Effect of imatinib mesylate and rapamycin on the preformed intimal hyperplasia in rat carotid injury model

Annals of Surgical Treatment and Research
Yang Jin ParkJongwon Ha

Abstract

Intimal hyperplasia (IH) is the main cause of restenosis or occlusion after vascular procedures. Imatinib mesylate and rapamycin are known to prevent IH. The purpose of this study was to evaluate the effect of these drugs on the regression of preformed IH in rat carotid injury model. IH was established in rat carotid arteries using a balloon catheter. The drug effects were assessed in vitro on proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMC) in the neointima. And in vivo studies were carried out in 4 groups: imatinib, rapamycin, combined, and no medication. After 2-week oral medication, morphometric analysis evaluated the number and density of neointimal cells, intima-to-media (I/M) ratio and cross-sectional area. Cell proliferation, apoptosis, and collagen changes were also investigated by immunohistochemical staining (IHCS). Imatinib and rapamycin significantly inhibited VSMC proliferation and migration, and promoted apoptosis in vitro. In morphometric analysis, the number and density of neointimal cells decreased significantly in all medication groups compared with control group (P < 0.01). However, there was no significant difference in neointimal cross-sectional area and I/M ratio among groups...Continue Reading

References

Nov 1, 1973·Beiträge Zur Pathologie·H PuchtlerL S Valentine
Nov 5, 1997·Progress in Cardiovascular Diseases·C Bauters, J M Isner
Jan 4, 2001·Journal of Dermatological Science·J Uitto, D Kouba
Mar 19, 2002·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·Allen M Gown, Mark C Willingham
Sep 25, 2003·Langenbeck's Archives of Surgery·Fred FändrichBernd Kremer
Oct 3, 2003·The New England Journal of Medicine·Jeffrey W MosesUNKNOWN SIRIUS Investigators
Oct 11, 2003·Arteriosclerosis, Thrombosis, and Vascular Biology·Chad Johnson, Zorina S Galis
Oct 31, 2003·The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation·Peter N RuygrokAnne Keogh
Feb 28, 2004·Arteriosclerosis, Thrombosis, and Vascular Biology·Markus LassilaMark E Cooper
Mar 23, 2004·Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology·Akimitsu NasunoYoshifusa Aizawa
Sep 24, 2004·Journal of Molecular and Cellular Cardiology·Hyo-Soo KimMyoung-Mook Lee
Mar 23, 2005·The Journal of Experimental Medicine·Amir AbdollahiPeter E Huber
Sep 15, 2005·JAMA : the Journal of the American Medical Association·Gregg W StoneUNKNOWN TAXUS V Investigators
Mar 8, 2006·Immunology and Cell Biology·Amit K MitraDevendra K Agrawal
Jan 6, 2007·Journal of Cardiovascular Pharmacology·Christian M MatterThomas F Lüscher
Oct 24, 2007·Journal of Vascular Surgery·Seung-Kee MinAlexander W Clowes

❮ Previous
Next ❯

Citations

Jul 4, 2019·Pharmaceutics·Bożena KarolewiczIgor Mucha

❮ Previous
Next ❯

Methods Mentioned

BETA
ELISA
fluorescence-activated cell sorter

Software Mentioned

LEICA
Modifit LT
LEICA application suite

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Cell Migration

Cell migration is involved in a variety of physiological and pathological processes such as embryonic development, cancer metastasis, blood vessel formation and remoulding, tissue regeneration, immune surveillance and inflammation. Here is the latest research.