II型糖尿病患者のヒト内皮原始細胞は,増殖,粘着,および血管構造への組み込みが低下しています
Oren M Tepper1, Robert D Galiano, Jennifer M Capla
1Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY 10016, USA.
Circulation
|November 27, 2002
まとめ
II型糖尿病は,内皮原始細胞 (EPC) の機能を低下させ,新しい血管の成長を抑制します. この機能障害は,糖尿病患者の血管閉塞イベントのリスクを増やす可能性があります.
科学分野:
- 血管生物学 血管生物学
- 糖尿病の病理生理学 糖尿病の病理生理学
- 細胞生物学 細胞生物学
背景:
- 循環する内皮原生細胞 (EPC) は,新しい血管形成に不可欠です.
- 糖尿病の合併症は,EPCが役割を果たす状態と関連しています.
- EPC機能不全は,糖尿病の血管合併症の病理生理学に寄与する可能性があります.
研究 の 目的:
- II型糖尿病患者におけるEPCの機能的状態を調査する.
- 糖尿病がEPCの増殖,粘着,およびチューブル形成能力に影響するかどうかを判断する.
主な方法:
- II型糖尿病患者と年齢マッチングされた対照群から単離されたEPC.
- マトリゲルアッセイでEPC増殖,様々な基板への粘着,およびチューブル形成を評価した.
- 患者のヘモグロビンA1Cレベルと相関するEPC機能.
主要な成果:
- 糖尿病のEPCは,対照群と比較して,増殖の48%の減少を示し,ヘモグロビンA1Cと逆相関していました.
- 糖尿病のEPCはフィブロネクチンとコラーゲンに正常な粘着を示したが,活性化された内皮細胞への粘着は低下した.
- 糖尿病のEPCは,マトリゲルアッセイでチューブルを形成する可能性が2.5倍低い.
結論:
- II型糖尿病は,EPC生物学に悪影響を及ぼし,新しい血管の成長のための重要なプロセスに影響を与えます.
- 糖尿病患者の変化したEPC機能は,血管閉塞イベントのリスクが高い個人を特定することができます.
- これらの発見は,糖尿病と心血管疾患の罹病率および死亡率の増加を結びつける潜在的なメカニズムを強調しています.
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