Alman B A, Greel D A, Ruby L K, Goldberg M J, Wolfe H J
Department of Orthopaedics and Pathology, New England Medical Center Hospitals, Boston, Massachusetts, USA.
J Orthop Res. 1996 Sep;14(5):722-8. doi: 10.1002/jor.1100140507.
Palmar fibromatosis (Dupuytren contracture) causes fibrosis of specific palmar fascial bands. These bands are subjected to repetitive mechanical strain in situ. Primary cell cultures were derived from (a) palmar fibromatosis from eight patients, (b) uninvolved palmar fascia (Skoog's fibers) from four of these patients, and (c) normal palmar fascia from four additional patients. The cells were plated onto collagen-coated membranes either subjected to cyclic strain (25% maximal strain at 1 Hz) or without strain. Bromodeoxyuridine incorporation showed an increase in proliferation in all cultures subjected to strain. This increase was highest for palmar fibromatosis (10 to 40% nuclear incorporation, p = 0.02). Skoog's fibers and fascia from the normal individuals showed a trend (not significant) toward increase with strain (8 to 25%, p = 0.15 for Skoog's fibers, and 8 to 15%, p = 0.45 for normal fascia). Cyclic strain increased the expression of platelet-derived growth factor-A relative to glyceraldehyde-3-phosphate dehydrogenase in palmar fibromatosis (2.2 to 3.5, p = 0.05) and Skoog's fibers (0.8 to 2.0, p = 0.04). The expression of platelet-derived growth factor-B relative to glyceraldehyde-3-phosphate dehydrogenase was enhanced by cyclic strain only in the fibromatosis tissue (0.7 to 2.1, p = 0.04). The normal fascia did not express platelet-derived growth factor. Platelet-derived growth factor neutralizing antibody decreased bromodeoxyuridine incorporation in fibromatosis cultures subjected to cyclic strain to near levels for those grown in the absence of strain (38 to 16%, p = 0.05). Conditioned medium from fibromatosis cells grown under stain showed a trend toward increased proliferation in additional fibromatosis cultures compared with conditioned medium from fibromatosis cells grown without strain (9 to 15% nuclear incorporation, p = 0.20). The observed palmar fibromatosis contracture can be partially explained on the basis of the cell's response to cyclic strain, which may be mediated by platelet-derived growth factor.
掌腱膜纤维瘤病（杜普伊特伦挛缩症）会导致特定掌腱膜束发生纤维化。这些束在原位受到重复性机械应变。原代细胞培养物来源于：(a) 8名患者的掌腱膜纤维瘤病组织；(b) 其中4名患者未受累的掌腱膜（斯库格纤维）；(c) 另外4名患者的正常掌腱膜。将细胞接种到涂有胶原蛋白的膜上，一部分膜施加循环应变（1Hz频率下25%最大应变），另一部分不施加应变。溴脱氧尿苷掺入实验表明，所有施加应变的培养物中细胞增殖均增加。掌腱膜纤维瘤病组织中这种增加最为显著（细胞核掺入率为10%至40%，p = 0.02）。斯库格纤维和正常个体的掌腱膜在施加应变后有增加的趋势（但不显著）（斯库格纤维为8%至25%，p = 0.15；正常掌腱膜为8%至15%，p = 0.45）。相对于甘油醛 - 3 - 磷酸脱氢酶，循环应变增加了掌腱膜纤维瘤病组织（2.2至3.5，p = 0.05）和斯库格纤维（0.8至2.0，p = 0.04）中血小板衍生生长因子 - A的表达。仅在纤维瘤病组织中，循环应变增强了相对于甘油醛 - 3 - 磷酸脱氢酶的血小板衍生生长因子 - B的表达（0.7至2.1，p = 0.04）。正常掌腱膜不表达血小板衍生生长因子。血小板衍生生长因子中和抗体将施加循环应变的纤维瘤病培养物中的溴脱氧尿苷掺入率降低至接近无应变培养物的水平（38%至16%，p = 0.05）。与无应变培养的纤维瘤病细胞的条件培养基相比，有应变培养的纤维瘤病细胞的条件培养基在其他纤维瘤病培养物中有增加增殖的趋势（细胞核掺入率为9%至15%，p = 0.20）。观察到的掌腱膜纤维瘤病挛缩可部分基于细胞对循环应变的反应来解释，这种反应可能由血小板衍生生长因子介导。
