Kaiser M, Weyand C M, Björnsson J, Goronzy J J
Mayo Clinic Foundation, Rochester, Minnesota 55905, USA.
Arthritis Rheum. 1998 Apr;41(4):623-33. doi: 10.1002/1529-0131(199804)41:4<623::AID-ART9>3.0.CO;2-6.
To explore whether vasoocclusion in giant cell (temporal) arteritis (GCA) is related to intimal hyperplasia and in situ production of platelet-derived growth factor (PDGF).
Temporal artery biopsy specimens from patients with GCA were analyzed for the presence of intimal hyperplasia. Expression of PDGF-A and PDGF-B was assessed by immunohistochemistry and digitized image analysis.
PDGF-A and PDGF-B were widely expressed in inflamed arteries. CD68+ macrophages, smooth muscle cells, and multinucleated giant cells produced PDGF, whereas hyperplastic intimal tissue did not. Arteries with marked luminal narrowing and those with no or minimal luminal narrowing differed in the extent and distribution of PDGF expression. Concentric intimal hyperplasia was associated with the accumulation of PDGF-A- and PDGF-B-producing CD68+ macrophages at the media-intima junction. PDGF+,CD68+ macrophages in close proximity to the internal elastic lamina frequently coproduced matrix metalloproteinase 2. Intimal hyperplasia of the temporal artery correlated with ischemic complications of GCA, such as ocular involvement, jaw claudication, and aortic arch syndrome.
Production of PDGF has a role in arterial occlusion in GCA. The excessive fibroproliferative response leading to luminal narrowing can be distinguished from the stenosing process in atherosclerosis and postangioplasty restenosis, suggesting that there are different response patterns to arterial injury. In GCA, macrophages at the media-intima border are the dominant source of PDGF. Since vasoocclusion is associated with a number of serious complications in GCA, inhibition of intimal proliferation should be a major goal of treatment.
探讨巨细胞（颞）动脉炎（GCA）中的血管闭塞是否与内膜增生及血小板衍生生长因子（PDGF）的原位产生有关。
对GCA患者的颞动脉活检标本进行内膜增生情况分析。通过免疫组织化学和数字化图像分析评估PDGF - A和PDGF - B的表达。
PDGF - A和PDGF - B在炎症动脉中广泛表达。CD68 +巨噬细胞、平滑肌细胞和多核巨细胞产生PDGF，而增生的内膜组织不产生。管腔明显狭窄的动脉与管腔无狭窄或轻度狭窄的动脉在PDGF表达程度和分布上存在差异。同心性内膜增生与在中膜 - 内膜交界处产生PDGF - A和PDGF - B的CD68 +巨噬细胞的积聚有关。紧邻内弹力层的PDGF +、CD68 +巨噬细胞常共同产生基质金属蛋白酶2。颞动脉的内膜增生与GCA的缺血性并发症相关，如眼部受累、颌部跛行和主动脉弓综合征。
PDGF的产生在GCA的动脉闭塞中起作用。导致管腔狭窄的过度纤维增生反应可与动脉粥样硬化和血管成形术后再狭窄中的狭窄过程相区分，提示对动脉损伤存在不同的反应模式。在GCA中，中膜 - 内膜边界处的巨噬细胞是PDGF的主要来源。由于血管闭塞在GCA中与许多严重并发症相关，抑制内膜增殖应是治疗的主要目标。
