scholarly journals Macrophage‐derived extracellular vesicles mediate smooth muscle hyperplasia: role of altered miRNA cargo in response to HIV infection and substance abuse

2018 ◽  
Vol 32 (9) ◽  
pp. 5174-5185 ◽  
Author(s):  
Himanshu Sharma ◽  
Mahendran Chinnappan ◽  
Stuti Agarwal ◽  
Pranjali Dalvi ◽  
Sumedha Gunewardena ◽  
...  
2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
H Mehrad

Abstract Background and aims Intimal hyperplasia refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in arterial wall thickening and decreased arterial lumen size. Neointimal hyperplasia is the major cause of restenosis after percutaneous carotid interventions such as stenting or angioplasty. The aim of this study was to investigate the effect of combined shock wave enhanced sonoporation therapy and catheter-based 90Y-mediated β-brachytherapy on neointimal hyperplasia regression in an animal model, wherein diagnostic B-mode ultrasound is combined with therapy system, with a goal of increased safety. Methods Endothelial balloon catheter denudation of the abdominal aorta of golden Syrian hamsters was performed. Histopathologic evaluation confirmed neointimal hyperplasia formation in all of the hamsters' arteries. The treatment group underwent intravenous lipid-based encapsulated paclitaxel nanoparticles (10mg/kg)-mediated extracorporeal confocal dual pulse low-level focused electrohydraulic shock wave (V=15 kV, F=2 Hz, Impulses = 50 and V=10 kV, F=0.2 Hz, Impulses = 150) enhanced sonoporation therapy accompanied by catheter-based 90Y-mediated β-brachytherapy (90Y, 15 Gy), guided by simultaneous B-mode ultrasound imaging. Results B-mode ultrasound guided combined shock wave enhanced sonoporation therapy and β-brachytherapy was feasible and appeared safe for the targeting of stenosis in the aorta artery. Furthermore, pathological results showed a significant reduction in the mean value for smooth muscle hyperplasia cells density, lumen wall thickness and percentage of luminal cross- sectional area of stenosis in the treatment group compared with the other groups (p<0.05). Conclusions Enhanced toxicity effect of paclitaxel, induced by enhanced sonoporation effect of shock wave therapy, due to inertial cavitation effect of collapsed capsules and dual pulse system application accompanied by apoptotic effect of brachytherapy, can cause to neointimal hyperplasia regression. Combined shock wave enhanced sonoporation therapy and β-brachytherapy is significantly associated with reduced aorta artery stenosis in hamsters. The mechanism may relate to reduced smooth muscle hyperplasia cells and inflammation in the tunica intima. FUNDunding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Mehrad Research Lab


1999 ◽  
Vol 38 (10) ◽  
pp. 775-777 ◽  
Author(s):  
Young Min Park ◽  
Hoon Kang ◽  
Baik Kee Cho

2009 ◽  
Vol 28 (7) ◽  
pp. 963-965 ◽  
Author(s):  
Dal Mo Yang ◽  
Hyun Cheol Kim ◽  
Hyung Lae Lee ◽  
Gyo Young Kim

2009 ◽  
Vol 296 (6) ◽  
pp. G1230-G1237 ◽  
Author(s):  
Krystina B. Hazelgrove ◽  
Robert S. Flynn ◽  
Li-Ya Qiao ◽  
John R. Grider ◽  
John F. Kuemmerle

Endogenous insulin-like growth factor-I (IGF-I) regulates intestinal smooth muscle growth by concomitantly stimulating proliferation and inhibiting apoptosis. IGF-I-stimulated growth is augmented by the αvβ3 integrin ligands vitronectin and fibronectin. IGF-I expression in smooth muscle is increased in both TNBS-induced colitis and Crohn's disease. We hypothesized that intestinal inflammation increased vitronectin and fibronectin expression by smooth muscle and, along with IGF-I upregulation, increased intestinal muscle growth. Intestinal smooth muscle cells were examined 7 days following the induction of TNBS-induced colitis. Although αvβ3 integrin expression was not altered by TNBS-induced colitis, vitronectin and fibronectin levels were increased by 80 ± 10% and 90 ± 15%, above control levels, respectively. Basal IGF-I receptor phosphorylation in inflamed muscle from TNBS-treated rats was increased by 86 ± 8% over vehicle-treated controls. Basal ERK1/2, p70S6 kinase, and GSK-3β phosphorylation in muscle cells of TNBS-treated rats were also increased by 140–180%. TNBS treatment increased basal muscle cell proliferation by 130 ± 15% and decreased apoptosis by 20 ± 2% compared with that in vehicle-treated controls. The changes in proliferation and apoptosis were reversed by an IGF-I receptor tyrosine kinase inhibitor or an αvβ3 integrin antagonist. The results suggest that smooth muscle hyperplasia in TNBS-induced colitis partly results from the upregulation of endogenous IGF-I and ligands of αvβ3 integrin that mediate increased smooth muscle cell proliferation and decreased apoptosis. This paper has identified one mechanism regulating smooth muscle hyperplasia, a feature of stricture formation that occurs in the chronically inflamed intestine of TNBS-induced colitis and potentially Crohn's disease.


2006 ◽  
Vol 174 (9) ◽  
pp. 1025-1033 ◽  
Author(s):  
Laurence Dewachter ◽  
Serge Adnot ◽  
Elie Fadel ◽  
Marc Humbert ◽  
Bernard Maitre ◽  
...  

Author(s):  
B. Ramesh ◽  
Rachana Ghanti ◽  
Veena Devadiga

Adenomyosis is the presence of endometrial glands and stroma in the context of the myometrium, with adjacent smooth muscle hyperplasia. It may be diffuse or cystic. Adenomyotic cysts of the uterus are extremely rare. A 31 years old nulligravida woman presented to our OPD with complaints of severe dysmenorrhea and back pain since 8 months. Transvaginal ultrasound revealed retroverted uterus with diffuse adenomyosis with intramyometrial endometriotic cysts in both cornual areas, both adnexa showing multiple small endometriotic cysts. On Laparoscopy – cystic masses around 5x4cm was found near the cornua and anterior uterine wall, which were excised and diagnosed as adenomyotic cyst on histopathology.


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