中华眼底病杂志
中華眼底病雜誌
중화안저병잡지
Chinese Journal of Ocular Fundus Diseases
2015年
5期
462-466
,共5页
玻璃体视网膜病,增生性/病理生理学%HSP47热休克蛋白质类%转化生长因子β2
玻璃體視網膜病,增生性/病理生理學%HSP47熱休剋蛋白質類%轉化生長因子β2
파리체시망막병,증생성/병리생이학%HSP47열휴극단백질류%전화생장인자β2
Vitreoretinopathy,proliferative/physiopathology%HSP47 heat-shock proteins%Transforming growth factor beta2
目的 观察探讨热休克蛋白(HSP)47和转化生长因子(TGF)-β2在增生性玻璃体视网膜疾病患眼玻璃体组织与视网膜前增生膜组织中的表达及其意义.方法 临床确诊为增生性玻璃体视网膜病变(PVR)的48例48只眼及增生型糖尿病视网膜病变(PDR)的50例50只眼纳入研究.同时纳入特发性黄斑裂孔(IMH)患者20例20只眼作为对照.收集患眼玻璃体及PVR、PDR患眼视网膜前增生膜、IMH患眼内界膜组织.采用酶联免疫吸附测定法检测所有患眼玻璃体组织中HSP47、TGF-β2的表达;免疫组织化学染色观察PVR、PDR患眼视网膜前增生膜以及IMH患眼内界膜组织中HSP47、TGF-β2及Ⅰ、Ⅲ型胶原蛋白的表达.分析PVR、PDR患眼视网膜前增生膜组织中HSP47阳性表达与TGF-β2和Ⅰ、Ⅲ型胶原蛋白阳性表达之间的相关性.结果 PVR、PDR、IMH患眼玻璃体组织中HSP47表达分别为(212.35±23.32)、(231.30±26.79)、(171.06±28.91) pg/ml;TGF-β2表达分别为(1 919.96土318.55)、(1 939.39±177.57)、(1 194.61±234.20) pg/ml.与IMH患眼比较,PVR、PDR患眼玻璃体组织中HSP47、TGF-β2表达明显增强,差异有统计学意义(F=12.952、34.532,P＜0.01).PVR、PDR患眼视网膜前增生膜组织中HSP47、TGF-β2及Ⅰ、Ⅲ型胶原蛋白均呈强阳性表达,HSP47、TGF-β2表达在细胞浆及细胞间质中,Ⅰ、Ⅲ型胶原蛋白表达在细胞浆及细胞外基质中.IMH患眼内界膜组织中HSP47及Ⅲ型胶原蛋白表达呈阴性,TGF-β2表达呈弱阳性,Ⅰ型胶原蛋白表达呈阳性.PVR、PDR患眼视网膜前增生膜组织中HSP47、TGF-β2及Ⅰ、Ⅲ型胶原蛋白表达较IMH患眼明显提高,差异有统计学意义(F=13.469、18.752、12.875、20.358,P＜0.01).PVR(r=0.475、0.556、0.468)、PDR(r=0.484、0.589、0.512)患眼视网膜前增生膜组织中HSP47阳性表达与TGF-β2和Ⅰ、Ⅲ型胶原蛋白阳性表达均呈正相关(P＜0.05).结论 HSP47、TGF-β2在PVR、PDR患眼玻璃体及视网膜前增生膜组织中表达增强;其表达部位均在细胞浆及细胞外间质中.HSP47和TGF-β2可能通过促进胶原蛋白合成参与PVR与PDR的病理过程.
目的 觀察探討熱休剋蛋白(HSP)47和轉化生長因子(TGF)-β2在增生性玻璃體視網膜疾病患眼玻璃體組織與視網膜前增生膜組織中的錶達及其意義.方法 臨床確診為增生性玻璃體視網膜病變(PVR)的48例48隻眼及增生型糖尿病視網膜病變(PDR)的50例50隻眼納入研究.同時納入特髮性黃斑裂孔(IMH)患者20例20隻眼作為對照.收集患眼玻璃體及PVR、PDR患眼視網膜前增生膜、IMH患眼內界膜組織.採用酶聯免疫吸附測定法檢測所有患眼玻璃體組織中HSP47、TGF-β2的錶達;免疫組織化學染色觀察PVR、PDR患眼視網膜前增生膜以及IMH患眼內界膜組織中HSP47、TGF-β2及Ⅰ、Ⅲ型膠原蛋白的錶達.分析PVR、PDR患眼視網膜前增生膜組織中HSP47暘性錶達與TGF-β2和Ⅰ、Ⅲ型膠原蛋白暘性錶達之間的相關性.結果 PVR、PDR、IMH患眼玻璃體組織中HSP47錶達分彆為(212.35±23.32)、(231.30±26.79)、(171.06±28.91) pg/ml;TGF-β2錶達分彆為(1 919.96土318.55)、(1 939.39±177.57)、(1 194.61±234.20) pg/ml.與IMH患眼比較,PVR、PDR患眼玻璃體組織中HSP47、TGF-β2錶達明顯增彊,差異有統計學意義(F=12.952、34.532,P＜0.01).PVR、PDR患眼視網膜前增生膜組織中HSP47、TGF-β2及Ⅰ、Ⅲ型膠原蛋白均呈彊暘性錶達,HSP47、TGF-β2錶達在細胞漿及細胞間質中,Ⅰ、Ⅲ型膠原蛋白錶達在細胞漿及細胞外基質中.IMH患眼內界膜組織中HSP47及Ⅲ型膠原蛋白錶達呈陰性,TGF-β2錶達呈弱暘性,Ⅰ型膠原蛋白錶達呈暘性.PVR、PDR患眼視網膜前增生膜組織中HSP47、TGF-β2及Ⅰ、Ⅲ型膠原蛋白錶達較IMH患眼明顯提高,差異有統計學意義(F=13.469、18.752、12.875、20.358,P＜0.01).PVR(r=0.475、0.556、0.468)、PDR(r=0.484、0.589、0.512)患眼視網膜前增生膜組織中HSP47暘性錶達與TGF-β2和Ⅰ、Ⅲ型膠原蛋白暘性錶達均呈正相關(P＜0.05).結論 HSP47、TGF-β2在PVR、PDR患眼玻璃體及視網膜前增生膜組織中錶達增彊;其錶達部位均在細胞漿及細胞外間質中.HSP47和TGF-β2可能通過促進膠原蛋白閤成參與PVR與PDR的病理過程.
목적 관찰탐토열휴극단백(HSP)47화전화생장인자(TGF)-β2재증생성파리체시망막질병환안파리체조직여시망막전증생막조직중적표체급기의의.방법 림상학진위증생성파리체시망막병변(PVR)적48례48지안급증생형당뇨병시망막병변(PDR)적50례50지안납입연구.동시납입특발성황반렬공(IMH)환자20례20지안작위대조.수집환안파리체급PVR、PDR환안시망막전증생막、IMH환안내계막조직.채용매련면역흡부측정법검측소유환안파리체조직중HSP47、TGF-β2적표체;면역조직화학염색관찰PVR、PDR환안시망막전증생막이급IMH환안내계막조직중HSP47、TGF-β2급Ⅰ、Ⅲ형효원단백적표체.분석PVR、PDR환안시망막전증생막조직중HSP47양성표체여TGF-β2화Ⅰ、Ⅲ형효원단백양성표체지간적상관성.결과 PVR、PDR、IMH환안파리체조직중HSP47표체분별위(212.35±23.32)、(231.30±26.79)、(171.06±28.91) pg/ml;TGF-β2표체분별위(1 919.96토318.55)、(1 939.39±177.57)、(1 194.61±234.20) pg/ml.여IMH환안비교,PVR、PDR환안파리체조직중HSP47、TGF-β2표체명현증강,차이유통계학의의(F=12.952、34.532,P＜0.01).PVR、PDR환안시망막전증생막조직중HSP47、TGF-β2급Ⅰ、Ⅲ형효원단백균정강양성표체,HSP47、TGF-β2표체재세포장급세포간질중,Ⅰ、Ⅲ형효원단백표체재세포장급세포외기질중.IMH환안내계막조직중HSP47급Ⅲ형효원단백표체정음성,TGF-β2표체정약양성,Ⅰ형효원단백표체정양성.PVR、PDR환안시망막전증생막조직중HSP47、TGF-β2급Ⅰ、Ⅲ형효원단백표체교IMH환안명현제고,차이유통계학의의(F=13.469、18.752、12.875、20.358,P＜0.01).PVR(r=0.475、0.556、0.468)、PDR(r=0.484、0.589、0.512)환안시망막전증생막조직중HSP47양성표체여TGF-β2화Ⅰ、Ⅲ형효원단백양성표체균정정상관(P＜0.05).결론 HSP47、TGF-β2재PVR、PDR환안파리체급시망막전증생막조직중표체증강;기표체부위균재세포장급세포외간질중.HSP47화TGF-β2가능통과촉진효원단백합성삼여PVR여PDR적병리과정.
Objective To observe the expression of heat shock protein 47 (HSP47) and transforming growth factor-β2 (TGF-β2) in vitreous specimens and epiretinal membranes of patients with proliferative vitreoretinopathy diseases.Methods Vitreous specimens and epiretinal membranes were obtained from 48 patients (48 eyes) with proliferative vitreoretinopathy (PVR) and 50 patients (50 eyes) with proliferative diabetic retinopathy (PDR).Vitreous specimens and internal limiting membranes were collected from 20 patients (20 eyes) with idiopathic macular hole (IMH) as control group.The expression of HSP47 and TGF-β2 in the vitreous specimens was evaluated using enzyme linked immunosorbent assay.The expression of HSP47,TGF-β2,types Ⅰ and Ⅲ collagen in epiretinal membrane and internal limiting membrane specimens were observed for immunohistochemical staining method.The correlation between the positive expression of HSP47 and TGF-β2,types Ⅰ and Ⅲ collagen in epiretinal membrane specimens of patients with PVR and PDR were analyzed.Results The expression of HSP47 in vitreous specimens of patients with PVR,PDR and IMH were (212.35±23.32),(231.30±26.79),(171.06±28.91) pg/ml,respectively.The expression of TGF β2 in vitreous specimens of patients with PVR,PDR and IMH were (1919.96 ± 318.55),(1939.39 ± 177.57),(1194.61 ± 234.20) pg/ml,respectively.The expression of HSP47,TGF-β2 in the vitreous specimens of patients with PVR and PDR were significantly increased compared with patients with IMH and the difference was statistically significant (F=12.952,34.532;P＜0.01).The epiretinal membrane of patients with PVR and PDR showed markedly increased expression of HSP47,TGF β2,types Ⅰ and Ⅲ collagen in the cytoplasm and extracellular matrix.The expression of HSP47 and type Ⅲ collagen was negative and the expression of TGF-β2 was weakly positive and the expression of types Ⅰ collagen was positive in internal limiting membrane of patients with IMH.The expression of HSP47,TGF β2,types Ⅰ and Ⅲ collagen in the epiretinal membrane of patients with PVR and PDR were significantly increased compared with patients with IMH and the difference was statistically significant (F=13.469,18.752,12.875,20.358;P＜0.01).The expression of HSP47 was positively correlated with thepositive expression of TGF-~,types Ⅰ and Ⅲ collagen in epiretinal membrane specimens of patients withPVR (r=0.475,0.556,0.468;P＜0.05) and PDR (r=0.484,0.589,0.512;P＜0.05).Conclusions This study showed increased consistent expression of HSP47 and TGF-β2 in vitreous and epiretinal membrane specimens of patients with PVR and PDR.Both HSP47 and TGF-β2 were expressed in the cytoplasm and extracellular matrix.HSP47 and TGF-β2 may be involved in the pathological process of PDR and PVR by promoting collagen synthesis.
