to a myofibroblastic reaction.
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http://dx.doi.org/10.1161/01.cir.103.6.882 | DOI Listing |
J Cardiothorac Surg
January 2025
The First Department of Cardiology, Beidahuang Industry Group General Hospital, Harbin, 150000, Heilongjiang Province, China.
Objective: it was to evaluate the efficacy and safety of rapamycin-eluting stents at different doses in the treatment of coronary artery narrowing in miniature pigs.
Methods: a total of 20 miniature pigs were randomly assigned into four groups: S1 group (low-dose rapamycin-coated stent, 55 µg/mm), S2 group (medium-dose rapamycin-coated stent, 120 µg/mm), S3 group (high-dose rapamycin-coated stent, 415 µg/mm), and D0 group (bare metal stent). The stent size was 3.
J Mater Sci Mater Med
January 2025
Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, PR China.
In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
February 2025
Department of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
It has been proposed that bone marrow contributes to the pathogenesis of arteriosclerosis. Nerve growth factor receptor (NGFR) is expressed in bone marrow stromal cells; it is also present in peripheral blood and ischemic coronary arteries. We hypothesized that bone marrow-derived NGFR-positive (NGFR) cells regulate arterial remodeling.
View Article and Find Full Text PDFTheranostics
January 2025
Department of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, 200032, PR China.
J Vasc Interv Radiol
December 2024
Vascular and Interventional Radiology Translational Research Lab, Mayo Clinic, Rochester, MN, USA; Department of Radiology, Mayo Clinic, Rochester, MN, USA. Electronic address:
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