胶质瘤细胞血小板源生长因子B链的纯合二聚体与其受体基因？…

目的 探讨胶质瘤细胞血小板源生长因子Ｂ链的纯合二聚合（ＰＤＧＦＢＢ）及其受体（ＤＧＦＲ）基因表达和ＰＤＧＦＲ活化汪洋在胶质瘤发生、发展听作用。方法 用原位杂交和免疫组化染色观察了７３例不同级别的人胶质瘤组织标本。结果 ６２例（８４．９％）的肿瘤细胞表达ＰＤＧＦＢｍＲＮＡ,基阳性率和阳性肿瘤细胞含量均随肿瘤恶性程度升高而递增。ＰＤＧＦＲα、ＰＤＧＦＲβ和这两种受体及其信号传递通路活化标记物酪氨酸磷酸     

胶质瘤细胞血小板源生长因子B链的纯合二聚体自分泌环活性与肿瘤细胞增殖和凋亡的关系

目的探讨胶质瘤细胞血小板源生长因子Ｂ链的纯合二聚体（ＰＤＧＦＢＢ）自分泌环活性与其细胞增殖和凋亡的关系。方法用原位杂交、原位细胞凋亡检测和免疫组化ＡＢＣ法染色观察了７３例不同级别的胶质瘤组织。结果胶质瘤细胞ＰＤＧＦＢＢ自分泌环活性与其增殖活性呈显著性正相关，两者均随肿瘤恶性程度升高而增强。肿瘤细胞凋亡随肿瘤恶性程度升高而减少，并与肿瘤细胞ＰＤＧＦＢＢ自分泌环活性和增殖活性呈显著性负相关。结论以上指标对评价胶质瘤生物学行为均有参考价值。胶质瘤细胞ＰＤＧＦＢＢ自分泌环活性异常增加可能是刺激肿瘤细胞增殖和抑制其凋亡的重要因素，并在胶质瘤发生及恶性进展过程中起重要作用。     

缺氧内皮细胞介导肺动脉平滑肌细胞血小板源性生长因子mRNA表达

目的探讨缺氧时肺动脉内皮细胞对肺动脉平滑肌细胞ＰＤＧＦ自分泌的影响。方法实验分３组：无血清培养组、常氧性内皮细胞条件培养液组及缺氧性内皮细胞条件培养液组。应用原位杂交和图像分析技术检测猪肺动脉平滑肌细胞ＰＤＧＦＡ和ＰＤＧＦＢ链ｍＲＮＡ表达。结果无血清培养的肺动脉平滑肌细胞有ＰＤＧＦＡ和ＰＤＧＦＢ链ｍＲＮＡ弱表达;内皮细胞条件培养液明显增加肺动脉平滑肌细胞ＰＤＧＦＡ和ＰＤＧＦＢ链ｍＲＮＡ表达,两者分别为无血清培养组的１．８倍和１．７倍（Ｐ＜０．０１）,为常氧内皮细胞条件培养液培养组的１．４倍和１．５倍（Ｐ＜０．０１）。结论缺氧时肺动脉内皮细胞可以介导肺动脉平滑肌细胞ＰＤＧＦ的自分泌,可能在缺氧性肺动脉高压血管构形改建中具有重要作用     

血小板源生长因子—B及其受体在哮喘豚鼠气道中的表达

为探讨血小板源生长因子－Ｂ多肽（ＰＤＧＦ－Ｂ）在哮喘发病中的作用，应用免疫组织化学方法，检测了豚鼠哮喘模型气道及肺组织中ＰＤＧＦ－Ｂ多肽及其受体（ＰＤＧＦＲ－β）的表达。结果表明：实验组气道壁及周围组织有大量ＰＤＧＦ－Ｂ多肽阳性细胞，主要为气道上皮细胞及浸润的炎症细胞。ＰＤＧＦＲ－β阳性细胞主要分布在气道基底膜及周围结缔组织，偶见于平滑肌和肺间质。提示ＰＤＧＦ－Ｂ多肽及ＰＤＧＦＲ－β的表达与哮喘发     

血小板源生长因子-B及其受体在哮喘豚鼠气道中的表达

为探讨血小板源生长因子－Ｂ多肽（ＰＤＧＦ－Ｂ）在哮喘发病中的作用，应用免疫组织化学方法，检测了豚鼠哮喘模型气道及肺组织中ＰＤＧＦ－Ｂ多肽及其受体（ＰＤＧＦＲ－β）的表达。结果表明：实验组气道壁及周围组织有大量ＰＤＧＦ－Ｂ多肽阳性细胞，主要为气道上皮细胞及浸润的炎症细胞。ＰＤＧＦＲ－β阳性细胞主要分布在气道基底膜及周围结缔组织，偶见于平滑肌和肺间质。提示ＰＤＧＦ－Ｂ多肽及ＰＤＧＦＲ－β的表达与哮喘发病关系密切。     

血小板衍生生长因子及其受体与病毒性肝炎肝纤维化的关系

目的研究血小板衍生生长因子在病毒性肝炎肝纤维化中的作用。方法以免疫组化技术检测血小板衍生生长因子（ＰＤＧＦ）－ＢＢ以及ＰＤＧＦ的β受体（ＰＤＧＦＲ－β）在病毒性肝炎肝组织中的表达。结果ＰＤＧＦ－ＢＢ及ＰＤＧＦＲ－β在肝组织中的表达与肝纤维化程度明显相关，肝硬变及慢性肝炎Ｓ３～４期患者肝组织ＰＤＧＦ－ＢＢ及ＰＤＧＦＲ－β表达强度明显高于急性肝炎及慢性肝炎Ｓ０～２期患者，同时与结蛋白、Ⅲ型前胶原肽在肝组织中的表达以及血清金属蛋白酶组织抑制因子－１（ＴＩＭＰ－１）呈明显正相关。结论ＰＤＧＦ－ＢＢ及ＰＤＧＦＲ－β不仅对星状细胞的活化、分裂、增殖及其合成胶原等细胞外基质（ＥＣＭ）均有明显的促进作用，而且可能通过上调ＴＩＭＰ－１减少ＥＣＭ的降解，促进肝纤维化的发生和进展过程。     

血小板源生长因子及其受体基因表达在低氧大鼠肺中的变化

本文观察了血小板源生长因子（ＰＤＧＦ）Ａ、Ｂ链及其α、β受体基因表达在低氧大鼠肺中的变化。Ｎｏｒｔｈｅｒｎ印迹杂交显示正常大鼠肺中可表达ＰＤＧＦ－Ａ链、Ｂ链和ＰＤＧＦ－α受体、β受体的ｍＲＮＡ。随着低氧时间的延长，ｍＲＮＡ水平迅速增加。ＰＤＧＦ－Ａ、Ｂ链ｍＲＮＡ均在低氧的第二天达高峰，分别为正常的１．５１倍及１．６９倍，且Ｂ链ｍＲＮＡ基本维持在该水平至第七天。ＰＤＧＦ－α、β受体的ｍＲＮＡ在低氧第     

血管内皮生长因子及其受体在卵巢癌中表达的免疫组化检测

目的： 检测血管内皮生长因子（ＶＥＧＦ） 及其受体（ＫＤＲ） 在卵巢癌中的表达, 并探讨其与卵巢癌发生的关系。方法： 采用ＳＡＢＣ免疫组化染色法, 对６６ 例卵巢肿瘤中, ＶＥＧＦ 和ＫＤＲ 的表达进行检测。结果： 恶性、交界性及良性卵巢肿瘤中, ＶＥＧＦ 和ＫＤＲ 的表达率分别为７２－９％ 、７５－００ ％ 、３８－４６ ％ 及５４－０５％ 、４３－７５％ 、７－６９ ％ ; 恶性肿瘤及交界性肿瘤ＶＥＧＦ和ＫＤＲ的表达, 明显高于良性肿瘤（Ｐ＜ ０－０５） 。ＫＤＲ 不仅表达于肿瘤血管内皮细胞, 在肿瘤细胞内也有强表达。有淋巴结转移的卵巢癌ＶＥＧＦ 的表达与无淋巴结转移者相比较, 有显著差异（Ｐ＜ ０－０５）; ＫＤＲ 的表达与卵巢癌淋巴结转移无关（Ｐ＞ ０－０５）; 卵巢癌的不同临床分期、病理类型及病理分级间ＶＥＧＦ和ＫＤＲ的表达, 无显著性差异（ Ｐ＞ ０－０５） 。结论： ＶＥＧＦ和ＫＤＲ 的表达可能与卵巢癌的发生有关。     

血管内皮细胞生长因子和血管生成与胃癌发展的关系

目的探讨血管内皮细胞生长因子（ＶＥＧＦ）和血管生成与胃癌发展的关系。方法应用免疫组织化学和原位分子杂交技术,检测５６例人胃癌组织ＶＥＧＦ蛋白表达和微血管密度（ＭＶＤ）及部分胃癌ＶＥＧＦｍＲＮＡ表达,分析ＶＥＧＦ和ＭＶＤ、及其与胃癌组织学分型、浸润深度、生长方式、淋巴结转移、远处转移和预后的关系。结果ＶＥＧＦ阳性者ＭＶＤ值显著高于阴性者（Ｐ＜００１）,ＶＥＧＦ表达和ＭＶＤ与胃癌浸润深度（Ｐ＜００１）、淋巴结转移（Ｐ＜００５）和远处转移（Ｐ＜０．０５）密切相关,而与组织学分型和生长方式无关（Ｐ＞００５）;ＶＥＧＦ表达阳性或ＭＶＤ≥４３的胃癌患者５年生存率较低;ＶＥＧＦｍＲＮＡ表达与ＶＥＧＦ蛋白表达具有一致性,但其分布不同。结论ＶＥＧＦ与胃癌的血管生成密切相关,对胃癌的生长和浸润转移有促进作用,ＶＥＧＦ和ＭＶＤ可作为反映胃癌生物学行为的指标之一     

大肠癌表皮生长因子受体和p53蛋白表达与临床病理特？…

为了研究大肠癌表皮生长因子受体（ＥＧＦＲ）和ｐ５３蛋白表达与病理特征和预后的关系，应用免疫组化检测ＥＧＦＲ和ｐ５３在６１例大肠癌中的表达，结果提示：正常大肠粘膜未发现ＥＧＦＲ和ｐ５３阳性表达，而两者在大肠癌均有较高表达（７７．０４％和５５．７５％）。ＥＧＦＲ表达与大肠癌Ｄｕｋｅｓ分期有关（Ｐ〈０．０５）。ｐ５３表达与大肠癌分化程度及Ｄｕｋｅｓ分期有关（Ｐ〈０．０５）。大肠癌生存率随ＥＧＦＲ和ｐ５３     

养精种玉汤对小鼠卵母细胞体外成熟及PDGFA和PDGFRα表达的影响

目的:探讨养精种玉汤对小鼠卵母细胞体外成熟及血小板源性生长因子A亚基(platelet-derived growth factor subunit A,PDGFA)和血小板源性生长因子受体α(platelet-derived growth factor receptorα,PDGFRα)表达的影响。方法:SPF级雌性KM小鼠灌胃养精种玉汤后取血制备血清,养精种玉汤血清用于未成熟卵母细胞-颗粒细胞复合体培养。体外培养后,观察并计算小鼠卵母细胞成熟率、受精率和卵裂率,采用Western blot和real-time PCR分别检测卵母细胞PDGFA和PDGFRα的蛋白及mRNA表达情况。结果:养精种玉汤能明显提高卵母细胞体外成熟率和受精率(P<0.05或P<0.01),下调PDGFA和PDGFRα的蛋白和mRNA表达(P<0.01)。结论:养精种玉汤可能通过下调PDGFA和PDGFRα的表达促进小鼠卵母细胞体外成熟。     

Platelet-derived growth factor receptors and ligands are up-regulated in paediatric fibromatoses

AIMS: Platelet-derived growth factors (PDGF) and their receptors (PDGFR) play an essential role in pathways involved in the regulation of cell proliferation, growth and function. Overexpression of PDGF/R is reported in a wide range of solid tumours. The aim was to determine levels of PDGF/R expression in paediatric fibromatoses and myofibromatosis. METHODS AND RESULTS: Quantitative real-time polymerase chain reaction was used to examine the expression level of alpha and beta isoforms of PDGF/R in 17 fibromatoses, four myofibromatoses and three dermatofibrosarcoma protuberans (DFSP) in children. Fifteen of 17 (88%) fibromatoses and all myofibromatoses and DFSPs demonstrated increased expression of PDGFalpha and beta compared with a panel of normal tissues. In terms of the cognate receptors, 13/17 (76%) fibromatoses demonstrated increased expression for PDGFRalpha and Rbeta, whereas 3/4 myofibromatoses demonstrated increased expression of PDGFRalpha and all four had increased PDGFRbeta expression. All DFSPs were associated with increased expression of both PDGFRalpha and PDGFRbeta compared with normal control tissues. CONCLUSIONS: Increased expression of PDGF/Ralphabeta may play an important role in the mechanism of growth of these paediatric fibromatous lesions and warrants further investigation, since novel therapeutic interventions could potentially be developed in the light of the expression patterns.     

PDGFRα signaling drives adipose tissue fibrosis by targeting progenitor cell plasticity

Fibrosis is a common disease process in which profibrotic cells disturb organ function by secreting disorganized extracellular matrix (ECM). Adipose tissue fibrosis occurs during obesity and is associated with metabolic dysfunction, but how profibrotic cells originate is still being elucidated. Here, we use a developmental model to investigate perivascular cells in white adipose tissue (WAT) and their potential to cause organ fibrosis. We show that a Nestin-Cre transgene targets perivascular cells (adventitial cells and pericyte-like cells) in WAT, and Nestin-GFP specifically labels pericyte-like cells. Activation of PDGFRα signaling in perivascular cells causes them to transition into ECM-synthesizing profibrotic cells. Before this transition occurs, PDGFRα signaling up-regulates mTOR signaling and ribosome biogenesis pathways and perturbs the expression of a network of epigenetically imprinted genes that have been implicated in cell growth and tissue homeostasis. Isolated Nestin-GFP⁺ cells differentiate into adipocytes ex vivo and form WAT when transplanted into recipient mice. However, PDGFRα signaling opposes adipogenesis and generates profibrotic cells instead, which leads to fibrotic WAT in transplant experiments. These results identify perivascular cells as fibro/adipogenic progenitors in WAT and show that PDGFRα targets progenitor cell plasticity as a profibrotic mechanism.     

Platelet-derived growth factor and its receptors are related to the progression of human muscular dystrophy: an immunohistochemical study

This study has examined the immunological localization of platelet-derived growth factor (PDGF)-A, PDGF-B, and PDGF receptor (PDGFR) alpha and beta to clarify their role in the progression of muscular dystrophy. Biopsied frozen muscles from patients with Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD), and congenital muscular dystrophy (CMD) were analysed immunohistochemically using antibodies raised against PDGF-A, PDGF-B, and PDGFR alpha and beta. Muscles from two dystrophic mouse models (dy and mdx mice) were also immunostained with antibodies raised against PDGFR alpha and beta. In normal human control muscle, neuromuscular junctions and vessels were positively stained with antibodies against PDGF-A, PDGF-B, PDGFR alpha and PDGFR beta. In human dystrophic muscles, PDGF-A, PDGF-B, PDGFR alpha and PDGFR beta were strongly immunolocalized in regenerating muscle fibres and infiltrating macrophages. PDGFR alpha was also immunolocalized to the muscle fibre sarcolemma and necrotic fibres. The most significant finding in this study was a remarkable overexpression of PDGFR beta and, to a lesser extent, PDGFR alpha in the endomysium of DMD and CMD muscles. PDGFR was also overexpressed in the interstitium of muscles from dystrophic mice, particularly dy mice. Double immunolabelling revealed that activated interstitial fibroblasts were clearly positive for PDGFR alpha and beta. However, DMD and CMD muscles with advanced fibrosis showed very poor reactivity against PDGF and PDGFR. Those findings were confirmed by immunoblotting with PDGFR beta. These findings indicate that PDGF and its receptors are significantly involved in the active stage of tissue destruction and are associated with the initiation or promotion of muscle fibrosis. They also have roles in muscle fibre regeneration and signalling at neuromuscular junctions in both normal and diseased muscle.     

Platelet-derived growth factor and platelet-derived growth factor receptor-α expression in the normal human thymus and thymoma

Platelet-derived growth factor (PDGF) and its receptors (PDGFRs) are strongly involved in the normal development of several organs, tumour angiogenesis and malignant progression and metastasis. Few studies concerning their expression, distribution and role in normal and pathological human thymus are available in the literature. The aim of this study has been to analyse the immunohistochemical expression of PDGF and PDGFR-α in prenatal and postnatal normal human thymus and thymomal biopsy specimens. The results demonstrated immunoreactivity to both PDGF and PDGFR-α in all specimens, but the intensity, distribution and number of positive cells were different in normal thymus and thymomas, and also among different tumour types. PDGF and PDGFR-α were weakly expressed in foetal and postnatal humans with a different distribution between cortex and medulla in both blood vessels and epithelial cells, whereas they were overexpressed in thymoma, especially in type B2 and B3, in the tumour epithelial cells. Overall, these data suggest that PDGF and PDGFR-α may be involved in the pathophysiology of the human thymus.     

The effects of inflammatory response associated with traumatic spinal cord injury in cutaneous wound healing and on expression of transforming growth factor-beta1 (TGF-β1) and platelet-derived growth factor (PDGF)-A at the wound site in rats

At the cellular level, spinal cord injury (SCI) provokes an inflammatory response that generates substantial secondary damage within the cord, but also may contribute to its repair. The aim of this study was to investigate the effects of inflammatory response associated with SCI in cutaneous wound healing and on expression of transforming growth factor-beta1 (TGF-β₁) and platelet-derived growth factor (PDGF)-A at the wound site in rats. At the 14th day analysis, the mean TGF-β₁ score in trauma group (I) was significantly lower than that in control group (C) (2.60 ± 0.90 vs. 3.64 ± 0.37, respectively; p < 0.05). The mean score for PDGF-A expression in group I was similar to the corresponding value in group C (2.42 ± 0.74 vs. 2.94 ± 0.72, respectively). Compared to group C, group I had significantly lower mean scores for epidermal and dermal regeneration, but higher mean scores for granulation tissue thickness and similar scores for angiogenesis. The dermal layer contains diffuse deposition of collagen fibers that are not organised as in control rat skin, and intraepidermal and subepidermal vasocongestion is distinct. Based on the results on the parameters evaluated in the study, experimental SCI in rats results in delay in wound healing and low intensity of TGF-β₁ in the dorsal wound-tissue specimens.     

氧环境对血管内皮生长因子、色素上皮衍生因子的影响及其与血管发育的关系

目的：研究视网膜发育过程中血管内皮生长因子(VEGF)和色素上皮衍生因子(PEDF)所起的调节作用及其机制。方法：C57BL/6J 小鼠从出生后7～12 d 饲养于75%氧环境,分别用抗 VEGF、抗 PEDF 和抗 CD31抗体作免疫组织化学标记视网膜切片。结果：持续处于高氧环境时,VEGF 表达处于低水平而 PEDF 快速上升,血管生长减缓。高氧处理5 d 后回到普通环境,VEGF 的表达迅速上升而 PEDF 却逐渐减少,出现了一过性的血管快速增长现象。结论：氧含量变化可调节 VEGF 和 PEDF 表达,参与视网膜血管发育。