Related Experiment Videos
Differences in cellular responses to mitogens in arterial smooth muscle cells derived from patients with moyamoya
M Yamamoto1, M Aoyagi, N Fukai
1Department of Cell Biology, Tokyo Metropolitan Institute of Gerontology, Japan.
Background And Purpose:
Moyamoya disease is a progressive cerebrovascular occlusive disease affecting primarily children. The etiology remains unknown. We examined the chemotactic and proliferative activities of inflammatory cell products from arterial smooth muscle cells (SMCs) derived from moyamoya patients and compared them with those from control subjects.
Methods:
We used 12 SMC strains from moyamoya patients and eight from control subjects. SMC migration was examined in a micro chemotaxis chamber. DNA synthesis was measured by an immunoperoxidase technique.
Results:
Platelet-derived growth factor (PDGF)-BB markedly stimulated cell migration and DNA synthesis in control SMCs. PDGF-AA stimulated only DNA synthesis in control SMCs. In moyamoya SMCs, PDGF-AA and PDGF-BB stimulated cell migration but not DNA synthesis. Basic fibroblast growth factor had little migratory activity but stimulated DNA synthesis in moyamoya SMCs and control SMCs. Conversely, hepatocyte growth factor stimulated cell migration but not DNA synthesis in moyamoya SMCs and control SMCs. In contrast, interleukin-1 beta (IL-1 beta) significantly stimulated the migration and DNA synthesis of control SMCs, while it inhibited moyamoya SMC migration. The levels of IL-1 beta-induced nitric oxide production did not differ between moyamoya SMCs and control SMCs, suggesting that IL-1 beta inhibits the migration of moyamoya SMCs through a nitric oxide-independent pathway.
Conclusions:
The differences in responses to PDGF and IL-1 in moyamoya SMCs are involved in the mechanism by which intimal thickening develops in moyamoya disease.
Insights
Smooth muscle cells (SMCs) from moyamoya disease patients show altered responses to growth factors, impacting intimal thickening. Interleukin-1 beta inhibits moyamoya SMC migration via a nitric oxide-independent pathway.
Area of Science:
- Cerebrovascular diseases
- Cell biology
- Immunology
Background:
- Moyamoya disease is a progressive cerebrovascular occlusive disease primarily affecting children.
- The exact etiology of moyamoya disease remains unknown.
- This study investigates the role of inflammatory cell products in moyamoya disease pathogenesis.
Purpose of the Study:
- To examine the chemotactic and proliferative activities of arterial smooth muscle cells (SMCs) from moyamoya patients.
- To compare these activities with those of SMCs from control subjects.
- To elucidate the cellular mechanisms underlying intimal thickening in moyamoya disease.
Main Methods:
- Utilized 12 SMC strains from moyamoya patients and 8 from control subjects.
- Assessed SMC migration using a micro chemotaxis chamber.
- Measured DNA synthesis via an immunoperoxidase technique.
Main Results:
- Platelet-derived growth factor (PDGF)-BB stimulated migration and DNA synthesis in control SMCs, while PDGF-AA primarily stimulated DNA synthesis.
- Moyamoya SMCs showed migration in response to both PDGF-AA and PDGF-BB but not increased DNA synthesis.
- Interleukin-1 beta (IL-1 beta) stimulated migration and DNA synthesis in control SMCs but inhibited moyamoya SMC migration through a nitric oxide-independent pathway.
Conclusions:
- Differential responses of moyamoya SMCs to PDGF and IL-1 are implicated in the intimal thickening characteristic of moyamoya disease.
- The findings suggest a novel mechanism involving inflammatory responses in moyamoya disease progression.
- Further research into these cellular mechanisms could lead to targeted therapies.