Expression of transforming growth factor-β_1 and its typeⅠ receptor in different phases of post-burn hypertrophic scars

Objective: To analyze and compare the expression pattern of the transforming growth factor-β1(TGF-β1) and its type I receptor (TGF-β RI ) in nounal human skin and various phases of post-burn hypertrophic scars (HTS). Method: The immunohistochemical ABC method was employed. Results: In nounal human skin, no evident immunoreactivity of TGF-β1 and TGF-β R I was observed. In activation phase of post-burn HTS, TGF-β R I and TGF-β1 were highly expressed in most dermal fibroblasts which seemed to be the same subset. However, in remission phase, no staining was seen in der mal fibroblasts. Conclusion: The formation of all may involve the increase of TGF-β responsiveness in fibroblasts The ac cumulation at the wound site and failure of apoptosis of over-resposive fibroblasts may contribute to the formation of HTS.

Correlation between expression of two transforming growth factor-beta 1 receptors and microvascular density in a rat model of cerebral ischemia and reperfusion injury

The effects of transforming growth factor-β1 （TGF-β1） are currently controversial. Whether TGF-β1 promotes or inhibits revascularization under different conditions remains poorly understood. Based on previous studies, the current experiment established rat models of cerebral ischemia and reperfusion injury （IRI）, and demonstrated that pathological and functional damage was also increased after IRI. The most serious damage was observed at 3 days after reperfusion, at which time microvascular density fell to its lowest level. Soon afterwards, microvascular density increased, new collateral circulation was gradually established at 4 to 7 days after reperfusion, and pathological damage and neurological deficits were improved. TGF-β1, activin receptor-like kinase 5 （ALK5） mRNA and protein expression levels increased gradually over time. In contrast, ALK1 mRNA and protein expression decreased over the same period. A significant negative correlation was detected between microvascular density and expression of the ALK5 gene transcript. There was no correlation between microvascular density and ALK1 gene transcriptional expression following cerebral IRI in a rat model. These findings suggest that ALK5, rather than ALK1, is the critical receptor in the TGF-β1 signal pathways after cerebral IRI.

Overexpression of insulin-like growth factor-Ⅰ receptor as a pertinent biomarker for hepatocytes malignant transformation

AIM:To investigate the dynamic features of insulinlike growth factor-Ⅰreceptor(IGF-ⅠR)expression in rat hepatocarcinogenesis,and the relationship between IGF-ⅠR and hepatocytes malignant transformation at mRNA or protein level.METHODS:Hepatoma models were made by inducing with 2-fluorenylacetamide(2-FAA)on male SpragueDawley rats.Morphological changes of hepatocytes were observed by pathological Hematoxylin and eosin staining,the dynamic expressions of liver and serum IGF-ⅠR were quantitatively analyzed by an enzymelinked immunosorbent assay.The distribution of hepatic IGF-ⅠR was located by immunohistochemistry.The fragments of IGF-ⅠR gene were amplified by reverse transcription-polymerase chain reaction,and confirmed by sequencing.RESULTS:Rat hepatocytes after induced by 2-FAA were changed dynamically from granule-like degeneration,precancerous to hepatoma formation with the progressing increasing of hepatic mRNA or IGF-ⅠR expression.The incidences of liver IGF-ⅠR,IGF-ⅠR mRNA,specific IGF-ⅠR concentration(ng/mg wet liver),and serum IGF-ⅠR level(ng/mL)were 0.0%,0.0%,0.63±0.17,and 1.33±0.47 in the control;50.0%,61.1%,0.65±0.2,and 1.51±0.46 in the degeneration;88.9%,100%,0.66±0.14,and 1.92±0.29 in the precancerosis;and 100%,100%,0.96±0.09,and2.43±0.57 in the cancerous group,respectively.IGF-ⅠR expression in the cancerous group was significantly higher(P<0.01)than that in any of other groups at mRNA or protein level.The closely positive IGF-ⅠR relationship was found between livers and sera(r=0.91,t=14.222,P<0.01),respectively.CONCLUSION:IGF-ⅠR expression may participate in rat hepatocarcinogenesis and its abnormality should be an early marker for hepatocytes malignant transformation.

Targeting Transforming Growth Factor-<i>β</i>(TGF-<i>β</i>) in Cancer and Non-Neoplastic Diseases

Transforming growth factor-β?(TGF-β) superfamily is a key player in the regulation of a wide variety of physiological processes from development to pathogenesis. Since the discovery of the prototypic member, TGF-β, almost three decades ago, there have been tremendous advances in our understanding of its complex biology. TGF-β?misregulation has been implicated in the pathogenesis of a variety of diseases, including cancer with a direct role in facilitating metastasis, fibrosis and inflammation. Consequently, TGF-β?is currently explored as a prognostic candidate biomarker of tumor invasiveness and metastasis;and it offers an attractive target for cancer therapy. Several anti-TGF-β?approaches, such as TGF-β?antibodies, antisense oligonucleotides and small molecules inhibitors of TGF-β?type 1 receptor kinase, have shown great promise in the preclinical studies. Here, we consider why the TGF-βsignaling pathway is a drug target, the potential clinical applications of TGF-β?inhibition, the issues arising with anti-TGF-β?therapy and how these might be adopted using personalized approaches with a special care for patient selection and timing of therapy so that we may bring forward all the potentials of targeting this pathway for therapeutic uses in both cancer, preferentially in combination therapy, and non-neoplastic diseases.

Immunohistochemical demonstration of transforming growth factor－β and bone morphogenetic protein in salivary gland tumors

Transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP)were related to embryonic development and the differentiation of many types of cells. Recent studies showed that they might play an important role in regulating the differentiation o

Expression of c-erbB-2 oncogene protein, epidermal growth factor receptor, and TGF-β1 in human pancreatic ductal adenocarcinoma

Objective: To detect the relations of c-erbB-2 onco-gene protein, epidermal growth factor receptor (EG-FR) and transforming growth factor-β1 (TGF-β1)to the progression or metastasis of pancreatic carci-noma.Methods: Using streptavidinbiotin complex (SABC)method, c-erbB-2 oncongene protein, we examinedimmunohistochemically EGFR and TGF-β1 expres-sions in wax-tissue sections from 10 individuals withnormal pancreas (NP), 13 patients with chronic pan-creatitis (CP) and 36 patients with pancreatic ductaladenocarcinoma (PC).Results: The positive expression rates of c-cerbB-2oncogene protein, EGFR and TGF-β1 in the NP, CPand PC groups were 0, 0, 10%; 7.7%, 7.7%,7.7%; and 41.7%, 50.0%, 44.4%, respectively.The positive expression rates of the three specific pro-teins increased more significantly in the PC groupthan in the NP and CP groups (P【0.05). The indi-vidual expression of c-erbB-2, EGFR and TGF-β1was not related to the age and sex of the patients aswell as the site, size and histopathological grade oftumors (P】0.05), but to the clinical stage of tumors(P【0.01). The coexpression rate of the three pro-teins was 27.8 % (10/36). This coexpression in thePC group was correlated with the histopathologicalgrades and clinical stages of tumors (P【0.01).Conclusion: Detection of c-erbB-2 oncogene protein,EGFR, and TGF-β1 expressions in pancreatic tissueis helpful to judge the malignancy, progression, andmetastasis of PC.

Influence of baicalin on the expression of receptor activator of nuclear factor-κB ligand and osteoprotegerin in human periodontal ligament cells

Objective To study the effect of baicalin on the expression of receptor activator of nuclear factor-κB ligand(RANKL)and osteoprotegerin(OPG)in cultured human periodontal ligament(HPDL)cells.Methods Small interfering RNA(siRNA)eukaryotic expression vector targeted transforming growth factor βⅡ receptor(TGF-β RⅡ)was constructed and transfected into T cells.HPDL cells with T cells transfected with siRNA or not were placed in the culture medium that had been added with lipopolysaccharide(LPS)and baicalin.The obtained solution was divided into six groups according to the components(group Ⅰ:HPDL cells+LPS+T cells transfected with siRNA1+baicalin;group Ⅱ:HPDL cells+LPS+T cells transfected with siRNA1;group Ⅲ:HPDL cells+LPS+T cells+baicalin;group Ⅳ:HPDL cells+LPS+T cells;group Ⅴ:HPDL cells+baicalin;group Ⅵ:HPDL cells)and was cultured for 48 hours.RT-PCR was used to observe the effect of baicalin on the expression of OPG-RANKL in HPDL cells.Results The ratio of RANKL/OPG in group Ⅰ was lower than that in group Ⅱ(P<0.01)and higher than that in group Ⅲ(P<0.01);The ratio of RANKL/OPG in group Ⅲ was lower than that in group Ⅳ(P<0.01);the ratio of RANKL/OPG in group Ⅳ was higher than that in group Ⅵ(P<0.01);the ratio of RANKL/OPG in group Ⅴ was lower than that in group Ⅵ(P<0.05).Conclusion ① Baicalin could decrease the ratio of RANKL/OPG in HPDL cells.② The TGF-β signaling transduction plays an important role in the effect of baicalin on the RANKL/OPG ratio in HPDL cells.③ Baicalin acts not only through TGF-β to regulate RANKL/OPG in HPDL cells,but also through other pathways.

Controlled release of transforming growth factor-beta receptor kinase inhibitor from thermosensitive Chitosan-based hydrogel Application for prevention of capsular contracture

Background Capsular contracture has become the most common complication associated with breast implant.Transforming growth factor-beta （TGF-β） is well known for a prominent role in fibrotic diseases.Due to the critical role of TGF-β in pathogenesis of capsular formation,we utilized thermosensitive C/GP hydrogel to controlled release of TGF-β receptor kinase inhibitor （SD208） and investigated their effects on capsular contracture.Methods In vitro degradation and drug release of C/GP hydrogel were performed.Twenty-four rabbits underwent subpanniculus implantation with 30 ml smooth silicone implants and were randomly divided into four groups as fellows：Group 1 received saline solution;Group 2 received SD208;Group 3 received SD208-C/GP;Group 4 received C/GP.At 8 weeks,the samples of capsular tissues were analyzed by hematoxylin and eosin and immunohistological staining.The mRNA expression of collagen Ⅲ and TGF-β1 was detected by RT-PCR assay.Results C/GP hydrogel could be applied as an ideal drug delivery vehicle which supported the controlled release of SD208.SD208-C/GP treatment showed a significant reduction in capsule thickness with fewer vessels.The histological findings confirmed that the lower amounts of inflammatory cells and fibroblasts infiltrate in SD208-C/GP group.In contrast,typical capsules with more vessel predominance were developed in control group.We did not observe the same inhibitory effect of SD208 or C/GP treatment on capsular contracture.Moreover,SD208-C/GP therapy yielded an evident down-regulation of collagen Ⅲ and TGF-β1 mRNA expression.Conclusions This study demonstrated that controlled release of TGF-β receptor kinase inhibitor from thermosensitive C/GP hydrogel could significantly prevent capsule formation after mammary implants.

EGF、TGF-α及EGFR在大鼠胃溃疡自愈过程中的表达及意义

目的 研究表皮生长因子 (EGF)、转化生长因子 α(TGF α)及表皮生长因子受体 (EGFR)在大鼠胃溃疡自愈过程中的表达及其可能的生物学意义。方法 采用乙酸注射制作溃疡动物模型 ,应用免疫组织化学方法动态研究EGF、TGF α及EGFR的定位与表达特征。结果 正常大鼠胃黏膜EGF、TGF α及EGFR均为弱阳性表达 ,EGF、TGF α定位于细胞质 ,EGFR在胞质及胞膜均有表达 ,但以后者为主 ,三者的表达部位有重叠。EGF主要集中胃腺颈部 ,TGF α、EGFR在胃腺颈部、基底部都有表达。阳性表达以胃黏膜的壁细胞、颈部细胞为主。取材组在溃疡自愈过程中EGF、TGF α及EGFR的表达发生了明显的规律性的变化 ,溃疡旁组织表达比正常组织高 ,坏死组织无表达 ,肉芽组织、瘢痕组织少有表达 ,溃疡的早期表达不明显 ,溃疡的愈合期及瘢痕期表达明显。结论 ①在正常情况下TGF α/EGFR自分泌系统对维护大鼠黏膜完整性可能起主导作用 ;②溃疡在自愈过程中EGF/EGFR和TGF α/EGFR自分泌系统可能对细胞增殖、分化。

转化生长因子β1及其受体在着床期小鼠子宫内膜中的免疫组织化学研究

目的 进一步证实转化生长因子 β1(transforming growth factorβ1,TGFβ1)在胚泡着床过程中的生物学作用。 方法 利用昆明小鼠 ,在着床前后不同时期取材 ,通过改良的免疫组织化学方法 ,检测了 TGFβ1及其受体 (TGFR1)在子宫内膜中的表达状况。 结果 受精后第 4d,子宫内膜表面上皮和腺上皮细胞中 TGFβ1及其受体均较未孕期增加 ,成纤维细胞周围的细胞外基质 (extracellular matrix,ECM)也呈 TGFβ1阳性着色。受精后第 5、6 d,TGFβ1及其受体主要表达于初级蜕膜带 (prim ary decidual zone,PDZ)。随着胚泡植入的深入 ,TGFβ1及其受体广泛分布于蜕膜细胞。 结论 TGFβ1及其受体的表达与胚泡植入过程密切相关。

TGF-β1及其受体在不孕患者粘连、闭锁输卵管伞部的表达及意义

目的初步探讨转化生长因子-β1(TGF-β1)在输卵管伞粘连发病机制中的作用及意义。方法应用免疫组化SP法检测TGF-β1及其受体在粘连组(30例)与不粘连组(15例)的分布与定位,用Image-ProPlus6.0图像分析系统对其进行定量分析。结果TGF-β1、TGF-βR1、TGF-βR2主要在输卵管上皮细胞表达,成纤维细胞和血管内皮细胞中也有表达,这3种因子在粘连组的表达均高于不粘连组(P<0.05),粘连组中TGF-β1与TGF-βR1、TGF-βR2的表达呈正相关(P<0.05),TGF-βR1与TGF-βR2的表达无相关性。不粘连组3个因子间均无相关性。结论TGF-β1信号系统可能在不孕患者输卵管伞粘连的发生过程中起促进作用。

转化生长因子β1及其受体在横纹肌肉瘤中的表达

目的 :探讨横纹肌肉瘤 (RMS)中转化生长因子 β1(TGFβ1)及其Ⅰ、Ⅱ型受体 (TGFβRⅠ ,TGFβRⅡ )表达及其意义。 方法 :应用免疫组化技术 (S P法 )检测 4 9例经电镜或 (和 )免疫组化证实的横纹肌肉瘤及 2 0例正常横纹肌组织中的TGFβ1、TGFβRⅠ和TGFβRⅡ表达水平 ,并结合临床病理资料进行分析。 结果 :TGFβ1在RMS中的高表达率高于正常横纹肌组织 (P<0 0 1) ;TGFβRⅠ、TGFβRⅡ在 98% (48/ 4 9)的RMS及所有正常横纹肌组织中均有表达 ,两组无差异。TGFβ1表达与肌球蛋白重链呈负相关 (r=- 0 6 6 1,P <0 0 1)。TGFβ1在低分化组高表达率为 79% ,高分化组为 38%。 结论 :横纹肌肉瘤中存在TGFβ1自分泌和旁分泌现象 ,且肿瘤细胞表达相关受体。TGFβ1的表达与肌源性分化程度有关。

TGF-βRⅡ和Smad4蛋白在葡萄膜黑色素瘤中的表达

目的研究转化生长因子Ⅱ型受体(TGFβRⅡ)及其下游的抑癌基因Smad4蛋白在葡萄膜黑色素瘤中的表达。方法应用免疫组织化学SP法对24例葡萄膜黑色素瘤瘤组织中TGFβRⅡ和Smad4蛋白的表达进行检测。结果在24例葡萄膜黑色素瘤组织切片中,可见瘤细胞TGFβRⅡ阳性12例(50%),Smad4阳性11例(45.8%),两者均阳性5例,两者均阴性6例。结论葡萄膜黑色素瘤组织中存在TGFβRⅡ和/或Smad4的蛋白表达异常,可能与葡萄膜黑色素瘤的发病有关。

整合素和TGF-β受体在增生性瘢痕成纤维细胞中的表达研究

目的 了解增生性瘢痕成纤维细胞表面整合素α1-3、αv、β1和转化生长因子β(TGF-β)受体1分布的情况及相互关系。方法 采用免疫组化染色的方法,观察10例人体增生性瘢痕和10例正常人皮肤组织成纤维细胞表面各整合素亚单位和TGF-β受体I表达的差异,以了解两者间的相关程度。结果 增生性瘢痕成纤维细胞表面整合素α1-3、αv、β1和TGF-β受体I的表达均明显高于正常对照组(P<0.01),其中以整合素α1、α3和β1的表达更为显著。增生性瘢痕成纤维细胞表面各整合素亚单位(除了α2以外)与TGF-β受体I在表达强度上呈正相关(P<0.05)。结论 增生性瘢痕成纤维细胞表面各整合素亚单位的高度表达是瘢痕产生与发展的重要因素之一;TGF-β受体I的高度表达提示增生性瘢痕成纤维细胞对于TGF-β的高反应性;整合素与TGF-β受体I在瘢痕形成过程中相互影响。

转化生长因子-β受体Ⅱ在增生性玻璃体视网膜病变增生膜中的表达

目的:观察及评估转化生长因子-β受体Ⅱ(TGF-βRⅡ)在增生性玻璃体视网膜病变(PVR)增生膜中的表达及临床意义。 方法:采用免疫组化和原位杂交方法,对13例PVR患者行玻璃体手术增生膜获得的16例进行TGF-βRⅡ的蛋白和mRNA的检测。 结果:免疫组化结果为:9例C2～C3级膜中,染色反应为阳性的有8例,总阳性率为88.9％。7例D1～D3级膜中有6例为阳性,总阳性率为85.7％。阳性细胞多是一类胞体为长圆形,胞核呈圆形或卵圆形的上皮样细胞。统计学分析TGF-βRⅡ标记与膜分级间无相关性(P>0.05)。原位杂交结果与免疫组化基本一致。 结论:PVR发生过程中视网膜色素上皮细胞在生长因子等的刺激下,TGF-βRⅡ表达显著上调,表明了TGF-β参与PVR增生膜的形成。眼科学报 2003;19:244-247。

α-转化生长因子及其受体在人原发性肝细胞肝癌中的表达意义

目的 探讨α－ 转化生长因子（ ＴＧＦα） 及其受体———表皮生长因子受体（ＥＧＦＲ） 在人原发性肝细胞肝癌（ ＨＣＣ） 组织蛋白和分子水平上的表达及意义．方法 运用免疫组织化学和原位杂交方法对７０ 例ＨＣＣ 进行研究，并采用５ 例正常人类肝脏做为对照．结果 ①７０ 例ＨＣＣ 中ＴＧＦ－ α的阳性率为７４－３ ％ ；ＥＧＦＲ 的阳性率为３８－６ ％ ． ②ＴＧＦα与 ＨＣＣ 的分化程度有关（ Ｐ ＜０－０５） ，在高分化ＨＣＣ 中ＴＧＦα的阳性率明显高于低分化的ＨＣＣ． ③有９３－６ ％ 的ＥＧＦＲ 阳性组织同时表现为ＴＧＦα阳性，二者的表达在 ＨＣＣ 组织中呈显著正相关（ Ｐ＜ ０－０５ ，γ＝ ０－４０） ． ④在 ＨＣＣ 癌旁组织中，ＴＧＦ － α的阳性率为８８－１ ％ ，ＥＧＦＲ 的阳性率为５４－２ ％ ，与其在ＨＣＣ 组织中相比，无显著差异（ Ｐ ＞ ０－０５ ） ，ＴＧＦα与 ＥＧＦＲ 呈显著正相关（ Ｐ＜ ０－０５ ，γ＝ ０－３５） ． ⑤ＴＧＦα与ＥＧＦＲ 的原位杂交结果略高于免疫组织化学结果，但二者之间无显著差异（ Ｐ＞ ０－０５） ．结论 ＴＧＦα，ＥＧＦＲ 可能与ＨＣＣ 的发生有关，在ＨＣＣ 发生中可能存在ＴＧＦα的自?

肝外胆管癌中TGF-β_1,TGF-β_2,TGF-βRI和TGF-βRⅡ的表达及意义

目的 探讨 TGF- β1 ,TGF- β2 ,TGF- βR 及 TGF- βR 在肝外胆管癌中的表达及其与肿瘤的临床分期、病理分级的关系 .方法 用抗 TGF-β1 ,TGF-β2 ,TGF-βR 及 TGF-βR 的多克隆抗体 ,进行免疫组化染色 ,分别检测 38例肝外胆管癌、14例非肿瘤胆管组织 (8例胆总管囊肿、6例正常胆管 )中 TGF- β1 ,TGF- β2 ,TGF- βR 及 TGF- βR 的表达 .结果 1TGF-β1 及 TGF-β2 的阳性表达率增高 (94.75 %与92 .11%) ;TGF-βRI及 TGF-βR 的阳性表达率明显降低(31.5 8%与 2 8.95 %) .2 TGF-βRI,TGF-βR 的阳性表达率在转移组中明显低于未转移组 (12 .5 %,14.2 9%,33.33%对 6 6 .6 7%及 18.75 %,14.2 9%,0对 5 8.33%) .结论 TGF- β1 ,TGF- β2 ,TGF- βRI及 TGF- βR 在肝外胆管癌中的异常表达 ,提示它们在肝外胆管癌的发生中起着重要作用 ,对其进行检测可作为肝外胆管癌的辅助诊断参考指标之一 ,并可为肝外胆管癌自然病程的判断和治疗方法的选择提供部分依据 .

表皮生长因子受体和转化生长因子β1在慢性鼻窦炎黏膜上皮的表达

目的观察表皮生长因子受体(epidermal growth factor receptor,EGFR)和转化生长因子β1(transforming growth factor-β1,TGF-β1)在慢性鼻窦炎患者鼻窦黏膜上皮的表达及分布,探讨EGFR和TGF-β1在慢性鼻窦炎发生发展中的作用。方法选取鼻内镜手术患者30例,实验组慢性鼻窦炎伴/不伴鼻息肉组各10例,对照组为10例无鼻窦炎症接受经鼻手术患者。所有患者均于术中取钩突黏膜置于10%福尔马林中固定,应用HE染色方法和免疫组织化学方法,分别观察EGFR和TGF-β1在两组鼻窦黏膜上皮的表达情况。结果对照组和实验组鼻窦黏膜上皮内EGFR和TGF-β1均有表达,EGFR在实验组两组鼻窦黏膜上皮内的表达均显著高于对照组(P<0.05),EGFR在实验组两组鼻窦黏膜上皮内的表达无显著性差异(P>0.05);TGF-β1在实验组两组鼻窦黏膜上皮内的表达显著高于对照组(P<0.05),TGF-β1在实验组鼻窦炎不伴鼻息肉组鼻窦黏膜上皮内的表达显著高于鼻窦炎伴鼻息肉组(P<0.05)。结论 EGFR和TGF-β1在鼻窦炎伴/不伴鼻息肉患者鼻窦黏膜中的异常表达可能与慢性鼻窦炎的发生、发展有关。

细支气管肺泡细胞增生和细支气管肺泡细胞癌内生长因子和蛋白激酶C的表达

表皮生长因子（ＥＧＦ）、转化生长因子－α（ＴＧＦα）、表皮生长因子受体（ＥＧＦＲ）和蛋白激酶Ｃ（ＰＫＣ）与细胞生长、增殖分化调节和细胞癌变有密切关系。作者用免疫组织化学方法检测了细支气管肺泡细胞增生（ＢＡＨ）和细支气管肺泡细胞癌（ＢＡＣ）的ＥＧＦ、ＴＧＦα、ＥＧＦＲ和ＰＫＣ表达。结果表明：ＢＡＣ中的ＥＧＦ、ＴＧＦα阳性率和阳性强度以及ＥＧＦＲ、ＰＫＣ阳性强度均明显高于ＢＡＨ。ＢＡＨ的重度不典型增生病例，其ＥＧＦ、ＴＧＦα、ＥＧＦＲ和ＰＫＣ均呈高表达。ＴＧＦα、ＥＧＦＲ和ＰＫＣ三者在ＢＡＣ和ＢＡＨ中的表达存在明显相关性。提示：ＴＧＦα及其受体ＥＧＦＲ和ＰＫＣ是细支气管肺泡细胞增生、恶性转化和肺泡癌细胞失控生长的重要因素。

增生性瘢痕不同时期TGF β_1及其受体的表达

目的：研究ＴＧＦ－β１及其受体ＴＧＦ－βＲⅠ在烧伤后增生性瘢痕不同时期的表达．方法：免疫组化ＡＢＣ法．结果：在正常真皮成纤维细胞中ＴＧＦ－β１及ＴＧＦ－βＲⅠ未检测到阳性表达；增生期的增生性瘢痕的真皮中ＴＧＦ－β１及ＴＧＦ－βＲⅠ在相同的成纤维细胞亚群中高表达，而萎缩期的增生性瘢痕中两者表达均为阴性．结论：提示增生性瘢痕的形成与成纤维细胞对ＴＧＦ－β１的反应性增高有关，同时也与伤口愈合高表达ＴＧＦ－βＲⅠ的成纤维细胞亚群不能及时发生凋亡有关．