TY - JOUR
T1 - Exploring the Histopathological Features of Thrombus-Associated Localized Amyloid Deposition
T2 - Comprehensive Analysis Employing Immunohistochemistry and Proteomics
AU - Ichimata, Shojiro
AU - Yoshinaga, Tsuneaki
AU - Sato, Mitsuto
AU - Katoh, Nagaaki
AU - Kametani, Fuyuki
AU - Yazaki, Masahide
AU - Sekijim, Yoshiki
AU - Hata, Yukiko
AU - Nishida, Naoki
PY - 2025/5/8
Y1 - 2025/5/8
N2 - Amyloid deposition has been reported to localize within thrombi; however, its pathological characteristics, particularly its precursor proteins, remain poorly understood. This study aimed to elucidate the pathological features of thrombus-associated amyloid deposition by immunohistochemistry combined with proteomic analyses using liquid chromatography-tandem mass spectrometry with laser microdissection. Our findings revealed that thrombus-associated amyloid deposits within the thrombus and vessel wall primarily comprised apolipoprotein A-I, with a mixture of amyloid fibrils derived from amyloidogenic proteins, including transthyretin and lactoferrin. Given that these proteins are present in the blood, our results support a previous hypothesis that proteins denatured during thrombus aging are a source of amyloid. Furthermore, phagocytes were infiltrated around the intramural and extravascular deposits rather than around the amyloid deposits within the thrombus. Therefore, amyloid deposits generated within the thrombus may be transported from regions with limited blood flow to the vessel wall and surrounding tissues, where blood flow is present, during thrombus processing. These deposits were primarily removed by phagocytic cells. Our results suggest that a facilitative effect on deposition occurs via a cross-seeding mechanism between amyloid fibrils and that phagocytes can remove amyloid deposits. These findings help elucidate the pathogenesis of localized amyloidosis.
AB - Amyloid deposition has been reported to localize within thrombi; however, its pathological characteristics, particularly its precursor proteins, remain poorly understood. This study aimed to elucidate the pathological features of thrombus-associated amyloid deposition by immunohistochemistry combined with proteomic analyses using liquid chromatography-tandem mass spectrometry with laser microdissection. Our findings revealed that thrombus-associated amyloid deposits within the thrombus and vessel wall primarily comprised apolipoprotein A-I, with a mixture of amyloid fibrils derived from amyloidogenic proteins, including transthyretin and lactoferrin. Given that these proteins are present in the blood, our results support a previous hypothesis that proteins denatured during thrombus aging are a source of amyloid. Furthermore, phagocytes were infiltrated around the intramural and extravascular deposits rather than around the amyloid deposits within the thrombus. Therefore, amyloid deposits generated within the thrombus may be transported from regions with limited blood flow to the vessel wall and surrounding tissues, where blood flow is present, during thrombus processing. These deposits were primarily removed by phagocytic cells. Our results suggest that a facilitative effect on deposition occurs via a cross-seeding mechanism between amyloid fibrils and that phagocytes can remove amyloid deposits. These findings help elucidate the pathogenesis of localized amyloidosis.
KW - Thrombosis/pathology
KW - Humans
KW - Proteomics/methods
KW - Amyloid/metabolism
KW - Immunohistochemistry
KW - Male
KW - Female
KW - Tandem Mass Spectrometry
KW - Prealbumin/metabolism
KW - Lactoferrin/metabolism
KW - Phagocytes/metabolism
KW - Amyloidosis/pathology
KW - Aged
KW - Middle Aged
U2 - 10.3390/ijms26104505
DO - 10.3390/ijms26104505
M3 - 学術論文
C2 - 40429650
SN - 1661-6596
VL - 26
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 10
ER -