2001 Fiscal Year Final Research Report Summary

Mechanisms of graft sclerosis by advanced glycation end product deposition - With the aim of elucidation of arteriosclerosis and development of therapy for arteriosclerosis

Research Project

Project/Area Number	11470236
Research Category	Grant-in-Aid for Scientific Research (B)
Allocation Type	Single-year Grants
Section	一般
Research Field	General surgery
Research Institution	Asahikawa Medical College
Principal Investigator	SASAJIMA Tadahiro Asahikawa Medical University, Professor, 医学部, 教授 (20109515)
Co-Investigator(Kenkyū-buntansha)	CHINO Yukihiro Taisho Pharmaceutical Co. Ltd., Researcher, 開発研究所, 研究員 HAGA Masae Asahikawa Medical University, Assistant Professor, 医学部, 助手 (80271766) YAMAZAKI Kosuke Asahikawa Medical University, Associate Professor, 医学部, 講師 (20281884)
Project Period (FY)	1999 – 2001
Keywords	advanced glycation end product / graft sclerosis / arteriosclerosis / medial elastic lamella / vascular smooth muscle cell / apoptosis
Research Abstract	Purpose Medial elastic lamellae works as a barrier against atherosclerotic risk factors: Advanced glycation end product (AGE) causes egg shell calcification in arteries of diabetic patients. This study assessed AGE deposition in medial elastic lamellae of internal thoracic arteries. Materials and Methods Internal thoracic arteries were obtained from 13 males and 3 females (aged 15-79 years) who did not suffer from arteriosclerosis and diabes at autopsy. AGE deposition in internal thoracic arteries was studied by autofluorescence detection method. Medial thickness and number of medial elastic lamellae of internal thoracic arteries were measured by morphometry. Results AGE deposition was detected in all internal thoracic arteries of 16 cadavers. Degree of AGE deposition in internal thoracic arteries was increased with aging. Medial thickness of internal thoracic arteries also increased with aging, while number of elastic lamellae of internal thoracic arteries decreased. Conclusion Defense mechanism of medial elastic lamellae against atherosclerosis may reduce due to AGE deposition with aging.